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1000 | TSC2 is a gene on chromosome 16p13.3 associated with the autosomal dominant neurocutaneous disorder , tuberous sclerosis complex ( TSC ) . | <dna>TSC2</dna> is a gene on <dna>chromosome 16p13.3</dna> associated with the autosomal dominant neurocutaneous disorder , tuberous sclerosis complex ( TSC ) . |
1001 | By using a partial nucleotide sequence from the cloned TSC2 and polymerase chain reaction methodology , we constructed a digoxigenin-labeled complementary DNA probe to examine TSC2 gene expression in autopsy- or biopsy-derived human tissues by in situ hybridization . | By using a partial nucleotide sequence from the cloned <dna>TSC2</dna> and polymerase chain reaction methodology , we constructed a <dna>digoxigenin-labeled complementary DNA probe</dna> to examine <dna>TSC2</dna> gene expression in autopsy- or biopsy-derived human tissues by in situ hybridization . |
1002 | TSC2 messenger RNA was widely expressed in various cell types throughout the body , including epithelia , lymphocytes , and cells with endocrine functions , e.g. , adrenal cortex and anterior pituitary . | <rna>TSC2 messenger RNA</rna> was widely expressed in various cell types throughout the body , including epithelia , <cell_type>lymphocytes</cell_type> , and cells with endocrine functions , e.g. , adrenal cortex and anterior pituitary . |
1003 | It was prominently and selectively ( within the central nervous system ) expressed in pyramidal cells of the cerebral cortex and other motor neurons , e.g. , in spinal cord and brainstem nuclei . | It was prominently and selectively ( within the central nervous system ) expressed in <cell_type>pyramidal cells</cell_type> of the cerebral cortex and other <cell_type>motor neurons</cell_type> , e.g. , in spinal cord and brainstem nuclei . |
1004 | Visceral TSC2 expression was comparable in autopsy tissues from patients with and without TSC ; TSC2 messenger RNA expression was most prominent in cells with a rapid mitotic rate and turnover , e.g. , epithelia and lymphocytes , with central nervous system pyramidal cells and other neurons being an obvious exception ,... | Visceral <dna>TSC2</dna> expression was comparable in autopsy tissues from patients with and without TSC ; <dna>TSC2</dna> messenger RNA expression was most prominent in cells with a rapid mitotic rate and turnover , e.g. , epithelia and <cell_type>lymphocytes</cell_type> , with central nervous system <cell_type>pyrami... |
1005 | This widespread expression of the TSC2 gene supports the view that it encodes a protein vital to cell growth and metabolism or one that functions as a tumor/growth suppressor . | This widespread expression of the <dna>TSC2 gene</dna> supports the view that it encodes a protein vital to cell growth and metabolism or one that functions as a tumor/growth suppressor . |
1006 | Apoptosis signaling pathways in normal T cells : differential activity of Bcl-2 and IL-1beta-converting enzyme family protease inhibitors on glucocorticoid- and Fas-mediated cytotoxicity . | Apoptosis signaling pathways in normal <cell_type>T cells</cell_type> : differential activity of <protein>Bcl-2</protein> and <protein>IL-1beta-converting enzyme family</protein> protease inhibitors on glucocorticoid- and Fas-mediated cytotoxicity . |
1007 | Fas -mediated apoptosis plays an important role in regulating the immune response in peripheral T cells . | <protein>Fas</protein> -mediated apoptosis plays an important role in regulating the immune response in <cell_type>peripheral T cells</cell_type> . |
1008 | Restimulation of T cell blasts up-regulates Fas and Fas ligand expression , with subsequent interaction leading to cell death . | Restimulation of <cell_type>T cell blasts</cell_type> up-regulates <protein>Fas</protein> and <protein>Fas</protein> ligand expression , with subsequent interaction leading to cell death . |
1009 | Overexpression of Bcl-2 in tumor cells blocks apoptosis induced by many stimuli , but inhibition of Fas -mediated killing has not been consistently observed . | Overexpression of <protein>Bcl-2</protein> in <cell_type>tumor cells</cell_type> blocks apoptosis induced by many stimuli , but inhibition of <protein>Fas</protein> -mediated killing has not been consistently observed . |
1010 | To examine the behavior of Bcl-2 in normal cells , T cell blasts were transiently transfected with Bcl-2 and related gene products to determine the effect on apoptotic signaling . | To examine the behavior of <protein>Bcl-2</protein> in <cell_type>normal cells</cell_type> , <cell_type>T cell blasts</cell_type> were transiently transfected with <protein>Bcl-2</protein> and related <protein>gene products</protein> to determine the effect on apoptotic signaling . |
1011 | Transient overexpression of Bcl-2 in mouse and human T cell blasts did not block Fas -mediated apoptosis , whereas etoposide- and glucocorticoid-induced cytotoxicity was potently inhibited . | Transient overexpression of <protein>Bcl-2</protein> in mouse and human <cell_type>T cell blasts</cell_type> did not block <protein>Fas</protein> -mediated apoptosis , whereas etoposide- and glucocorticoid-induced cytotoxicity was potently inhibited . |
1012 | Expression of Bcl-xL and adenovirus E1B 19K did not interfere with anti- Fas killing . | Expression of <protein>Bcl-xL</protein> and <protein>adenovirus E1B 19K</protein> did not interfere with anti- <protein>Fas</protein> killing . |
1013 | In contrast , interleukin-1beta-converting enzyme family protease inhibitors Ac-DEVD-CHO and CrmA blocked Fas -mediated apoptosis . | In contrast , interleukin-1beta-converting enzyme family protease inhibitors Ac-DEVD-CHO and CrmA blocked <protein>Fas</protein> -mediated apoptosis . |
1014 | These results suggest that peripheral T cells use distinct apoptosis signaling pathways with differential sensitivity to Bcl-2 and interleukin-1beta-converting enzyme family protease inhibitors . | These results suggest that <cell_type>peripheral T cells</cell_type> use distinct apoptosis signaling pathways with differential sensitivity to <protein>Bcl-2</protein> and interleukin-1beta-converting enzyme family protease inhibitors . |
1015 | Since T cells normally express Bcl-2 and Bcl-xL following activation , their inability to block Fas -mediated apoptosis may allow for the elimination of self-reactive cells and the appropriate regulation of immune responses . | Since <cell_type>T cells</cell_type> normally express <protein>Bcl-2</protein> and <protein>Bcl-xL</protein> following activation , their inability to block <protein>Fas</protein> -mediated apoptosis may allow for the elimination of <cell_type>self-reactive cells</cell_type> and the appropriate regulation of immune res... |
1016 | Increased interleukin 2 transcription in murine lymphocytes by ciprofloxacin . | Increased <protein>interleukin 2</protein> transcription in <cell_type>murine lymphocytes</cell_type> by ciprofloxacin . |
1017 | The fluoroquinolone antibiotic , ciprofloxacin ( cipro ) , induces hyperproduction of interleukin 2 ( IL-2 ) and interferon-gamma ( IFN-gamma ) in stimulated human peripheral blood lymphocytes . | The fluoroquinolone antibiotic , ciprofloxacin ( cipro ) , induces hyperproduction of <protein>interleukin 2</protein> ( <protein>IL-2</protein> ) and <protein>interferon-gamma</protein> ( <protein>IFN-gamma</protein> ) in stimulated <cell_type>human peripheral blood lymphocytes</cell_type> . |
1018 | In this investigation an enhanced and prolonged IL-2 and IL-2 mRNA response was also detected in both stimulated ( T cell mitogens or alloantigens ) murine splenocytes and in the stimulated murine T cell line EL-4 in the presence of ciprofloxacin ( 5-80 micrograms/ml ) as compared to control cells without antibiotics . | In this investigation an enhanced and prolonged <protein>IL-2</protein> and <rna>IL-2 mRNA</rna> response was also detected in both stimulated ( <protein>T cell mitogens</protein> or <protein>alloantigens</protein> ) <cell_type>murine splenocytes</cell_type> and in the stimulated <cell_line>murine T cell line EL-4</cel... |
1019 | However , in contrast to human lymphocytes , IFN-gamma production was inhibited and IFN-gamma mRNA levels were unaffected at 24 h and only slightly upregulated at 48 and 72 h of culture in murine splenocytes incubated with cipro ( 20 micrograms/ml ) . | However , in contrast to <cell_type>human lymphocytes</cell_type> , <protein>IFN-gamma</protein> production was inhibited and <rna>IFN-gamma mRNA</rna> levels were unaffected at 24 h and only slightly upregulated at 48 and 72 h of culture in <cell_type>murine splenocytes</cell_type> incubated with cipro ( 20 micrograms... |
1020 | EL-4 cells were transfected with a plasmid containing the IL-2 promoter and enhancer region linked to the chloramphenicol acetyltransferase ( CAT ) reporter gene . | <cell_type>EL-4 cells</cell_type> were transfected with a plasmid containing the <dna>IL-2 promoter</dna> and <dna>enhancer region</dna> linked to the <dna>chloramphenicol acetyltransferase ( CAT ) reporter gene</dna> . |
1021 | Analysis of CAT activity revealed that cipro enhanced IL-2 gene induction . | Analysis of <protein>CAT</protein> activity revealed that cipro enhanced IL-2 gene induction . |
1022 | In addition , EL-4 cells incubated with ciprofloxacin showed an early peak and more activated nuclear factor of activated T cells ( NFAT-1 ) as compared to control cells without antibiotics . | In addition , <cell_type>EL-4 cells</cell_type> incubated with ciprofloxacin showed an early peak and more activated nuclear factor of <cell_type>activated T cells</cell_type> ( <protein>NFAT-1</protein> ) as compared to control cells without antibiotics . |
1023 | Cipro did not affect the nuclear transcription factors AP-1 or NFIL-2A . | Cipro did not affect the <protein>nuclear transcription factors</protein> <protein>AP-1</protein> or <protein>NFIL-2A</protein> . |
1024 | Taken together , cipro inhibited IFN-gamma synthesis , but enhanced IL-2 production in murine lymphocytes by means of influencing NFAT-1 and causing an increased IL-2 transcription . | Taken together , cipro inhibited <protein>IFN-gamma</protein> synthesis , but enhanced <protein>IL-2</protein> production in <cell_type>murine lymphocytes</cell_type> by means of influencing <protein>NFAT-1</protein> and causing an increased <protein>IL-2</protein> transcription . |
1025 | Human T-cell leukemia virus type I Tax associates with and is negatively regulated by the NF-kappa B2 p100 gene product : implications for viral latency . | Human T-cell leukemia virus type I <protein>Tax</protein> associates with and is negatively regulated by the <protein>NF-kappa B2 p100 gene product</protein> : implications for viral latency . |
1026 | Human T-cell leukemia virus type I ( HTLV-I ) is the etiologic agent of the adult T-cell leukemia , an aggressive and often fatal malignancy of activated human CD4 T cells . | Human T-cell leukemia virus type I ( HTLV-I ) is the etiologic agent of the adult T-cell leukemia , an aggressive and often fatal malignancy of <cell_line>activated human CD4 T cells</cell_line> . |
1027 | HTLV-I encodes an essential 40-kDa protein termed Tax that not only transactivates the long terminal repeat of this retrovirus but also induces an array of cellular genes . | HTLV-I encodes an essential <protein>40-kDa protein</protein> termed <protein>Tax</protein> that not only transactivates the long terminal repeat of this retrovirus but also induces an array of <dna>cellular genes</dna> . |
1028 | Tax -mediated transformation of T cells likely involves the deregulated expression of various cellular genes that normally regulate lymphocyte growth produced by altered activity of various endogenous host transcription factors . | <protein>Tax</protein> -mediated transformation of <cell_type>T cells</cell_type> likely involves the deregulated expression of various <dna>cellular genes</dna> that normally regulate <cell_type>lymphocyte</cell_type> growth produced by altered activity of various endogenous host <protein>transcription factors</protei... |
1029 | In particular , Tax is capable of modulating the expression or activity of various host transcription factors , including members of the NF-kappa B/Rel and CREB/ATF families , as well as the cellular factors HEB-1 and p67SRF . | In particular , <protein>Tax</protein> is capable of modulating the expression or activity of various host <protein>transcription factors</protein> , including members of the <protein>NF-kappa B/Rel</protein> and <protein>CREB/ATF families</protein> , as well as the <protein>cellular factors</protein> <protein>HEB-1</p... |
1030 | An additional distinguishing characteristic of HTLV-I infection is the profound state of viral latency that is present in circulating primary leukemic T cells . | An additional distinguishing characteristic of HTLV-I infection is the profound state of viral latency that is present in circulating <cell_type>primary leukemic T cells</cell_type> . |
1031 | In this study , we demonstrate that HTLV-I Tax can physically associate with p100 , the product of the Rel-related NF-kappa B2 gene , both in transfected cells and in HTLV-I-infected leukemic T-cell lines . | In this study , we demonstrate that HTLV-I <protein>Tax</protein> can physically associate with <protein>p100</protein> , the product of the <dna>Rel-related NF-kappa B2 gene</dna> , both in <cell_line>transfected cells</cell_line> and in <cell_line>HTLV-I-infected leukemic T-cell lines</cell_line> . |
1032 | Furthermore , the physical interaction of Tax with p100 leads to the inhibition of Tax -induced activation of the HTLV-I and human immunodeficiency virus type 1 long terminal repeats , reflecting p100 -mediated cytoplasmic sequestration of the normally nuclearly expressed Tax protein . | Furthermore , the physical interaction of <protein>Tax</protein> with <protein>p100</protein> leads to the inhibition of <protein>Tax</protein> -induced activation of the HTLV-I and <dna>human immunodeficiency virus type 1 long terminal repeats</dna> , reflecting <protein>p100</protein> -mediated cytoplasmic sequestrat... |
1033 | In contrast , a mutant of Tax that selectively fails to activate nuclear NF-kappa B expression does not associate with p100 . | In contrast , a mutant of <protein>Tax</protein> that selectively fails to activate nuclear <protein>NF-kappa B</protein> expression does not associate with <protein>p100</protein> . |
1034 | ( ABSTRACT TRUNCATED AT 250 WORDS ) | ( ABSTRACT TRUNCATED AT 250 WORDS ) |
1035 | Rhabdomyosarcomas do not contain mutations in the DNA binding domains of myogenic transcription factors . | Rhabdomyosarcomas do not contain mutations in the DNA binding domains of myogenic <protein>transcription factors</protein> . |
1036 | Skeletal myogenesis is regulated by a group of transcription factors ( MyoD , myogenin , myf5 , and myf6 ) that are `` basic helix-loop-helix '' proteins that bind to the promoters of muscle-specific genes and promote their expression . | Skeletal myogenesis is regulated by a group of <protein>transcription factors</protein> ( <protein>MyoD</protein> , <protein>myogenin</protein> , <protein>myf5</protein> , and <protein>myf6</protein> ) that are <protein>`` basic helix-loop-helix '' proteins</protein> that bind to the <dna>promoters</dna> of <dna>muscle... |
1037 | We have previously shown that after a mutation of Leu122 to Arg the DNA binding basic domain of MyoD confers c-myc -like functional characteristics to the protein . | We have previously shown that after a mutation of Leu122 to Arg the <protein>DNA binding basic domain</protein> of <protein>MyoD</protein> confers <dna>c-myc</dna> -like functional characteristics to the protein . |
1038 | In this study we used single-strand conformation polymorphism analysis to determine whether such mutations occur naturally in rhabdomyosarcomas . | In this study we used single-strand conformation polymorphism analysis to determine whether such mutations occur naturally in rhabdomyosarcomas . |
1039 | We have found that the basic domains of all the myogenic factors remain unaltered in rhabdomyosarcomas . | We have found that the <protein>basic domains</protein> of all the <protein>myogenic factors</protein> remain unaltered in rhabdomyosarcomas . |
1040 | Selection against such mutations may be the result of functional redundancy of these myogenic transcription factors . | Selection against such mutations may be the result of functional redundancy of these <protein>myogenic transcription factors</protein> . |
1041 | Function and activation of NF-kappa B in the immune system . | Function and activation of <protein>NF-kappa B</protein> in the immune system . |
1042 | NF-kappa B is a ubiquitous transcription factor . | <protein>NF-kappa B</protein> is a <protein>ubiquitous transcription factor</protein> . |
1043 | Nevertheless , its properties seem to be most extensively exploited in cells of the immune system . | Nevertheless , its properties seem to be most extensively exploited in cells of the immune system . |
1044 | Among these properties are NF-kappa B 's rapid posttranslational activation in response to many pathogenic signals , its direct participation in cytoplasmic/nuclear signaling , and its potency to activate transcription of a great variety of genes encoding immunologically relevant proteins . | Among these properties are <protein>NF-kappa B</protein> 's rapid posttranslational activation in response to many pathogenic signals , its direct participation in cytoplasmic/nuclear signaling , and its potency to activate transcription of a great variety of genes encoding <protein>immunologically relevant proteins</p... |
1045 | In vertebrates , five distinct DNA binding subunits are currently known which might extensively heterodimerize , thereby forming complexes with distinct transcriptional activity , DNA sequence specificity , and cell type- and cell stage-specific distribution . | In vertebrates , five distinct <protein>DNA binding subunits</protein> are currently known which might extensively heterodimerize , thereby forming complexes with distinct transcriptional activity , DNA sequence specificity , and cell type- and cell stage-specific distribution . |
1046 | The activity of DNA binding NF-kappa B dimers is tightly controlled by accessory proteins called I kappa B subunits of which there are also five different species currently known in vertebrates . | The activity of <protein>DNA binding NF-kappa B dimers</protein> is tightly controlled by <protein>accessory proteins</protein> called <protein>I kappa B subunits</protein> of which there are also five different species currently known in vertebrates . |
1047 | I kappa B proteins inhibit DNA binding and prevent nuclear uptake of NF-kappa B complexes . | <protein>I kappa B proteins</protein> inhibit DNA binding and prevent nuclear uptake of <protein>NF-kappa B complexes</protein> . |
1048 | An exception is the Bcl-3 protein which in addition can function as a transcription activating subunit in th nucleus . | An exception is the <protein>Bcl-3 protein</protein> which in addition can function as a <protein>transcription activating subunit</protein> in th nucleus . |
1049 | Other I kappa B proteins are rather involved in terminating NF-kappa B 's activity in the nucleus . | Other <protein>I kappa B proteins</protein> are rather involved in terminating <protein>NF-kappa B</protein> 's activity in the nucleus . |
1050 | The intracellular events that lead to the inactivation of I kappa B , i.e. the activation of NF-kappa B , are complex . | The intracellular events that lead to the inactivation of <protein>I kappa B</protein> , i.e. the activation of <protein>NF-kappa B</protein> , are complex . |
1051 | They involve phosphorylation and proteolytic reactions and seem to be controlled by the cells ' redox status . | They involve phosphorylation and proteolytic reactions and seem to be controlled by the cells ' redox status . |
1052 | Interference with the activation or activity of NF-kappa B may be beneficial in suppressing toxic/septic shock , graft-vs-host reactions , acute inflammatory reactions , acute phase response , and radiation damage . | Interference with the activation or activity of <protein>NF-kappa B</protein> may be beneficial in suppressing toxic/septic shock , graft-vs-host reactions , acute inflammatory reactions , acute phase response , and radiation damage . |
1053 | The inhibition of NF-kappa B activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes . | The inhibition of <protein>NF-kappa B</protein> activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes . |
1054 | Lack of T-cell-mediated recognition of the fusion region of the pml/RAR-alpha hybrid protein by lymphocytes of acute promyelocytic leukemia patients . | Lack of T-cell-mediated recognition of the fusion region of the <protein>pml/RAR-alpha hybrid protein</protein> by <cell_type>lymphocytes</cell_type> of acute promyelocytic leukemia patients . |
1055 | In previous studies , it was shown that the fusion region of the pml/RAR-alpha protein , expressed by acute promyelocytic leukemia ( APL ) cells , can be specifically recognized in vitro by donor ( D. E. ) CD4 T cells in a HLA class II DR11-restricted fashion . | In previous studies , it was shown that the fusion region of the <protein>pml/RAR-alpha protein</protein> , expressed by <cell_line>acute promyelocytic leukemia ( APL ) cells</cell_line> , can be specifically recognized in vitro by donor ( D. E. ) <cell_line>CD4 T cells</cell_line> in a <protein>HLA class II</protein> ... |
1056 | We present here the results on the recognition of several pml/RAR-alpha peptides by APL patients expressing HLA DR11 . | We present here the results on the recognition of several pml/RAR-alpha peptides by APL patients expressing <protein>HLA DR11</protein> . |
1057 | The in vitro immunization of peripheral blood lymphocytes from four patients in remission ( S.R. , F.R. , M.M. , P. G. ) with BCR1/25 , a 25-mer pml/ RAR-alpha , did not elicit either a polyclonal or a clonal immune response specific to the peptide . | The in vitro immunization of <cell_type>peripheral blood lymphocytes</cell_type> from four patients in remission ( S.R. , F.R. , M.M. , P. G. ) with BCR1/25 , a 25-mer pml/ <protein>RAR-alpha</protein> , did not elicit either a polyclonal or a clonal immune response specific to the peptide . |
1058 | We then generated new donor anti-pml/RAR-alpha CD4 ( + ) T-cell clones . | We then generated new donor <cell_line>anti-pml/RAR-alpha CD4 ( + ) T-cell clones</cell_line> . |
1059 | These clones were tested for their recognition of BCR1/25 . | These clones were tested for their recognition of BCR1/25 . |
1060 | One clone ( C3/5 , CD3 ( + ) , CD4 ( + ) , CD8 ( - ) ) was selected for further analysis . | One clone ( <cell_line>C3/5 , CD3 ( + ) , CD4 ( + ) , CD8 ( - )</cell_line> ) was selected for further analysis . |
1061 | Clone C3/5 showed specific proliferation , cytotoxicity , and cytokine ( tumor necrosis factor alpha , granulocyte-macrophage colony-stimulating factor ) production when challenged with autologous lymphoblastic cell lines pulsed with peptide BCR1/25 . | <cell_line>Clone C3/5</cell_line> showed specific proliferation , cytotoxicity , and cytokine ( <protein>tumor necrosis factor alpha</protein> , <protein>granulocyte-macrophage colony-stimulating factor</protein> ) production when challenged with <cell_line>autologous lymphoblastic cell lines</cell_line> pulsed with pe... |
1062 | C3/5 cells developed specific proliferation and cytotoxicity when challenged with peptide-pulsed lymphoblastic cell lines and peripheral blood lymphocytes from the four DR11 ( + ) APL patients . | <cell_line>C3/5 cells</cell_line> developed specific proliferation and cytotoxicity when challenged with <cell_line>peptide-pulsed lymphoblastic cell lines</cell_line> and <cell_type>peripheral blood lymphocytes</cell_type> from the four DR11 ( + ) APL patients . |
1063 | APL blasts , available only from patients F.R. and P.G. , were not lysed by C3/5 and were unable to present peptide BCR1/25 . | <cell_type>APL blasts</cell_type> , available only from patients F.R. and P.G. , were not lysed by <cell_line>C3/5</cell_line> and were unable to present peptide BCR1/25 . |
1064 | Incubation of APL cells with IFN-gamma failed to induce HLA class II molecules and recognition by the C3/5 clone . | Incubation of <cell_line>APL cells</cell_line> with <protein>IFN-gamma</protein> failed to induce <protein>HLA class II molecules</protein> and recognition by the <cell_line>C3/5 clone</cell_line> . |
1065 | Since APL cells do not express HLA class II molecules , we tested in two donors ( D.E. and C.H.R. ) and in patients S.R.and P.G.whether the use of 9-mer peptides ( BCR1/9 ) would generate a CD8 /HLA class I -restricted response . | Since <cell_line>APL cells</cell_line> do not express <protein>HLA class II molecules</protein> , we tested in two donors ( D.E. and C.H.R. ) and in patients S.R.and P.G.whether the use of 9-mer peptides ( BCR1/9 ) would generate a <protein>CD8</protein> <protein>/HLA class I</protein> -restricted response . |
1066 | No peptide-specific T-cell line or clone could be generated from both donors and patients . | No <cell_line>peptide-specific T-cell line</cell_line> or clone could be generated from both donors and patients . |
1067 | These findings are discussed in relation to possible therapeutic approaches to the immunotherapy of APL . | These findings are discussed in relation to possible therapeutic approaches to the immunotherapy of APL . |
1068 | The proximal regulatory element of the interferon-gamma promoter mediates selective expression in T cells . | The proximal regulatory element of the <dna>interferon-gamma promoter</dna> mediates selective expression in <cell_type>T cells</cell_type> . |
1069 | Interferon-gamma ( IFN-gamma ) is produced by natural killer cells and certain subsets of T cells , but the basis for its selective expression is unknown . | <protein>Interferon-gamma</protein> ( <protein>IFN-gamma</protein> ) is produced by <cell_type>natural killer cells</cell_type> and certain subsets of <cell_type>T cells</cell_type> , but the basis for its selective expression is unknown . |
1070 | Within the region between -108 and -40 base pairs of the IFN-gamma promoter are two conserved and essential regulatory elements , which confer activation-specific expression in T cells . | Within the region between -108 and -40 base pairs of the <protein>IFN-gamma</protein> promoter are two conserved and essential <dna>regulatory elements</dna> , which confer activation-specific expression in <cell_type>T cells</cell_type> . |
1071 | This report describes studies indicating that the most proximal of these two regulatory elements is an important determinant of its restricted expression . | This report describes studies indicating that the most proximal of these two <dna>regulatory elements</dna> is an important determinant of its restricted expression . |
1072 | The proximal element is a composite site that binds members of the CREB/ATF , AP-1 , and octamer families of transcription factors . | The proximal element is a composite site that binds members of the <protein>CREB/ATF</protein> , <protein>AP-1</protein> , and <protein>octamer families</protein> of <protein>transcription factors</protein> . |
1073 | Jun is essential for activation-induced transcription and binds preferably as a heterodimer with ATF-2 . | <protein>Jun</protein> is essential for activation-induced transcription and binds preferably as a heterodimer with <protein>ATF-2</protein> . |
1074 | In contrast , CREB appears to dampen transcription from this element . | In contrast , <protein>CREB</protein> appears to dampen transcription from this element . |
1075 | The CpG dinucleotide in this element is selectively methylated in Th2 T cells and other cells that do not express IFN-gamma , and methylation markedly reduces transcription factor binding . | The CpG dinucleotide in this <dna>element</dna> is selectively methylated in <cell_type>Th2 T cells</cell_type> and other cells that do not express <protein>IFN-gamma</protein> , and methylation markedly reduces <protein>transcription factor</protein> binding . |
1076 | As a target for DNA methylation and for binding of transcription factors that mediate or impede transcription , this element appears to play a central role in controlling IFN-gamma expression . | As a target for DNA methylation and for binding of <protein>transcription factors</protein> that mediate or impede transcription , this element appears to play a central role in controlling <protein>IFN-gamma</protein> expression . |
1077 | CD40 , but not lipopolysaccharide and anti-IgM stimulation of primary B lymphocytes , leads to a persistent nuclear accumulation of RelB . | <protein>CD40</protein> , but not lipopolysaccharide and <protein>anti-IgM</protein> stimulation of <cell_type>primary B lymphocytes</cell_type> , leads to a persistent nuclear accumulation of <protein>RelB</protein> . |
1078 | In this study we analyzed the effect of CD40 stimulation on the activity and nuclear appearance of Rel/nuclear factor kappaB ( NF-kappaB ) factors in primary murine B lymphocytes . | In this study we analyzed the effect of <protein>CD40</protein> stimulation on the activity and nuclear appearance of <protein>Rel/nuclear factor kappaB ( NF-kappaB ) factors</protein> in <cell_type>primary murine B lymphocytes</cell_type> . |
1079 | We show that triggering of CD40 signaling pathway ( s ) by CD40 ligands expressed on L cells led to strong activation of an NF-kappaB-controlled beta-globin reporter gene in primary B lymphocytes from transgenic mice . | We show that triggering of <protein>CD40</protein> signaling pathway ( s ) by <protein>CD40 ligands</protein> expressed on <cell_type>L cells</cell_type> led to strong activation of an <dna>NF-kappaB-controlled beta-globin reporter gene</dna> in <cell_type>primary B lymphocytes</cell_type> from transgenic mice . |
1080 | Analyses of nuclear translocation of individual members of Rel proteins after CD40 induction of primary B cells showed a strong and long-lasting accumulation of RelB and , less pronounced , of c-Rel . | Analyses of nuclear translocation of individual members of <protein>Rel proteins</protein> after <protein>CD40</protein> induction of <cell_type>primary B cells</cell_type> showed a strong and long-lasting accumulation of <protein>RelB</protein> and , less pronounced , of <protein>c-Rel</protein> . |
1081 | LPS stimulation did not give rise to a persistent nuclear accumulation of RelB and c-Rel , whereas nuclear c-Rel , but not RelB , accumulated after B cell receptor stimulation . | LPS stimulation did not give rise to a persistent nuclear accumulation of <protein>RelB</protein> and <protein>c-Rel</protein> , whereas nuclear <protein>c-Rel</protein> , but not <protein>RelB</protein> , accumulated after B cell receptor stimulation . |
1082 | CD40 induced not only nuclear translocation but also de novo synthesis of RelB RNA and protein . | <protein>CD40</protein> induced not only nuclear translocation but also de novo synthesis of <rna>RelB RNA</rna> and protein . |
1083 | S107 plasmacytoma cells , which express CD40 but are defective for the nuclear appearance of p50/p65-NF-kappaB , do not express RelB after CD40 stimulation . | <cell_line>S107 plasmacytoma cells</cell_line> , which express <protein>CD40</protein> but are defective for the nuclear appearance of <protein>p50/p65-NF-kappaB</protein> , do not express <protein>RelB</protein> after <protein>CD40</protein> stimulation . |
1084 | In S107 cells stably transfected with relB genes , stimulation of nuclear RelB translocation by CD40 was observed . | In <cell_line>S107 cells</cell_line> stably transfected with <dna>relB genes</dna> , stimulation of nuclear <protein>RelB</protein> translocation by <protein>CD40</protein> was observed . |
1085 | These results indicate that stimulation of CD40 signaling pathways exerts a long-lasting stimulatory effect on both the transcription and nuclear translocation of RelB . | These results indicate that stimulation of <protein>CD40</protein> signaling pathways exerts a long-lasting stimulatory effect on both the transcription and nuclear translocation of <protein>RelB</protein> . |
1086 | Since LPS and anti-IgM were unable to activate RelB , CD40 appears to trigger a special program of gene expression involved in the proliferation and/or differentiation of B lymphocytes . | Since LPS and <protein>anti-IgM</protein> were unable to activate <protein>RelB</protein> , <protein>CD40</protein> appears to trigger a special program of gene expression involved in the proliferation and/or differentiation of <cell_type>B lymphocytes</cell_type> . |
1087 | Identification and characterization of a leukocyte-specific component of the nuclear body . | Identification and characterization of a leukocyte-specific component of the nuclear body . |
1088 | The nuclear body ( NB ) is a cellular organelle that is involved in the pathogenesis of acute promyelocytic leukemia and viral infection . | The nuclear body ( NB ) is a cellular organelle that is involved in the pathogenesis of acute promyelocytic leukemia and viral infection . |
1089 | The NB is also a target of antibodies in the serum of patients with the autoimmune disease primary biliary cirrhosis . | The NB is also a target of <protein>antibodies</protein> in the serum of patients with the autoimmune disease primary biliary cirrhosis . |
1090 | In this study , serum from a patient with primary biliary cirrhosis was used to identify a cDNA encoding a novel component of the NB , a 140-kDa protein designated Sp140 . | In this study , serum from a patient with primary biliary cirrhosis was used to identify a cDNA encoding a novel component of the NB , a <protein>140-kDa protein</protein> designated <protein>Sp140</protein> . |
1091 | The predicted amino acid sequence of the amino-terminal portion of Sp140 was similar to Sp100 , a previously identified NB protein . | The predicted amino acid sequence of the <protein>amino-terminal portion</protein> of <protein>Sp140</protein> was similar to <protein>Sp100</protein> , a previously identified <protein>NB protein</protein> . |
1092 | The carboxyl portion of Sp140 contained a zinc-finger domain and a bromodomain , motifs that are present in proteins regulating gene transcription . | The <protein>carboxyl portion</protein> of <protein>Sp140</protein> contained a <protein>zinc-finger domain</protein> and a <protein>bromodomain</protein> , motifs that are present in proteins regulating gene transcription . |
1093 | High levels of Sp140 mRNA were detected in human spleen and peripheral blood leukocytes , but not other human tissues . | High levels of <rna>Sp140 mRNA</rna> were detected in human spleen and <cell_type>peripheral blood leukocytes</cell_type> , but not other human tissues . |
1094 | The level of SP140 mRNA in myeloid precursor cell lines HL60 and NB4 markedly increased in response to chemically induced cellular differentiation . | The level of <rna>SP140 mRNA</rna> in <cell_line>myeloid precursor cell lines</cell_line> <cell_line>HL60</cell_line> and <cell_line>NB4</cell_line> markedly increased in response to chemically induced cellular differentiation . |
1095 | Immunohistochemical techniques were used to demonstrate that SP140 localized to the NB in differentiated HL60 and NB4 cells . | Immunohistochemical techniques were used to demonstrate that <protein>SP140</protein> localized to the NB in differentiated <cell_line>HL60</cell_line> and <cell_line>NB4 cells</cell_line> . |
1096 | The location of Sp140 in the NB , and expression of this gene in cells involved in host defense , suggest that Sp140 may be involved in the pathogenesis of acute promyelocytic leukemia and viral infection . | The location of <protein>Sp140</protein> in the NB , and expression of this gene in cells involved in host defense , suggest that <protein>Sp140</protein> may be involved in the pathogenesis of acute promyelocytic leukemia and viral infection . |
1097 | Regulation of cytokine and cytokine receptor expression by glucocorticoids . | Regulation of <protein>cytokine</protein> and <protein>cytokine receptor</protein> expression by glucocorticoids . |
1098 | Glucocorticoids ( GCS ) profoundly inhibit several aspects of T cell immunity largely through inhibition of cytokine expression at the transcriptional and posttranscriptional levels . | Glucocorticoids ( GCS ) profoundly inhibit several aspects of T cell immunity largely through inhibition of <protein>cytokine</protein> expression at the transcriptional and posttranscriptional levels . |
1099 | GCS were also reported to act indirectly by inducing transforming growth factor-beta expression , which in turn blocks T cell immunity . | GCS were also reported to act indirectly by inducing transforming <protein>growth factor-beta</protein> expression , which in turn blocks T cell immunity . |
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