Datasets:
vgainullin
/
xciting_data

Dataset card Data Studio Files
xet
 Community
1
paragraph_index
int64
sec
string
p_has_citation
int64
cites
string
citeids
list
pmid
int64
cited_id
string
sentences
string
all_sent_cites
list
sent_len
int64
sentence_batch_index
int64
sent_has_citation
float64
qc_fail
bool
cited_sentence
string
cites_in_sentence
list
cln_sentence
string
is_cap
bool
is_alpha
bool
ends_wp
bool
cit_qc
bool
lgtm
bool
__index_level_0__
int64
1
INTRODUCTION
1
8
[ "b8", "b10", "b5", "b11", "b12", "b13", "b14", "b17" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Due to the defect in the DNA-PK dependent pathway (D-NHEJ), end joining must be carried out in these mutants by an alternative process prone to missjoining and possibly utilizing microhomologies (8–10).
[ "8", "10", "5", "11", "12", "13", "14", "17" ]
202
11,500
0
false
Due to the defect in the DNA-PK dependent pathway (D-NHEJ), end joining must be carried out in these mutants by an alternative process prone to missjoining and possibly utilizing microhomologies.
[ "8–10" ]
Due to the defect in the DNA-PK dependent pathway (D-NHEJ), end joining must be carried out in these mutants by an alternative process prone to missjoining and possibly utilizing microhomologies.
true
true
true
true
true
1,840
1
INTRODUCTION
1
13
[ "b8", "b10", "b5", "b11", "b12", "b13", "b14", "b17" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Alternative pathways of end joining are also implicated in genomic instability (5,11,12), in the formation of soft tissue sarcomas (13) and in the aberrant coding and signal joints formed during V(D)J recombination (14–17) in NHEJ mutant mice.
[ "8", "10", "5", "11", "12", "13", "14", "17" ]
243
11,501
1
false
Alternative pathways of end joining are also implicated in genomic instability, in the formation of soft tissue sarcomas and in the aberrant coding and signal joints formed during V(D)J recombination in NHEJ mutant mice.
[ "5,11,12", "13", "14–17" ]
Alternative pathways of end joining are also implicated in genomic instability, in the formation of soft tissue sarcomas and in the aberrant coding and signal joints formed during V(D)J recombination in NHEJ mutant mice.
true
true
true
true
true
1,840
2
INTRODUCTION
1
18
[ "b18", "b20", "b20" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
Furthermore, alternative forms of end joining operate in the repair of IR-induced DSBs.
[ "18", "20", "20" ]
87
11,502
0
false
Furthermore, alternative forms of end joining operate in the repair of IR-induced DSBs.
[]
Furthermore, alternative forms of end joining operate in the repair of IR-induced DSBs.
true
true
true
true
true
1,841
2
INTRODUCTION
1
18
[ "b18", "b20", "b20" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
Mutants with defects in NHEJ show pronounced inhibition but still rejoin the majority of DSBs by a slowly operating pathway (18–20).
[ "18", "20", "20" ]
132
11,503
0
false
Mutants with defects in NHEJ show pronounced inhibition but still rejoin the majority of DSBs by a slowly operating pathway.
[ "18–20" ]
Mutants with defects in NHEJ show pronounced inhibition but still rejoin the majority of DSBs by a slowly operating pathway.
true
true
true
true
true
1,841
2
INTRODUCTION
1
20
[ "b18", "b20", "b20" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
Because this repair pathway does not show dependence on genes of HRR (20), it is thought to reflect an alternative form of end joining that functions as backup (B-NHEJ) to the DNA-PK dependent pathway (D-NHEJ).
[ "18", "20", "20" ]
210
11,504
1
false
Because this repair pathway does not show dependence on genes of HRR, it is thought to reflect an alternative form of end joining that functions as backup (B-NHEJ) to the DNA-PK dependent pathway (D-NHEJ).
[ "20" ]
Because this repair pathway does not show dependence on genes of HRR, it is thought to reflect an alternative form of end joining that functions as backup (B-NHEJ) to the DNA-PK dependent pathway (D-NHEJ).
true
true
true
true
true
1,841
3
INTRODUCTION
1
8
[ "b8", "b9" ]
17,088,286
pmid-12110179|pmid-11870614|pmid-9308963|pmid-11359911|pmid-11432840
These results implicate alternative pathways of end joining in genomic integrity through contributions to DSB repair, particularly when D-NHEJ is compromised.
[ "8", "9" ]
158
11,505
0
false
These results implicate alternative pathways of end joining in genomic integrity through contributions to DSB repair, particularly when D-NHEJ is compromised.
[]
These results implicate alternative pathways of end joining in genomic integrity through contributions to DSB repair, particularly when D-NHEJ is compromised.
true
true
true
true
true
1,842
3
INTRODUCTION
1
8
[ "b8", "b9" ]
17,088,286
pmid-12110179|pmid-11870614|pmid-9308963|pmid-11359911|pmid-11432840
However, due to their low fidelity, the same repair pathways are directly implicated in genomic instability and cancer.
[ "8", "9" ]
119
11,506
0
false
However, due to their low fidelity, the same repair pathways are directly implicated in genomic instability and cancer.
[]
However, due to their low fidelity, the same repair pathways are directly implicated in genomic instability and cancer.
true
true
true
true
true
1,842
3
INTRODUCTION
1
8
[ "b8", "b9" ]
17,088,286
pmid-12110179|pmid-11870614|pmid-9308963|pmid-11359911|pmid-11432840
Despite the potentially grave consequences of their functions, little is known about the biochemistry of these pathways, as well as the mechanisms of their regulation and integration into the cellular DNA DSB processing machinery, beyond the observation that they frequently utilize microhomologies (8,9).
[ "8", "9" ]
305
11,507
0
false
Despite the potentially grave consequences of their functions, little is known about the biochemistry of these pathways, as well as the mechanisms of their regulation and integration into the cellular DNA DSB processing machinery, beyond the observation that they frequently utilize microhomologies.
[ "8,9" ]
Despite the potentially grave consequences of their functions, little is known about the biochemistry of these pathways, as well as the mechanisms of their regulation and integration into the cellular DNA DSB processing machinery, beyond the observation that they frequently utilize microhomologies.
true
true
true
true
true
1,842
4
INTRODUCTION
1
22
[ "b21", "b22", "b22", "b23", "b25" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
Recent work identifies DNA ligase III as a candidate factor in alternative pathways of NHEJ (21,22) and points to PARP-1 as an additional potential contributor (22).
[ "21", "22", "22", "23", "25" ]
165
11,508
1
false
Recent work identifies DNA ligase III as a candidate factor in alternative pathways of NHEJ and points to PARP-1 as an additional potential contributor.
[ "21,22", "22" ]
Recent work identifies DNA ligase III as a candidate factor in alternative pathways of NHEJ and points to PARP-1 as an additional potential contributor.
true
true
true
true
true
1,843
4
INTRODUCTION
1
21
[ "b21", "b22", "b22", "b23", "b25" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
PARP-1 is an abundant nuclear enzyme of higher eukaryotes that has been implicated in many cellular processes including DNA repair.
[ "21", "22", "22", "23", "25" ]
131
11,509
0
false
PARP-1 is an abundant nuclear enzyme of higher eukaryotes that has been implicated in many cellular processes including DNA repair.
[]
PARP-1 is an abundant nuclear enzyme of higher eukaryotes that has been implicated in many cellular processes including DNA repair.
true
true
true
true
true
1,843
4
INTRODUCTION
1
21
[ "b21", "b22", "b22", "b23", "b25" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
It is a member of a superfamily of eighteen proteins containing PARP domains, of which only PARP-2 has also been implicated in DNA damage response (23–25).
[ "21", "22", "22", "23", "25" ]
155
11,510
0
false
It is a member of a superfamily of eighteen proteins containing PARP domains, of which only PARP-2 has also been implicated in DNA damage response.
[ "23–25" ]
It is a member of a superfamily of eighteen proteins containing PARP domains, of which only PARP-2 has also been implicated in DNA damage response.
true
true
true
true
true
1,843
4
INTRODUCTION
1
21
[ "b21", "b22", "b22", "b23", "b25" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
The 116 kDa PARP-1 has two zinc finger motifs that mediate binding to single strand breaks (SSBs) and DSBs.
[ "21", "22", "22", "23", "25" ]
107
11,511
0
false
The 116 kDa PARP-1 has two zinc finger motifs that mediate binding to single strand breaks (SSBs) and DSBs.
[]
The 116 kDa PARP-1 has two zinc finger motifs that mediate binding to single strand breaks (SSBs) and DSBs.
true
true
true
true
true
1,843
4
INTRODUCTION
1
21
[ "b21", "b22", "b22", "b23", "b25" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
This binding enables the protein to cleave NAD+ to nicotinamide and ADP-ribose and to form branched ADP-ribose polymers on glutamic acid residues of target proteins, including itself.
[ "21", "22", "22", "23", "25" ]
183
11,512
0
false
This binding enables the protein to cleave NAD+ to nicotinamide and ADP-ribose and to form branched ADP-ribose polymers on glutamic acid residues of target proteins, including itself.
[]
This binding enables the protein to cleave NAD+ to nicotinamide and ADP-ribose and to form branched ADP-ribose polymers on glutamic acid residues of target proteins, including itself.
true
true
true
true
true
1,843
5
INTRODUCTION
1
26
[ "b26", "b27", "b28", "b29", "b30", "b33", "b23", "b34", "b35" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
PARP-1 is involved in SSB repair, BER or NER, together with XRCC1, DNA ligase III, as well as polynucleotide kinase (PNK), PCNA and FEN1 (26,27) and plays an essential role in removing lesions converted to DSBs during DNA replication (28,29).
[ "26", "27", "28", "29", "30", "33", "23", "34", "35" ]
242
11,513
0
false
PARP-1 is involved in SSB repair, BER or NER, together with XRCC1, DNA ligase III, as well as polynucleotide kinase (PNK), PCNA and FEN1 and plays an essential role in removing lesions converted to DSBs during DNA replication.
[ "26,27", "28,29" ]
PARP-1 is involved in SSB repair, BER or NER, together with XRCC1, DNA ligase III, as well as polynucleotide kinase (PNK), PCNA and FEN1 and plays an essential role in removing lesions converted to DSBs during DNA replication.
true
true
true
true
true
1,844
5
INTRODUCTION
1
26
[ "b26", "b27", "b28", "b29", "b30", "b33", "b23", "b34", "b35" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
Although PARP-1 is implicated in DSB repair (30–33) the results are variable and the mechanism unknown (23,34,35).
[ "26", "27", "28", "29", "30", "33", "23", "34", "35" ]
114
11,514
0
false
Although PARP-1 is implicated in DSB repair the results are variable and the mechanism unknown.
[ "30–33", "23,34,35" ]
Although PARP-1 is implicated in DSB repair the results are variable and the mechanism unknown.
true
true
true
true
true
1,844
5
INTRODUCTION
1
26
[ "b26", "b27", "b28", "b29", "b30", "b33", "b23", "b34", "b35" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
Here, we present experiments demonstrating that PARP-1 contributes to DSB repair as a component of an alternative pathway of NHEJ.
[ "26", "27", "28", "29", "30", "33", "23", "34", "35" ]
130
11,515
0
false
Here, we present experiments demonstrating that PARP-1 contributes to DSB repair as a component of an alternative pathway of NHEJ.
[]
Here, we present experiments demonstrating that PARP-1 contributes to DSB repair as a component of an alternative pathway of NHEJ.
true
true
true
true
true
1,844
0
DISCUSSION
1
21
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
Taken together the results presented identify PARP-1 as a component of an alternative pathway of NHEJ and provide evidence that DNA end binding, in direct competition with Ku, is a key determinant of pathway selection.
[ "21", "22", "22", "52", "53", "54" ]
218
11,516
0
false
Taken together the results presented identify PARP-1 as a component of an alternative pathway of NHEJ and provide evidence that DNA end binding, in direct competition with Ku, is a key determinant of pathway selection.
[]
Taken together the results presented identify PARP-1 as a component of an alternative pathway of NHEJ and provide evidence that DNA end binding, in direct competition with Ku, is a key determinant of pathway selection.
true
true
true
true
true
1,845
0
DISCUSSION
1
21
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
Additional data provide biochemical evidence for an engagement of DNA ligase III, a known partner of PARP-1, in DSB repair (21,22).
[ "21", "22", "22", "52", "53", "54" ]
131
11,517
0
false
Additional data provide biochemical evidence for an engagement of DNA ligase III, a known partner of PARP-1, in DSB repair.
[ "21,22" ]
Additional data provide biochemical evidence for an engagement of DNA ligase III, a known partner of PARP-1, in DSB repair.
true
true
true
true
true
1,845
0
DISCUSSION
1
21
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
In a directly relevant biochemical study using a novel two-step in vitro DNA end joining assay, immune to interference by Ku, Audebert et al.
[ "21", "22", "22", "52", "53", "54" ]
141
11,518
0
false
In a directly relevant biochemical study using a novel two-step in vitro DNA end joining assay, immune to interference by Ku, Audebert et al.
[]
In a directly relevant biochemical study using a novel two-step in vitro DNA end joining assay, immune to interference by Ku, Audebert et al.
true
true
true
true
true
1,845
0
DISCUSSION
1
22
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
(22) reported that DNA end joining requires the synapsis activity of PARP-1 and the ligation activity of the XRCC1-DNA ligase III complex.
[ "21", "22", "22", "52", "53", "54" ]
138
11,519
1
false
reported that DNA end joining requires the synapsis activity of PARP-1 and the ligation activity of the XRCC1-DNA ligase III complex.
[ "22" ]
reported that DNA end joining requires the synapsis activity of PARP-1 and the ligation activity of the XRCC1-DNA ligase III complex.
false
true
true
true
false
1,845
0
DISCUSSION
1
21
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
Thus, the repair module PARP-1/DNA ligase III/XRCC1 (PLX), hitherto regarded as central in SSB repair (52,53), is implicated in the repair of DSBs.
[ "21", "22", "22", "52", "53", "54" ]
147
11,520
0
false
Thus, the repair module PARP-1/DNA ligase III/XRCC1 (PLX), hitherto regarded as central in SSB repair, is implicated in the repair of DSBs.
[ "52,53" ]
Thus, the repair module PARP-1/DNA ligase III/XRCC1 (PLX), hitherto regarded as central in SSB repair, is implicated in the repair of DSBs.
true
true
true
true
true
1,845
0
DISCUSSION
1
21
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
This function may not rely on novel activities, as DSBs form when SSBs occur in close proximity, in opposite DNA strands.
[ "21", "22", "22", "52", "53", "54" ]
121
11,521
0
false
This function may not rely on novel activities, as DSBs form when SSBs occur in close proximity, in opposite DNA strands.
[]
This function may not rely on novel activities, as DSBs form when SSBs occur in close proximity, in opposite DNA strands.
true
true
true
true
true
1,845
0
DISCUSSION
1
21
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
The much higher affinity of Ku for DNA ends will limit the contribution of this form of end joining to instances where the classical pathway is compromised.
[ "21", "22", "22", "52", "53", "54" ]
156
11,522
0
false
The much higher affinity of Ku for DNA ends will limit the contribution of this form of end joining to instances where the classical pathway is compromised.
[]
The much higher affinity of Ku for DNA ends will limit the contribution of this form of end joining to instances where the classical pathway is compromised.
true
true
true
true
true
1,845
0
DISCUSSION
1
54
[ "b21", "b22", "b22", "b52", "b53", "b54" ]
17,088,286
pmid-11242102|pmid-15189136|pmid-16439205|pmid-16439204|pmid-10761921|pmid-10786799|pmid-15899791|pmid-15498778|pmid-15498778|pmid-11340626|pmid-9363683|pmid-15162010
As a result, its function will be more that of a backup (B-NHEJ) and less of an ‘alternative’ repair pathway (54).
[ "21", "22", "22", "52", "53", "54" ]
114
11,523
1
false
As a result, its function will be more that of a backup (B-NHEJ) and less of an ‘alternative’ repair pathway.
[ "54" ]
As a result, its function will be more that of a backup (B-NHEJ) and less of an ‘alternative’ repair pathway.
true
true
true
true
true
1,845
1
DISCUSSION
1
5
[ "b5", "b8", "b11", "b12", "b55", "b14", "b15", "b17", "b55", "b56", "b21", "b22" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Several reports implicate inferior backup pathways of DNA end joining in the phenotypes of mutants of the classical NHEJ pathway.
[ "5", "8", "11", "12", "55", "14", "15", "17", "55", "56", "21", "22" ]
129
11,524
0
false
Several reports implicate inferior backup pathways of DNA end joining in the phenotypes of mutants of the classical NHEJ pathway.
[]
Several reports implicate inferior backup pathways of DNA end joining in the phenotypes of mutants of the classical NHEJ pathway.
true
true
true
true
true
1,846
1
DISCUSSION
1
5
[ "b5", "b8", "b11", "b12", "b55", "b14", "b15", "b17", "b55", "b56", "b21", "b22" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Thus, non-classical pathways of end joining bring together the c-myc and Igh locus and cause B-cell lymphomas in mice with defects in Ku, LIG4 or XRCC4 (5–8,11,12,55).
[ "5", "8", "11", "12", "55", "14", "15", "17", "55", "56", "21", "22" ]
167
11,525
0
false
Thus, non-classical pathways of end joining bring together the c-myc and Igh locus and cause B-cell lymphomas in mice with defects in Ku, LIG4 or XRCC4.
[ "5–8,11,12,55" ]
Thus, non-classical pathways of end joining bring together the c-myc and Igh locus and cause B-cell lymphomas in mice with defects in Ku, LIG4 or XRCC4.
true
true
true
true
true
1,846
1
DISCUSSION
1
5
[ "b5", "b8", "b11", "b12", "b55", "b14", "b15", "b17", "b55", "b56", "b21", "b22" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Functionally equivalent pathways may generate the aberrant junctions manifesting chromosome instability in the same mutants.
[ "5", "8", "11", "12", "55", "14", "15", "17", "55", "56", "21", "22" ]
124
11,526
0
false
Functionally equivalent pathways may generate the aberrant junctions manifesting chromosome instability in the same mutants.
[]
Functionally equivalent pathways may generate the aberrant junctions manifesting chromosome instability in the same mutants.
true
true
true
true
true
1,846
1
DISCUSSION
1
55
[ "b5", "b8", "b11", "b12", "b55", "b14", "b15", "b17", "b55", "b56", "b21", "b22" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Non-classical pathways of end joining generate the few V(D)J junctions observed in cells with defects in NHEJ (14,15,17) and are implicated in antibody class switching occurring under the same conditions (55).
[ "5", "8", "11", "12", "55", "14", "15", "17", "55", "56", "21", "22" ]
209
11,527
1
false
Non-classical pathways of end joining generate the few V(D)J junctions observed in cells with defects in NHEJ and are implicated in antibody class switching occurring under the same conditions.
[ "14,15,17", "55" ]
Non-classical pathways of end joining generate the few V(D)J junctions observed in cells with defects in NHEJ and are implicated in antibody class switching occurring under the same conditions.
true
true
true
true
true
1,846
1
DISCUSSION
1
5
[ "b5", "b8", "b11", "b12", "b55", "b14", "b15", "b17", "b55", "b56", "b21", "b22" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Although not formally demonstrated, PARP-1 may be participating in these forms of non-classical end joining [e.g.
[ "5", "8", "11", "12", "55", "14", "15", "17", "55", "56", "21", "22" ]
113
11,528
0
false
Although not formally demonstrated, PARP-1 may be participating in these forms of non-classical end joining [e.g.
[]
Although not formally demonstrated, PARP-1 may be participating in these forms of non-classical end joining [e.g.
true
true
true
true
true
1,846
1
DISCUSSION
1
5
[ "b5", "b8", "b11", "b12", "b55", "b14", "b15", "b17", "b55", "b56", "b21", "b22" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
Furthermore, the substantial DNA end joining observed after exposure to IR of cells with defects in DNA ligase IV, Ku and DNA–PK (Figures 1 and 2, and Supplementary Figure 1) directly implicates alternative forms of DNA end joining.
[ "5", "8", "11", "12", "55", "14", "15", "17", "55", "56", "21", "22" ]
232
11,529
0
false
Furthermore, the substantial DNA end joining observed after exposure to IR of cells with defects in DNA ligase IV, Ku and DNA–PK (Figures 1 and 2, and Supplementary Figure 1) directly implicates alternative forms of DNA end joining.
[]
Furthermore, the substantial DNA end joining observed after exposure to IR of cells with defects in DNA ligase IV, Ku and DNA–PK (Figures 1 and 2, and Supplementary Figure 1) directly implicates alternative forms of DNA end joining.
true
true
true
true
true
1,846
1
DISCUSSION
1
5
[ "b5", "b8", "b11", "b12", "b55", "b14", "b15", "b17", "b55", "b56", "b21", "b22" ]
17,088,286
pmid-12110179|pmid-3025650|pmid-10761921|pmid-10607596|pmid-10823907|pmid-11779495|pmid-9252118|pmid-15084256|pmid-10761921|pmid-12110179|pmid-10607596|pmid-10823907|pmid-16400328|pmid-9252118|pmid-8548796|pmid-15084256|pmid-16400328|pmid-11930007|pmid-15899791|pmid-15498778
The results presented here and published data (21,22) implicate PARP-1 and DNA Ligase III in this function.
[ "5", "8", "11", "12", "55", "14", "15", "17", "55", "56", "21", "22" ]
107
11,530
0
false
The results presented here and published data implicate PARP-1 and DNA Ligase III in this function.
[ "21,22" ]
The results presented here and published data implicate PARP-1 and DNA Ligase III in this function.
true
true
true
true
true
1,846
2
DISCUSSION
1
9
[ "b9", "b10", "b19", "b54", "b57" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
PARP-1/DNA Ligase III dependent end joining, when utilized, helps the cell to restore its genome and thus presumably to avert cell death.
[ "9", "10", "19", "54", "57" ]
137
11,531
0
false
PARP-1/DNA Ligase III dependent end joining, when utilized, helps the cell to restore its genome and thus presumably to avert cell death.
[]
PARP-1/DNA Ligase III dependent end joining, when utilized, helps the cell to restore its genome and thus presumably to avert cell death.
true
true
true
true
true
1,847
2
DISCUSSION
1
9
[ "b9", "b10", "b19", "b54", "b57" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
However, its error prone nature causes genomic instability and cancer in the affected organism.
[ "9", "10", "19", "54", "57" ]
95
11,532
0
false
However, its error prone nature causes genomic instability and cancer in the affected organism.
[]
However, its error prone nature causes genomic instability and cancer in the affected organism.
true
true
true
true
true
1,847
2
DISCUSSION
1
9
[ "b9", "b10", "b19", "b54", "b57" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
The adverse consequences of this repair pathway may derive from inefficient synapsis of the DNA ends, which is probably supported only by microhomologies (9,10) and is therefore inefficient and slow [Figures 1 and 2, and Supplementary Figure 1; and (19,54,57)].
[ "9", "10", "19", "54", "57" ]
261
11,533
0
false
The adverse consequences of this repair pathway may derive from inefficient synapsis of the DNA ends, which is probably supported only by microhomologies and is therefore inefficient and slow.
[ "9,10", "Figures 1 and 2, and Supplementary Figure 1; and (19,54,57)" ]
The adverse consequences of this repair pathway may derive from inefficient synapsis of the DNA ends, which is probably supported only by microhomologies and is therefore inefficient and slow.
true
true
true
true
true
1,847
2
DISCUSSION
1
9
[ "b9", "b10", "b19", "b54", "b57" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
The resulting persistence of DNA ends in the cell can lead to incorrect rejoining and thus to translocations.
[ "9", "10", "19", "54", "57" ]
109
11,534
0
false
The resulting persistence of DNA ends in the cell can lead to incorrect rejoining and thus to translocations.
[]
The resulting persistence of DNA ends in the cell can lead to incorrect rejoining and thus to translocations.
true
true
true
true
true
1,847
2
DISCUSSION
1
9
[ "b9", "b10", "b19", "b54", "b57" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
In addition, it may facilitate DNA end degradation and thus loss of genetic information.
[ "9", "10", "19", "54", "57" ]
88
11,535
0
false
In addition, it may facilitate DNA end degradation and thus loss of genetic information.
[]
In addition, it may facilitate DNA end degradation and thus loss of genetic information.
true
true
true
true
true
1,847
2
DISCUSSION
1
9
[ "b9", "b10", "b19", "b54", "b57" ]
17,088,286
pmid-9146698|pmid-11402316|pmid-11402316|pmid-11870614|pmid-3025650|pmid-10728683|pmid-15162010|pmid-11292837
Both phenomena have been described in mutants of the classical pathway of DNA end joining (see above).
[ "9", "10", "19", "54", "57" ]
102
11,536
0
false
Both phenomena have been described in mutants of the classical pathway of DNA end joining (see above).
[]
Both phenomena have been described in mutants of the classical pathway of DNA end joining (see above).
true
true
true
true
true
1,847
3
DISCUSSION
1
58
[ "b58", "b59", "b60" ]
17,088,286
pmid-12110179|pmid-11870614|pmid-9308963|pmid-11359911|pmid-11432840
While prominent when the classical pathway is compromised, the backup pathway may theoretically be utilized to a limited degree in cells with functional D-NHEJ as well.
[ "58", "59", "60" ]
168
11,537
0
false
While prominent when the classical pathway is compromised, the backup pathway may theoretically be utilized to a limited degree in cells with functional D-NHEJ as well.
[]
While prominent when the classical pathway is compromised, the backup pathway may theoretically be utilized to a limited degree in cells with functional D-NHEJ as well.
true
true
true
true
true
1,848
3
DISCUSSION
1
58
[ "b58", "b59", "b60" ]
17,088,286
pmid-12110179|pmid-11870614|pmid-9308963|pmid-11359911|pmid-11432840
This can occur when a DSB is induced in a nuclear region where Ku or other key components of D-NHEJ, are not immediately available; for example because they are already recruited to a neighboring DSB.
[ "58", "59", "60" ]
200
11,538
0
false
This can occur when a DSB is induced in a nuclear region where Ku or other key components of D-NHEJ, are not immediately available; for example because they are already recruited to a neighboring DSB.
[]
This can occur when a DSB is induced in a nuclear region where Ku or other key components of D-NHEJ, are not immediately available; for example because they are already recruited to a neighboring DSB.
true
true
true
true
true
1,848
3
DISCUSSION
1
58
[ "b58", "b59", "b60" ]
17,088,286
pmid-12110179|pmid-11870614|pmid-9308963|pmid-11359911|pmid-11432840
Such contributions may underlie micronuclei observed in PARP-1−/− cells (58), as well as genomic instability and occasionally tumor development in PARP-1−/− mice on p53−/− background (59,60).
[ "58", "59", "60" ]
191
11,539
1
false
Such contributions may underlie micronuclei observed in PARP-1−/− cells, as well as genomic instability and occasionally tumor development in PARP-1−/− mice on p53−/− background.
[ "58", "59,60" ]
Such contributions may underlie micronuclei observed in PARP-1−/− cells, as well as genomic instability and occasionally tumor development in PARP-1−/− mice on p53−/− background.
true
true
true
true
true
1,848
4
DISCUSSION
1
22
[ "b22", "b28", "b29" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
Our results further show that the function of PARP-1 in DSB repair will be competed by its canonical function in SSB repair.
[ "22", "28", "29" ]
124
11,540
0
false
Our results further show that the function of PARP-1 in DSB repair will be competed by its canonical function in SSB repair.
[]
Our results further show that the function of PARP-1 in DSB repair will be competed by its canonical function in SSB repair.
true
true
true
true
true
1,849
4
DISCUSSION
1
22
[ "b22", "b28", "b29" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
Reduced engagement in the repair of a highly dangerous lesion as the DSB through competition by a less severe one, a SSB, is a limitation of the pathway and justifies its ranking as a backup.
[ "22", "28", "29" ]
191
11,541
0
false
Reduced engagement in the repair of a highly dangerous lesion as the DSB through competition by a less severe one, a SSB, is a limitation of the pathway and justifies its ranking as a backup.
[]
Reduced engagement in the repair of a highly dangerous lesion as the DSB through competition by a less severe one, a SSB, is a limitation of the pathway and justifies its ranking as a backup.
true
true
true
true
true
1,849
4
DISCUSSION
1
22
[ "b22", "b28", "b29" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
It follows that DSBs induced by agents generating higher ratios of DSBs to SSBs than IR, e.g.
[ "22", "28", "29" ]
93
11,542
0
false
It follows that DSBs induced by agents generating higher ratios of DSBs to SSBs than IR, e.g.
[]
It follows that DSBs induced by agents generating higher ratios of DSBs to SSBs than IR, e.g.
true
true
true
true
true
1,849
4
DISCUSSION
1
22
[ "b22", "b28", "b29" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
calicheamicin γ?, are more likely to engage PARP-1 (22).
[ "22", "28", "29" ]
56
11,543
1
false
calicheamicin γ?, are more likely to engage PARP-1.
[ "22" ]
calicheamicin γ?, are more likely to engage PARP-1.
false
true
true
true
false
1,849
4
DISCUSSION
1
22
[ "b22", "b28", "b29" ]
17,088,286
pmid-15899791|pmid-15498778|pmid-15498778|pmid-10455009|pmid-16140981|pmid-15498778|pmid-15829967|pmid-15829966
However, this distinction of severity between SSBs and DSBs may be altered during S phase, where SSBs can be converted to one-ended DSBs which, if not repaired by HRR, can have serious consequences for the cell (28,29).
[ "22", "28", "29" ]
219
11,544
0
false
However, this distinction of severity between SSBs and DSBs may be altered during S phase, where SSBs can be converted to one-ended DSBs which, if not repaired by HRR, can have serious consequences for the cell.
[ "28,29" ]
However, this distinction of severity between SSBs and DSBs may be altered during S phase, where SSBs can be converted to one-ended DSBs which, if not repaired by HRR, can have serious consequences for the cell.
true
true
true
true
true
1,849
5
DISCUSSION
1
61
[ "b61", "b62", "b63", "b64", "b65", "b66", "b67" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
Inhibition of a PARP-1 dependent backup pathway of DSB end joining partly explains the lethality of PARP-1−/−/Ku−/− mice (61), as normal development may not be compatible with inactivation of both NHEJ pathways.
[ "61", "62", "63", "64", "65", "66", "67" ]
211
11,545
1
false
Inhibition of a PARP-1 dependent backup pathway of DSB end joining partly explains the lethality of PARP-1−/−/Ku−/− mice, as normal development may not be compatible with inactivation of both NHEJ pathways.
[ "61" ]
Inhibition of a PARP-1 dependent backup pathway of DSB end joining partly explains the lethality of PARP-1−/−/Ku−/− mice, as normal development may not be compatible with inactivation of both NHEJ pathways.
true
true
true
true
true
1,850
5
DISCUSSION
1
62
[ "b61", "b62", "b63", "b64", "b65", "b66", "b67" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
Along similar lines it can be reasoned that the lethality of PARP-1−/−/ATM−/− mice partly derives from a contribution of ATM to a subset of radiation-induced complex DSBs that require D-NHEJ (62).
[ "61", "62", "63", "64", "65", "66", "67" ]
196
11,546
1
false
Along similar lines it can be reasoned that the lethality of PARP-1−/−/ATM−/− mice partly derives from a contribution of ATM to a subset of radiation-induced complex DSBs that require D-NHEJ.
[ "62" ]
Along similar lines it can be reasoned that the lethality of PARP-1−/−/ATM−/− mice partly derives from a contribution of ATM to a subset of radiation-induced complex DSBs that require D-NHEJ.
true
true
true
true
true
1,850
5
DISCUSSION
1
63
[ "b61", "b62", "b63", "b64", "b65", "b66", "b67" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
Also, tumor formation in PARP-1−/− mice engineered with Ku haploinsufficiency (63), or DNA–PK knock out (64), suggests that reduction in the efficiency of D-NHEJ favors PARP-1 dependent end joining and thus genomic instability and cancer.
[ "61", "62", "63", "64", "65", "66", "67" ]
238
11,547
1
false
Also, tumor formation in PARP-1−/− mice engineered with Ku haploinsufficiency, or DNA–PK knock out, suggests that reduction in the efficiency of D-NHEJ favors PARP-1 dependent end joining and thus genomic instability and cancer.
[ "63", "64" ]
Also, tumor formation in PARP-1−/− mice engineered with Ku haploinsufficiency, or DNA–PK knock out, suggests that reduction in the efficiency of D-NHEJ favors PARP-1 dependent end joining and thus genomic instability and cancer.
true
true
true
true
true
1,850
5
DISCUSSION
1
61
[ "b61", "b62", "b63", "b64", "b65", "b66", "b67" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
Finally, the rescue of LIG4−/− lethality and radiosensitivity by Ku knock out (65,66) can be explained by the relief of the dominant negative inhibition exerted by Ku on backup end joining in LIG4−/− cells.
[ "61", "62", "63", "64", "65", "66", "67" ]
206
11,548
0
false
Finally, the rescue of LIG4−/− lethality and radiosensitivity by Ku knock out can be explained by the relief of the dominant negative inhibition exerted by Ku on backup end joining in LIG4−/− cells.
[ "65,66" ]
Finally, the rescue of LIG4−/− lethality and radiosensitivity by Ku knock out can be explained by the relief of the dominant negative inhibition exerted by Ku on backup end joining in LIG4−/− cells.
true
true
true
true
true
1,850
5
DISCUSSION
1
67
[ "b61", "b62", "b63", "b64", "b65", "b66", "b67" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
However, the recent observation that PARP-1 protects HRR from interference by KU and DNA Ligase IV (67) also suggests that KU-mediated down regulation of HRR may partly underlie the above described phenomena.
[ "61", "62", "63", "64", "65", "66", "67" ]
208
11,549
1
false
However, the recent observation that PARP-1 protects HRR from interference by KU and DNA Ligase IV also suggests that KU-mediated down regulation of HRR may partly underlie the above described phenomena.
[ "67" ]
However, the recent observation that PARP-1 protects HRR from interference by KU and DNA Ligase IV also suggests that KU-mediated down regulation of HRR may partly underlie the above described phenomena.
true
true
true
true
true
1,850
5
DISCUSSION
1
61
[ "b61", "b62", "b63", "b64", "b65", "b66", "b67" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
Finally, it is also possible that defects in SSB repair resulting from PARP-1 deficiency contribute to the described effects.
[ "61", "62", "63", "64", "65", "66", "67" ]
125
11,550
0
false
Finally, it is also possible that defects in SSB repair resulting from PARP-1 deficiency contribute to the described effects.
[]
Finally, it is also possible that defects in SSB repair resulting from PARP-1 deficiency contribute to the described effects.
true
true
true
true
true
1,850
5
DISCUSSION
1
61
[ "b61", "b62", "b63", "b64", "b65", "b66", "b67" ]
17,088,286
pmid-12748298|pmid-12930846|pmid-15829967|pmid-15829966|pmid-7760811|pmid-14757832|pmid-10455009|pmid-12866953|pmid-15021907|pmid-12531386|pmid-15574327|pmid-12460917|pmid-9398855|pmid-12531011|pmid-11593023|pmid-16498404
More work is needed to discriminate between these possible contributions.
[ "61", "62", "63", "64", "65", "66", "67" ]
73
11,551
0
false
More work is needed to discriminate between these possible contributions.
[]
More work is needed to discriminate between these possible contributions.
true
true
true
true
true
1,850
6
DISCUSSION
1
49
[ "b49", "b68", "b56", "b34", "b69", "b22" ]
17,088,286
pmid-10082940|pmid-12205080|pmid-11930007|pmid-12866953|pmid-15286704|pmid-15498778
The biochemical properties of PARP-1 are compatible with its function in a backup pathway of NHEJ.
[ "49", "68", "56", "34", "69", "22" ]
98
11,552
0
false
The biochemical properties of PARP-1 are compatible with its function in a backup pathway of NHEJ.
[]
The biochemical properties of PARP-1 are compatible with its function in a backup pathway of NHEJ.
true
true
true
true
true
1,851
6
DISCUSSION
1
56
[ "b49", "b68", "b56", "b34", "b69", "b22" ]
17,088,286
pmid-10082940|pmid-12205080|pmid-11930007|pmid-12866953|pmid-15286704|pmid-15498778
PARP-1 binds and becomes activated by double-stranded DNA ends (49,68), even during V(D)J recombination (56), as it would be anticipated by a protein involved in DSB repair.
[ "49", "68", "56", "34", "69", "22" ]
173
11,553
1
false
PARP-1 binds and becomes activated by double-stranded DNA ends, even during V(D)J recombination, as it would be anticipated by a protein involved in DSB repair.
[ "49,68", "56" ]
PARP-1 binds and becomes activated by double-stranded DNA ends, even during V(D)J recombination, as it would be anticipated by a protein involved in DSB repair.
true
true
true
true
true
1,851
6
DISCUSSION
1
49
[ "b49", "b68", "b56", "b34", "b69", "b22" ]
17,088,286
pmid-10082940|pmid-12205080|pmid-11930007|pmid-12866953|pmid-15286704|pmid-15498778
The affinity of PARP-1 for DNA ends generates an activity analogous to Ku and offers an alternative mode of recognition of this type of lesion.
[ "49", "68", "56", "34", "69", "22" ]
143
11,554
0
false
The affinity of PARP-1 for DNA ends generates an activity analogous to Ku and offers an alternative mode of recognition of this type of lesion.
[]
The affinity of PARP-1 for DNA ends generates an activity analogous to Ku and offers an alternative mode of recognition of this type of lesion.
true
true
true
true
true
1,851
6
DISCUSSION
1
49
[ "b49", "b68", "b56", "b34", "b69", "b22" ]
17,088,286
pmid-10082940|pmid-12205080|pmid-11930007|pmid-12866953|pmid-15286704|pmid-15498778
Although PARP-1 has been repeatedly implicated in DSB repair, divergent results have hampered the formulation of a consistent model (34,69).
[ "49", "68", "56", "34", "69", "22" ]
140
11,555
0
false
Although PARP-1 has been repeatedly implicated in DSB repair, divergent results have hampered the formulation of a consistent model.
[ "34,69" ]
Although PARP-1 has been repeatedly implicated in DSB repair, divergent results have hampered the formulation of a consistent model.
true
true
true
true
true
1,851
6
DISCUSSION
1
22
[ "b49", "b68", "b56", "b34", "b69", "b22" ]
17,088,286
pmid-10082940|pmid-12205080|pmid-11930007|pmid-12866953|pmid-15286704|pmid-15498778
Our observations, as well as those published earlier (22), implicate this activity in a backup rather in the canonical pathway of end joining and provide a new dimension for re-evaluating these experiments.
[ "49", "68", "56", "34", "69", "22" ]
206
11,556
1
false
Our observations, as well as those published earlier, implicate this activity in a backup rather in the canonical pathway of end joining and provide a new dimension for re-evaluating these experiments.
[ "22" ]
Our observations, as well as those published earlier, implicate this activity in a backup rather in the canonical pathway of end joining and provide a new dimension for re-evaluating these experiments.
true
true
true
true
true
1,851
7
DISCUSSION
1
21
[ "b21", "b22" ]
17,088,286
pmid-15899791|pmid-15498778
Although inhibition of PARP-1 compromises DSB rejoining both in the plasmid assay as well as in irradiated cells, the inhibition is never complete and actually rather limited for DSBs induced in genomic DNA (Figures 1 and 2).
[ "21", "22" ]
225
11,557
0
false
Although inhibition of PARP-1 compromises DSB rejoining both in the plasmid assay as well as in irradiated cells, the inhibition is never complete and actually rather limited for DSBs induced in genomic DNA (Figures 1 and 2).
[]
Although inhibition of PARP-1 compromises DSB rejoining both in the plasmid assay as well as in irradiated cells, the inhibition is never complete and actually rather limited for DSBs induced in genomic DNA.
true
true
true
true
true
1,852
7
DISCUSSION
1
21
[ "b21", "b22" ]
17,088,286
pmid-15899791|pmid-15498778
This suggests that rejoining of DSBs remains possible in the absence of PARP-1 and may be carried out by DNA ligase III, possibly aided by its zinc finger domain (21,22).
[ "21", "22" ]
170
11,558
0
false
This suggests that rejoining of DSBs remains possible in the absence of PARP-1 and may be carried out by DNA ligase III, possibly aided by its zinc finger domain.
[ "21,22" ]
This suggests that rejoining of DSBs remains possible in the absence of PARP-1 and may be carried out by DNA ligase III, possibly aided by its zinc finger domain.
true
true
true
true
true
1,852
8
DISCUSSION
1
70
[ "b70", "b50", "b71", "b71" ]
17,088,286
pmid-9603959|pmid-10467406|pmid-16397295|pmid-16397295
The hierarchical organization of the classical and backup pathways of end joining may be regulated by interactions between the participating proteins.
[ "70", "50", "71", "71" ]
150
11,559
0
false
The hierarchical organization of the classical and backup pathways of end joining may be regulated by interactions between the participating proteins.
[]
The hierarchical organization of the classical and backup pathways of end joining may be regulated by interactions between the participating proteins.
true
true
true
true
true
1,853
8
DISCUSSION
1
70
[ "b70", "b50", "b71", "b71" ]
17,088,286
pmid-9603959|pmid-10467406|pmid-16397295|pmid-16397295
Thus, DNA–PKcs is poly(ADP-ribosyl)ated in vitro by PARP-1 and this modification stimulates DNA–PK activity (70).
[ "70", "50", "71", "71" ]
113
11,560
1
false
Thus, DNA–PKcs is poly(ADP-ribosyl)ated in vitro by PARP-1 and this modification stimulates DNA–PK activity.
[ "70" ]
Thus, DNA–PKcs is poly(ADP-ribosyl)ated in vitro by PARP-1 and this modification stimulates DNA–PK activity.
true
true
true
true
true
1,853
8
DISCUSSION
1
50
[ "b70", "b50", "b71", "b71" ]
17,088,286
pmid-9603959|pmid-10467406|pmid-16397295|pmid-16397295
On the other hand, DNA–PK suppresses PARP-1 activity but probably not through the associated phosphorylation (50).
[ "70", "50", "71", "71" ]
114
11,561
1
false
On the other hand, DNA–PK suppresses PARP-1 activity but probably not through the associated phosphorylation.
[ "50" ]
On the other hand, DNA–PK suppresses PARP-1 activity but probably not through the associated phosphorylation.
true
true
true
true
true
1,853
8
DISCUSSION
1
71
[ "b70", "b50", "b71", "b71" ]
17,088,286
pmid-9603959|pmid-10467406|pmid-16397295|pmid-16397295
Similarly, the BRCT1 domain of XRCC1 is phosphorylated by DNA–PK and this phosphorylation causes XRCC1 dimer dissociation (71).
[ "70", "50", "71", "71" ]
127
11,562
1
false
Similarly, the BRCT1 domain of XRCC1 is phosphorylated by DNA–PK and this phosphorylation causes XRCC1 dimer dissociation.
[ "71" ]
Similarly, the BRCT1 domain of XRCC1 is phosphorylated by DNA–PK and this phosphorylation causes XRCC1 dimer dissociation.
true
true
true
true
true
1,853
8
DISCUSSION
1
71
[ "b70", "b50", "b71", "b71" ]
17,088,286
pmid-9603959|pmid-10467406|pmid-16397295|pmid-16397295
At the same time, interaction between XRCC1 and DNA–PK stimulates the kinase activity towards p53 (71).
[ "70", "50", "71", "71" ]
103
11,563
1
false
At the same time, interaction between XRCC1 and DNA–PK stimulates the kinase activity towards p53.
[ "71" ]
At the same time, interaction between XRCC1 and DNA–PK stimulates the kinase activity towards p53.
true
true
true
true
true
1,853
8
DISCUSSION
1
70
[ "b70", "b50", "b71", "b71" ]
17,088,286
pmid-9603959|pmid-10467406|pmid-16397295|pmid-16397295
It is notable that all these inputs further consolidate the hierarchical organization of end joining by favoring the engagement of the classical pathway and suppressing the utilization of the backup pathway.
[ "70", "50", "71", "71" ]
207
11,564
0
false
It is notable that all these inputs further consolidate the hierarchical organization of end joining by favoring the engagement of the classical pathway and suppressing the utilization of the backup pathway.
[]
It is notable that all these inputs further consolidate the hierarchical organization of end joining by favoring the engagement of the classical pathway and suppressing the utilization of the backup pathway.
true
true
true
true
true
1,853
9
DISCUSSION
1
24
[ "b24" ]
17,088,286
pmid-15273990
Our results in aggregate implicate PARP-1 in DSB repair through participation in a backup pathway together with DNA Ligase III and possibly XRCC1.
[ "24" ]
146
11,565
0
false
Our results in aggregate implicate PARP-1 in DSB repair through participation in a backup pathway together with DNA Ligase III and possibly XRCC1.
[]
Our results in aggregate implicate PARP-1 in DSB repair through participation in a backup pathway together with DNA Ligase III and possibly XRCC1.
true
true
true
true
true
1,854
9
DISCUSSION
1
24
[ "b24" ]
17,088,286
pmid-15273990
This function is enabled by the considerable affinity of PARP-1 for double-stranded DNA ends, is under normal conditions competed by Ku and may further be down-regulated by DNA–PK.
[ "24" ]
180
11,566
0
false
This function is enabled by the considerable affinity of PARP-1 for double-stranded DNA ends, is under normal conditions competed by Ku and may further be down-regulated by DNA–PK.
[]
This function is enabled by the considerable affinity of PARP-1 for double-stranded DNA ends, is under normal conditions competed by Ku and may further be down-regulated by DNA–PK.
true
true
true
true
true
1,854
9
DISCUSSION
1
24
[ "b24" ]
17,088,286
pmid-15273990
Additional modulation of engagement for DSB repair is afforded by PARP-1 recruitment to SSB.
[ "24" ]
92
11,567
0
false
Additional modulation of engagement for DSB repair is afforded by PARP-1 recruitment to SSB.
[]
Additional modulation of engagement for DSB repair is afforded by PARP-1 recruitment to SSB.
true
true
true
true
true
1,854
9
DISCUSSION
1
24
[ "b24" ]
17,088,286
pmid-15273990
Our experiments focus on PARP-1.
[ "24" ]
32
11,568
0
false
Our experiments focus on PARP-1.
[]
Our experiments focus on PARP-1.
true
true
true
true
true
1,854
9
DISCUSSION
1
24
[ "b24" ]
17,088,286
pmid-15273990
However among the eighteen potential PARPs in the mammalian genome, PARP-2 has also been implicated in repair functions equivalent to those of PARP-1 (24).
[ "24" ]
155
11,569
1
false
However among the eighteen potential PARPs in the mammalian genome, PARP-2 has also been implicated in repair functions equivalent to those of PARP-1.
[ "24" ]
However among the eighteen potential PARPs in the mammalian genome, PARP-2 has also been implicated in repair functions equivalent to those of PARP-1.
true
true
true
true
true
1,854
9
DISCUSSION
1
24
[ "b24" ]
17,088,286
pmid-15273990
It remains to be seen whether PARP-2 can also contribute to backup end joining of DSBs as suggested here for PARP-1.
[ "24" ]
116
11,570
0
false
It remains to be seen whether PARP-2 can also contribute to backup end joining of DSBs as suggested here for PARP-1.
[]
It remains to be seen whether PARP-2 can also contribute to backup end joining of DSBs as suggested here for PARP-1.
true
true
true
true
true
1,854
0
INTRODUCTION
1
1
[ "B1", "B2", "B3 B4 B5 B6 B7", "B8", "B9", "B10", "B11", "B12", "B13" ]
17,517,774
pmid-8892734|pmid-11389461|pmid-16132046|pmid-16377561|pmid-16357213|pmid-17289582|pmid-17396147|pmid-12239151|pmid-11376695|pmid-14643432|pmid-15723711|pmid-12065746|pmid-16621732|pmid-16522646|pmid-16055725
Fanconi anemia (FA) is a genetic disease characterized by diverse congenital abnormalities, early predisposition to cancer and progressive bone marrow failure due to defective hematopoiesis (1,2).
[ "1", "2", "3–7", "8", "9", "10", "11", "12", "13" ]
196
11,571
0
false
Fanconi anemia (FA) is a genetic disease characterized by diverse congenital abnormalities, early predisposition to cancer and progressive bone marrow failure due to defective hematopoiesis.
[ "1,2" ]
Fanconi anemia (FA) is a genetic disease characterized by diverse congenital abnormalities, early predisposition to cancer and progressive bone marrow failure due to defective hematopoiesis.
true
true
true
true
true
1,855
0
INTRODUCTION
1
1
[ "B1", "B2", "B3 B4 B5 B6 B7", "B8", "B9", "B10", "B11", "B12", "B13" ]
17,517,774
pmid-8892734|pmid-11389461|pmid-16132046|pmid-16377561|pmid-16357213|pmid-17289582|pmid-17396147|pmid-12239151|pmid-11376695|pmid-14643432|pmid-15723711|pmid-12065746|pmid-16621732|pmid-16522646|pmid-16055725
Patients have mutations in one of at least 12 genes: FANCA, B, C, D1 (also known as BRCA2), D2, E, F, G, I, J (BRIP1/BACH1), L, M (Hef), and N (PALB2).
[ "1", "2", "3–7", "8", "9", "10", "11", "12", "13" ]
151
11,572
0
false
Patients have mutations in one of at least 12 genes: FANCA, B, C, D1, D2, E, F, G, I, J, L, M (Hef), and N.
[ "also known as BRCA2", "BRIP1/BACH1", "PALB2" ]
Patients have mutations in one of at least 12 genes: FANCA, B, C, D1, D2, E, F, G, I, J, L, M (Hef), and N.
true
true
true
true
true
1,855
0
INTRODUCTION
1
3–7
[ "B1", "B2", "B3 B4 B5 B6 B7", "B8", "B9", "B10", "B11", "B12", "B13" ]
17,517,774
pmid-8892734|pmid-11389461|pmid-16132046|pmid-16377561|pmid-16357213|pmid-17289582|pmid-17396147|pmid-12239151|pmid-11376695|pmid-14643432|pmid-15723711|pmid-12065746|pmid-16621732|pmid-16522646|pmid-16055725
Many of the FANC proteins (FANCA/B/C/E/F/G/L/M/FAAP24/FAAP100) form a nuclear ‘core complex’ (3–7), the integrity of which is essential for the monoubiquitination of FANCD2 in response to DNA damage, including that from mitomycin C crosslinking or oxidative lesions from ionizing radiation (IR).
[ "1", "2", "3–7", "8", "9", "10", "11", "12", "13" ]
295
11,573
1
false
Many of the FANC proteins form a nuclear ‘core complex’, the integrity of which is essential for the monoubiquitination of FANCD2 in response to DNA damage, including that from mitomycin C crosslinking or oxidative lesions from ionizing radiation (IR).
[ "FANCA/B/C/E/F/G/L/M/FAAP24/FAAP100", "3–7" ]
Many of the FANC proteins form a nuclear ‘core complex’, the integrity of which is essential for the monoubiquitination of FANCD2 in response to DNA damage, including that from mitomycin C crosslinking or oxidative lesions from ionizing radiation (IR).
true
true
true
true
true
1,855
0
INTRODUCTION
1
8
[ "B1", "B2", "B3 B4 B5 B6 B7", "B8", "B9", "B10", "B11", "B12", "B13" ]
17,517,774
pmid-8892734|pmid-11389461|pmid-16132046|pmid-16377561|pmid-16357213|pmid-17289582|pmid-17396147|pmid-12239151|pmid-11376695|pmid-14643432|pmid-15723711|pmid-12065746|pmid-16621732|pmid-16522646|pmid-16055725
During the cell cycle, monoubiquitinated FANCD2 appears during S phase and co-localizes at sites of putative double-strand breaks (DSBs) with nuclear foci of BRCA1 and Rad51(8), two key proteins in the DSB repair pathway of homologous recombination repair (HRR).
[ "1", "2", "3–7", "8", "9", "10", "11", "12", "13" ]
262
11,574
1
false
During the cell cycle, monoubiquitinated FANCD2 appears during S phase and co-localizes at sites of putative double-strand breaks (DSBs) with nuclear foci of BRCA1 and Rad51, two key proteins in the DSB repair pathway of homologous recombination repair (HRR).
[ "8" ]
During the cell cycle, monoubiquitinated FANCD2 appears during S phase and co-localizes at sites of putative double-strand breaks (DSBs) with nuclear foci of BRCA1 and Rad51, two key proteins in the DSB repair pathway of homologous recombination repair (HRR).
true
true
true
true
true
1,855
0
INTRODUCTION
1
1
[ "B1", "B2", "B3 B4 B5 B6 B7", "B8", "B9", "B10", "B11", "B12", "B13" ]
17,517,774
pmid-8892734|pmid-11389461|pmid-16132046|pmid-16377561|pmid-16357213|pmid-17289582|pmid-17396147|pmid-12239151|pmid-11376695|pmid-14643432|pmid-15723711|pmid-12065746|pmid-16621732|pmid-16522646|pmid-16055725
HRR uses the sister chromatid, when it is available, as a template for error-free repair of DSBs caused by insults such as ionizing radiation, as well as for restarting broken replication forks during DNA synthesis (9,10).
[ "1", "2", "3–7", "8", "9", "10", "11", "12", "13" ]
222
11,575
0
false
HRR uses the sister chromatid, when it is available, as a template for error-free repair of DSBs caused by insults such as ionizing radiation, as well as for restarting broken replication forks during DNA synthesis.
[ "9,10" ]
HRR uses the sister chromatid, when it is available, as a template for error-free repair of DSBs caused by insults such as ionizing radiation, as well as for restarting broken replication forks during DNA synthesis.
true
true
true
true
true
1,855
0
INTRODUCTION
1
11
[ "B1", "B2", "B3 B4 B5 B6 B7", "B8", "B9", "B10", "B11", "B12", "B13" ]
17,517,774
pmid-8892734|pmid-11389461|pmid-16132046|pmid-16377561|pmid-16357213|pmid-17289582|pmid-17396147|pmid-12239151|pmid-11376695|pmid-14643432|pmid-15723711|pmid-12065746|pmid-16621732|pmid-16522646|pmid-16055725
These processes are facilitated by the Rad51 recombinase, which requires mediator proteins including BRCA2 and five Rad51 paralogs (XRCC2, XRCC3, RAD51B, RAD51C, RAD51D) (11).
[ "1", "2", "3–7", "8", "9", "10", "11", "12", "13" ]
175
11,576
1
false
These processes are facilitated by the Rad51 recombinase, which requires mediator proteins including BRCA2 and five Rad51 paralogs.
[ "XRCC2, XRCC3, RAD51B, RAD51C, RAD51D", "11" ]
These processes are facilitated by the Rad51 recombinase, which requires mediator proteins including BRCA2 and five Rad51 paralogs.
true
true
true
true
true
1,855
0
INTRODUCTION
1
12
[ "B1", "B2", "B3 B4 B5 B6 B7", "B8", "B9", "B10", "B11", "B12", "B13" ]
17,517,774
pmid-8892734|pmid-11389461|pmid-16132046|pmid-16377561|pmid-16357213|pmid-17289582|pmid-17396147|pmid-12239151|pmid-11376695|pmid-14643432|pmid-15723711|pmid-12065746|pmid-16621732|pmid-16522646|pmid-16055725
The identification of FANCD1 as BRCA2 (12), and the physical associations between other FANC and HRR proteins such as XRCC3 (13), also suggest a role for the FANC ‘pathway’ in preventing or repairing broken replication forks, and highlight a potential link between the FA proteins and the better defined HRR pathway.
[ "1", "2", "3–7", "8", "9", "10", "11", "12", "13" ]
316
11,577
1
false
The identification of FANCD1 as BRCA2, and the physical associations between other FANC and HRR proteins such as XRCC3, also suggest a role for the FANC ‘pathway’ in preventing or repairing broken replication forks, and highlight a potential link between the FA proteins and the better defined HRR pathway.
[ "12", "13" ]
The identification of FANCD1 as BRCA2, and the physical associations between other FANC and HRR proteins such as XRCC3, also suggest a role for the FANC ‘pathway’ in preventing or repairing broken replication forks, and highlight a potential link between the FA proteins and the better defined HRR pathway.
true
true
true
true
true
1,855
1
INTRODUCTION
1
14
[ "B14", "B2", "B15", "B16", "B17", "B18", "B19", "B20", "B21", "B11", "B22", "B23", "B24 B25 B26", "B27", "B28", "B29" ]
17,517,774
NA|pmid-11389461|pmid-12509764|pmid-15084315|pmid-15668941|pmid-14726021|pmid-15907771|pmid-14522929|pmid-15498778|pmid-15723711|pmid-12427531|pmid-16522646|pmid-12861027|pmid-15601828|pmid-15650050|pmid-9287344|pmid-12748186|pmid-15671039|pmid-2159378|pmid-2236046|pmid-10635999
Cells from FA patients typically show increased spontaneous chromatid breaks and gaps (14), and consistently show high sensitivity for cell killing and chromosomal aberrations in response to DNA crosslinking agents (2,15).
[ "14", "2", "15", "16", "17", "18", "19", "20", "21", "11", "22", "23", "24–26", "27", "28", "29" ]
222
11,578
1
false
Cells from FA patients typically show increased spontaneous chromatid breaks and gaps, and consistently show high sensitivity for cell killing and chromosomal aberrations in response to DNA crosslinking agents.
[ "14", "2,15" ]
Cells from FA patients typically show increased spontaneous chromatid breaks and gaps, and consistently show high sensitivity for cell killing and chromosomal aberrations in response to DNA crosslinking agents.
true
true
true
true
true
1,856
1
INTRODUCTION
1
14
[ "B14", "B2", "B15", "B16", "B17", "B18", "B19", "B20", "B21", "B11", "B22", "B23", "B24 B25 B26", "B27", "B28", "B29" ]
17,517,774
NA|pmid-11389461|pmid-12509764|pmid-15084315|pmid-15668941|pmid-14726021|pmid-15907771|pmid-14522929|pmid-15498778|pmid-15723711|pmid-12427531|pmid-16522646|pmid-12861027|pmid-15601828|pmid-15650050|pmid-9287344|pmid-12748186|pmid-15671039|pmid-2159378|pmid-2236046|pmid-10635999
Treatment of FA cells with low doses of mitomycin C produces excessive chromosomal interchanges due to misrepair of chromatid breaks (16,17) (arising in S or G2 phases) by an end-joining repair pathway, such as DNA-PK-dependent (18,19) or PARP1-dependent (20,21) non-homologous end joining (NHEJ).
[ "14", "2", "15", "16", "17", "18", "19", "20", "21", "11", "22", "23", "24–26", "27", "28", "29" ]
297
11,579
0
false
Treatment of FA cells with low doses of mitomycin C produces excessive chromosomal interchanges due to misrepair of chromatid breaks by an end-joining repair pathway, such as DNA-PK-dependent or PARP1-dependent non-homologous end joining (NHEJ).
[ "16,17", "arising in S or G2 phases", "18,19", "20,21" ]
Treatment of FA cells with low doses of mitomycin C produces excessive chromosomal interchanges due to misrepair of chromatid breaks by an end-joining repair pathway, such as DNA-PK-dependent or PARP1-dependent non-homologous end joining (NHEJ).
true
true
true
true
true
1,856
1
INTRODUCTION
1
14
[ "B14", "B2", "B15", "B16", "B17", "B18", "B19", "B20", "B21", "B11", "B22", "B23", "B24 B25 B26", "B27", "B28", "B29" ]
17,517,774
NA|pmid-11389461|pmid-12509764|pmid-15084315|pmid-15668941|pmid-14726021|pmid-15907771|pmid-14522929|pmid-15498778|pmid-15723711|pmid-12427531|pmid-16522646|pmid-12861027|pmid-15601828|pmid-15650050|pmid-9287344|pmid-12748186|pmid-15671039|pmid-2159378|pmid-2236046|pmid-10635999
Such cellular phenotypes are reminiscent of cells defective in HRR, including the well-studied rodent cell lines deficient in the Rad51 paralogs (11,22,23), which show high levels of spontaneous chromosomal aberrations and high sensitivity to crosslinking agents, suggesting an overlapping role for the FANC and HRR prot...
[ "14", "2", "15", "16", "17", "18", "19", "20", "21", "11", "22", "23", "24–26", "27", "28", "29" ]
357
11,580
0
false
Such cellular phenotypes are reminiscent of cells defective in HRR, including the well-studied rodent cell lines deficient in the Rad51 paralogs, which show high levels of spontaneous chromosomal aberrations and high sensitivity to crosslinking agents, suggesting an overlapping role for the FANC and HRR proteins in mai...
[ "11,22,23" ]
Such cellular phenotypes are reminiscent of cells defective in HRR, including the well-studied rodent cell lines deficient in the Rad51 paralogs, which show high levels of spontaneous chromosomal aberrations and high sensitivity to crosslinking agents, suggesting an overlapping role for the FANC and HRR proteins in mai...
true
true
true
true
true
1,856
1
INTRODUCTION
1
24–26
[ "B14", "B2", "B15", "B16", "B17", "B18", "B19", "B20", "B21", "B11", "B22", "B23", "B24 B25 B26", "B27", "B28", "B29" ]
17,517,774
NA|pmid-11389461|pmid-12509764|pmid-15084315|pmid-15668941|pmid-14726021|pmid-15907771|pmid-14522929|pmid-15498778|pmid-15723711|pmid-12427531|pmid-16522646|pmid-12861027|pmid-15601828|pmid-15650050|pmid-9287344|pmid-12748186|pmid-15671039|pmid-2159378|pmid-2236046|pmid-10635999
HRR capacity in FA cells, as indicated by synthetic reporter genes, is reported to be decreased (24–26), increased (27,28) or unaltered (29).
[ "14", "2", "15", "16", "17", "18", "19", "20", "21", "11", "22", "23", "24–26", "27", "28", "29" ]
141
11,581
1
false
HRR capacity in FA cells, as indicated by synthetic reporter genes, is reported to be decreased, increased or unaltered.
[ "24–26", "27,28", "29" ]
HRR capacity in FA cells, as indicated by synthetic reporter genes, is reported to be decreased, increased or unaltered.
true
true
true
true
true
1,856
1
INTRODUCTION
1
14
[ "B14", "B2", "B15", "B16", "B17", "B18", "B19", "B20", "B21", "B11", "B22", "B23", "B24 B25 B26", "B27", "B28", "B29" ]
17,517,774
NA|pmid-11389461|pmid-12509764|pmid-15084315|pmid-15668941|pmid-14726021|pmid-15907771|pmid-14522929|pmid-15498778|pmid-15723711|pmid-12427531|pmid-16522646|pmid-12861027|pmid-15601828|pmid-15650050|pmid-9287344|pmid-12748186|pmid-15671039|pmid-2159378|pmid-2236046|pmid-10635999
These approaches have not helped assess the functional overlap between the FA and HRR pathways.
[ "14", "2", "15", "16", "17", "18", "19", "20", "21", "11", "22", "23", "24–26", "27", "28", "29" ]
95
11,582
0
false
These approaches have not helped assess the functional overlap between the FA and HRR pathways.
[]
These approaches have not helped assess the functional overlap between the FA and HRR pathways.
true
true
true
true
true
1,856
2
INTRODUCTION
1
26
[ "B26", "B30 B31 B32" ]
17,517,774
pmid-15650050|pmid-11124945|pmid-12361951|pmid-15199173
The role of the FA pathway in DSB repair through DNA end joining mechanisms also has not been established.
[ "26", "30–32" ]
106
11,583
0
false
The role of the FA pathway in DSB repair through DNA end joining mechanisms also has not been established.
[]
The role of the FA pathway in DSB repair through DNA end joining mechanisms also has not been established.
true
true
true
true
true
1,857
2
INTRODUCTION
1
26
[ "B26", "B30 B31 B32" ]
17,517,774
pmid-15650050|pmid-11124945|pmid-12361951|pmid-15199173
FA cells generally do not exhibit phenotypes associated with gross NHEJ deficiency, such as high IR sensitivity.
[ "26", "30–32" ]
112
11,584
0
false
FA cells generally do not exhibit phenotypes associated with gross NHEJ deficiency, such as high IR sensitivity.
[]
FA cells generally do not exhibit phenotypes associated with gross NHEJ deficiency, such as high IR sensitivity.
true
true
true
true
true
1,857
2
INTRODUCTION
1
26
[ "B26", "B30 B31 B32" ]
17,517,774
pmid-15650050|pmid-11124945|pmid-12361951|pmid-15199173
It is not understood why various NHEJ assays in FA cells provide conflicting results.
[ "26", "30–32" ]
85
11,585
0
false
It is not understood why various NHEJ assays in FA cells provide conflicting results.
[]
It is not understood why various NHEJ assays in FA cells provide conflicting results.
true
true
true
true
true
1,857
2
INTRODUCTION
1
26
[ "B26", "B30 B31 B32" ]
17,517,774
pmid-15650050|pmid-11124945|pmid-12361951|pmid-15199173
For example, studies based on chromosomally integrated reporter constructs containing a I–Sce-I restriction site and PCR analysis found no reduction in NHEJ activity in FA cells from three complementation groups (A, D2 and G) compared to gene-complemented control cells (26).
[ "26", "30–32" ]
275
11,586
1
false
For example, studies based on chromosomally integrated reporter constructs containing a I–Sce-I restriction site and PCR analysis found no reduction in NHEJ activity in FA cells from three complementation groups (A, D2 and G) compared to gene-complemented control cells.
[ "26" ]
For example, studies based on chromosomally integrated reporter constructs containing a I–Sce-I restriction site and PCR analysis found no reduction in NHEJ activity in FA cells from three complementation groups compared to gene-complemented control cells.
true
true
true
true
true
1,857
2
INTRODUCTION
1
30–32
[ "B26", "B30 B31 B32" ]
17,517,774
pmid-15650050|pmid-11124945|pmid-12361951|pmid-15199173
However, an intact FA pathway was required for the end-joining repair of DSBs in plasmid-based assays (both in vitro and in vivo) and for survival of cells after electroporation with restriction enzymes was reported (30–32).
[ "26", "30–32" ]
224
11,587
1
false
However, an intact FA pathway was required for the end-joining repair of DSBs in plasmid-based assays (both in vitro and in vivo) and for survival of cells after electroporation with restriction enzymes was reported.
[ "30–32" ]
However, an intact FA pathway was required for the end-joining repair of DSBs in plasmid-based assays (both in vitro and in vivo) and for survival of cells after electroporation with restriction enzymes was reported.
true
true
true
true
true
1,857
3
INTRODUCTION
1
23
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
Although chromosomal rearrangements such as those associated with FA and HRR deficiencies are known to play a role in carcinogenesis, single-gene mutation and amplification, are not well characterized in FA and HHR mutant cells.
[ "23", "23", "33", "34", "35", "36", "37" ]
228
11,588
0
false
Although chromosomal rearrangements such as those associated with FA and HRR deficiencies are known to play a role in carcinogenesis, single-gene mutation and amplification, are not well characterized in FA and HHR mutant cells.
[]
Although chromosomal rearrangements such as those associated with FA and HRR deficiencies are known to play a role in carcinogenesis, single-gene mutation and amplification, are not well characterized in FA and HHR mutant cells.
true
true
true
true
true
1,858
3
INTRODUCTION
1
23
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
Using an isogenic CHO rad51d knockout mutant, we recently showed that HRR deficiency causes a substantial increase (∼12-fold) in the rate of spontaneous mutagenesis in the X-linked hprt (hypoxanthine phosphoribosyltransferase) gene, and in the rate of amplification at two loci (dhfr, ∼10-fold; CAD, ∼4-fold) (23).
[ "23", "23", "33", "34", "35", "36", "37" ]
314
11,589
1
false
Using an isogenic CHO rad51d knockout mutant, we recently showed that HRR deficiency causes a substantial increase (∼12-fold) in the rate of spontaneous mutagenesis in the X-linked hprt (hypoxanthine phosphoribosyltransferase) gene, and in the rate of amplification at two loci (dhfr, ∼10-fold; CAD, ∼4-fold).
[ "23" ]
Using an isogenic CHO rad51d knockout mutant, we recently showed that HRR deficiency causes a substantial increase in the rate of spontaneous mutagenesis in the X-linked hprt (hypoxanthine phosphoribosyltransferase) gene, and in the rate of amplification at two loci (dhfr, ∼10-fold; CAD, ∼4-fold).
true
true
true
true
true
1,858
3
INTRODUCTION
1
23
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
This mutant phenotype suggests a major role for HRR in rescuing broken DNA replication forks (23).
[ "23", "23", "33", "34", "35", "36", "37" ]
98
11,590
1
false
This mutant phenotype suggests a major role for HRR in rescuing broken DNA replication forks.
[ "23" ]
This mutant phenotype suggests a major role for HRR in rescuing broken DNA replication forks.
true
true
true
true
true
1,858
3
INTRODUCTION
1
33
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
Mutagenesis studies in human FA cells have given seemingly conflicting results (33).
[ "23", "23", "33", "34", "35", "36", "37" ]
84
11,591
1
false
Mutagenesis studies in human FA cells have given seemingly conflicting results.
[ "33" ]
Mutagenesis studies in human FA cells have given seemingly conflicting results.
true
true
true
true
true
1,858
3
INTRODUCTION
1
23
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
FA lymphoblasts had a ‘reduced’ rate of mutagenesis in the hprt gene in response to treatments with monofunctional and bifunctional psoralens, whereas the spontaneous mutant frequencies were markedly ‘increased’ in FA patients at two autosomal loci: glycophorin
[ "23", "23", "33", "34", "35", "36", "37" ]
261
11,592
0
false
FA lymphoblasts had a ‘reduced’ rate of mutagenesis in the hprt gene in response to treatments with monofunctional and bifunctional psoralens, whereas the spontaneous mutant frequencies were markedly ‘increased’ in FA patients at two autosomal loci: glycophorin
[]
FA lymphoblasts had a ‘reduced’ rate of mutagenesis in the hprt gene in response to treatments with monofunctional and bifunctional psoralens, whereas the spontaneous mutant frequencies were markedly ‘increased’ in FA patients at two autosomal loci: glycophorin
true
true
false
true
false
1,858
3
INTRODUCTION
1
36
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
A (GPA) in erythrocytes (34,35) and PIG-A in lymphoblasts (36).
[ "23", "23", "33", "34", "35", "36", "37" ]
63
11,593
1
false
A (GPA) in erythrocytes and PIG-A in lymphoblasts.
[ "34,35", "36" ]
A (GPA) in erythrocytes and PIG-A in lymphoblasts.
true
true
true
true
true
1,858
3
INTRODUCTION
1
37
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
In chicken DT40 cells a requirement for a FANC protein (FANCC) to promote translesion synthesis (TLS) during crosslink repair was reported (37).
[ "23", "23", "33", "34", "35", "36", "37" ]
144
11,594
1
false
In chicken DT40 cells a requirement for a FANC protein (FANCC) to promote translesion synthesis (TLS) during crosslink repair was reported.
[ "37" ]
In chicken DT40 cells a requirement for a FANC protein (FANCC) to promote translesion synthesis (TLS) during crosslink repair was reported.
true
true
true
true
true
1,858
3
INTRODUCTION
1
23
[ "B23", "B23", "B33", "B34", "B35", "B36", "B37" ]
17,517,774
pmid-16522646|pmid-16522646|NA|pmid-7689157|pmid-15822129|pmid-16166284|pmid-15327776|pmid-2687881|pmid-16787682|pmid-16787682|pmid-8868464|pmid-9566927|pmid-10859355|pmid-12509235|pmid-11389084|pmid-16522646
Thus, the precise role of the FA proteins in mutagenesis remains unclear, and may indeed involve multiple cellular mechanisms of maintaining genomic integrity.
[ "23", "23", "33", "34", "35", "36", "37" ]
159
11,595
0
false
Thus, the precise role of the FA proteins in mutagenesis remains unclear, and may indeed involve multiple cellular mechanisms of maintaining genomic integrity.
[]
Thus, the precise role of the FA proteins in mutagenesis remains unclear, and may indeed involve multiple cellular mechanisms of maintaining genomic integrity.
true
true
true
true
true
1,858
4
INTRODUCTION
1
38
[ "B38", "B23", "B39", "B40" ]
17,517,774
pmid-15533833|pmid-16522646|pmid-927508|pmid-6273843|pmid-15561104
In this study, we use a model mutagenesis system of isogenic CHO fancg (38) and rad51d (23) knockout mutants to understand how the FA pathway influences spontaneous mutagenesis and to distinguish the roles of the FA and HRR pathways in mutation control.
[ "38", "23", "39", "40" ]
253
11,596
1
false
In this study, we use a model mutagenesis system of isogenic CHO fancg and rad51d knockout mutants to understand how the FA pathway influences spontaneous mutagenesis and to distinguish the roles of the FA and HRR pathways in mutation control.
[ "38", "23" ]
In this study, we use a model mutagenesis system of isogenic CHO fancg and rad51d knockout mutants to understand how the FA pathway influences spontaneous mutagenesis and to distinguish the roles of the FA and HRR pathways in mutation control.
true
true
true
true
true
1,859
4
INTRODUCTION
1
39
[ "B38", "B23", "B39", "B40" ]
17,517,774
pmid-15533833|pmid-16522646|pmid-927508|pmid-6273843|pmid-15561104
CHO cells have been widely used to perform highly quantitative mutagenesis studies at the hprt locus (39) and, using the dhfr locus to analyze gene amplification, to assay a specific type of carcinogenic mutagenesis (40).
[ "38", "23", "39", "40" ]
221
11,597
1
false
CHO cells have been widely used to perform highly quantitative mutagenesis studies at the hprt locus and, using the dhfr locus to analyze gene amplification, to assay a specific type of carcinogenic mutagenesis.
[ "39", "40" ]
CHO cells have been widely used to perform highly quantitative mutagenesis studies at the hprt locus and, using the dhfr locus to analyze gene amplification, to assay a specific type of carcinogenic mutagenesis.
true
true
true
true
true
1,859
4
INTRODUCTION
1
38
[ "B38", "B23", "B39", "B40" ]
17,517,774
pmid-15533833|pmid-16522646|pmid-927508|pmid-6273843|pmid-15561104
We find both a ‘reduced’ rate of occurrence of viable hprt mutants and ‘increased’ rates of gene amplification in fancg cells.
[ "38", "23", "39", "40" ]
126
11,598
0
false
We find both a ‘reduced’ rate of occurrence of viable hprt mutants and ‘increased’ rates of gene amplification in fancg cells.
[]
We find both a ‘reduced’ rate of occurrence of viable hprt mutants and ‘increased’ rates of gene amplification in fancg cells.
true
true
true
true
true
1,859
4
INTRODUCTION
1
38
[ "B38", "B23", "B39", "B40" ]
17,517,774
pmid-15533833|pmid-16522646|pmid-927508|pmid-6273843|pmid-15561104
In addition, we compare the spectra of hprt mutations in the fancg and rad51d mutant lines with those of their gene-complemented control cells.
[ "38", "23", "39", "40" ]
143
11,599
0
false
In addition, we compare the spectra of hprt mutations in the fancg and rad51d mutant lines with those of their gene-complemented control cells.
[]
In addition, we compare the spectra of hprt mutations in the fancg and rad51d mutant lines with those of their gene-complemented control cells.
true
true
true
true
true
1,859