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16400 | To understand the role of MARs in IgH enhancer regulation , we have identified a novel MAR-binding protein , MAR-BP1 , from soluble nuclear matrix preparations based on its ability to bind to the MARs associated with the IgH enhancer . | To understand the role of <protein>MARs</protein> in <dna>IgH enhancer</dna> regulation , we have identified a novel <protein>MAR-binding protein</protein> , <protein>MAR-BP1</protein> , from soluble nuclear matrix preparations based on its ability to bind to the <protein>MARs</protein> associated with the <dna>IgH enh... |
16401 | Purified MAR-BP1 migrates as a 33-kDa protein , and it can be found in nuclear matrix preparations from a number of different types of lymphoid cell lines . | Purified <protein>MAR-BP1</protein> migrates as a <protein>33-kDa protein</protein> , and it can be found in nuclear matrix preparations from a number of different types of <cell_line>lymphoid cell lines</cell_line> . |
16402 | Although specific binding sites have been difficult to localize by chemical or enzymatic footprinting procedures , NF-muNR binding sites are critical for efficient MAR-BP1 binding . | Although specific binding sites have been difficult to localize by chemical or enzymatic footprinting procedures , <protein>NF-muNR</protein> binding sites are critical for efficient <protein>MAR-BP1</protein> binding . |
16403 | Indeed , binding of the IgH enhancer to either intact nuclear matrix preparations or to MAR-BP1 is mutually exclusive to NF-muNR binding . | Indeed , binding of the <dna>IgH enhancer</dna> to either intact nuclear matrix preparations or to <protein>MAR-BP1</protein> is mutually exclusive to <protein>NF-muNR</protein> binding . |
16404 | These results are consistent with a model for cell-type specific regulation in which binding of the NF-muNR repressor to the IgH enhancer prevents nuclear matrix attachment in inappropriate cells by interfering with MAR-BP1 /enhancer interaction . | These results are consistent with a model for cell-type specific regulation in which binding of the <protein>NF-muNR repressor</protein> to the <dna>IgH enhancer</dna> prevents nuclear matrix attachment in inappropriate cells by interfering with <protein>MAR-BP1</protein> <dna>/enhancer</dna> interaction . |
16405 | PU.1 ( Spi-1 ) and C/EBP alpha regulate expression of the granulocyte-macrophage colony-stimulating factor receptor alpha gene . | <protein>PU.1</protein> ( <protein>Spi-1</protein> ) and <protein>C/EBP alpha</protein> regulate expression of the <dna>granulocyte-macrophage colony-stimulating factor receptor alpha gene</dna> . |
16406 | Growth factor receptors play an important role in hematopoiesis . | <protein>Growth factor receptors</protein> play an important role in hematopoiesis . |
16407 | In order to further understand the mechanisms directing the expression of these key regulators of hematopoiesis , we initiated a study investigating the transcription factors activating the expression of the granulocyte-macrophage colony-stimulating factor ( GM-CSF ) receptor alpha gene . | In order to further understand the mechanisms directing the expression of these key regulators of hematopoiesis , we initiated a study investigating the <protein>transcription factors</protein> activating the expression of the <dna>granulocyte-macrophage colony-stimulating factor ( GM-CSF ) receptor alpha gene</dna> . |
16408 | Here , we demonstrate that the human GM-CSF receptor alpha promoter directs reporter gene activity in a tissue-specific fashion in myelomonocytic cells , which correlates with its expression pattern as analyzed by reverse transcription PCR . | Here , we demonstrate that the <dna>human GM-CSF receptor alpha promoter</dna> directs <dna>reporter gene</dna> activity in a tissue-specific fashion in <cell_type>myelomonocytic cells</cell_type> , which correlates with its expression pattern as analyzed by reverse transcription PCR . |
16409 | The GM-CSF receptor alpha promoter contains an important functional site between positions -53 and -41 as identified by deletion analysis of reporter constructs . | The <dna>GM-CSF receptor alpha promoter</dna> contains an important functional site between positions -53 and -41 as identified by deletion analysis of <dna>reporter constructs</dna> . |
16410 | We show that the myeloid and B cell transcription factor PU.1 binds specifically to this site . | We show that the myeloid and <protein>B cell transcription factor</protein> <protein>PU.1</protein> binds specifically to this site . |
16411 | Furthermore , we demonstrate that a CCAAT site located upstream of the PU.1 site between positions -70 and -54 is involved in positive-negative regulation of the GM-CSF receptor alpha promoter activity . | Furthermore , we demonstrate that a <dna>CCAAT site</dna> located upstream of the <dna>PU.1 site</dna> between positions -70 and -54 is involved in positive-negative regulation of the <dna>GM-CSF receptor alpha promoter</dna> activity . |
16412 | C/EBP alpha is the major CCAAT/enhancer-binding protein ( C/EBP ) form binding to this site in nuclear extracts of U937 cells . | <protein>C/EBP alpha</protein> is the major <protein>CCAAT/enhancer-binding protein</protein> ( <protein>C/EBP</protein> ) form binding to this site in nuclear extracts of <cell_line>U937 cells</cell_line> . |
16413 | Point mutations of either the PU.1 site or the C/EBP site that abolish the binding of the respective factors result in a significant decrease of GM-CSF receptor alpha promoter activity in myelomonocytic cells only . | Point mutations of either the <dna>PU.1 site</dna> or the <dna>C/EBP site</dna> that abolish the binding of the respective factors result in a significant decrease of <dna>GM-CSF receptor alpha promoter</dna> activity in <cell_type>myelomonocytic cells</cell_type> only . |
16414 | Furthermore , we demonstrate that in myeloid and B cell extracts , PU.1 forms a novel , specific , more slowly migrating complex ( PU-SF ) when binding the GM-CSF receptor alpha promoter PU.1 site . | Furthermore , we demonstrate that in myeloid and B cell extracts , <protein>PU.1</protein> forms a novel , specific , more slowly migrating complex ( <protein>PU-SF</protein> ) when binding the <protein>GM-CSF receptor alpha</protein> promoter <dna>PU.1 site</dna> . |
16415 | This is the first demonstration of a specific interaction with PU.1 on a myeloid PU.1 binding site . | This is the first demonstration of a specific interaction with <protein>PU.1</protein> on a <dna>myeloid PU.1 binding site</dna> . |
16416 | The novel complex is distinct from that described previously as binding to B cell enhancer sites and can be formed by addition of PU.1 to extracts from certain nonmyeloid cell types which do not express PU.1 , including T cells and epithelial cells , but not from erythroid cells . | The novel complex is distinct from that described previously as binding to <dna>B cell enhancer sites</dna> and can be formed by addition of <protein>PU.1</protein> to extracts from certain <cell_type>nonmyeloid cell types</cell_type> which do not express <protein>PU.1</protein> , including <cell_type>T cells</cell_typ... |
16417 | Furthermore , we demonstrate that the PU-SF complex binds to PU.1 sites found on a number of myeloid promoters , and its formation requires an intact PU.1 site adjacent to a single-stranded region . | Furthermore , we demonstrate that the <protein>PU-SF complex</protein> binds to <protein>PU.1</protein> sites found on a number of <dna>myeloid promoters</dna> , and its formation requires an intact <dna>PU.1 site</dna> adjacent to a single-stranded region . |
16418 | Expression of PU.1 in nonmyeloid cells can activate the GM-CSF receptor alpha promoter . | Expression of <protein>PU.1</protein> in <cell_type>nonmyeloid cells</cell_type> can activate the <dna>GM-CSF receptor alpha promoter</dna> . |
16419 | Deletion of the amino-terminal region of PU.1 results in a failure to form the PU-SF complex and in a concomitant loss of transactivation , suggesting that formation of the PU-SF complex is of functional importance for the activity of the GM-CSF receptor alpha promoter . | Deletion of the <protein>amino-terminal region</protein> of <protein>PU.1</protein> results in a failure to form the <protein>PU-SF</protein> complex and in a concomitant loss of transactivation , suggesting that formation of the <protein>PU-SF complex</protein> is of functional importance for the activity of the <dna>... |
16420 | Finally , we demonstrate that C/EBP alpha can also active the GM-CSF receptor alpha promoter in nonmyeloid cells . | Finally , we demonstrate that <protein>C/EBP alpha</protein> can also active the <dna>GM-CSF receptor alpha promoter</dna> in <cell_type>nonmyeloid cells</cell_type> . |
16421 | ( ABSTRACT TRUNCATED AT 400 WORDS ) | ( ABSTRACT TRUNCATED AT 400 WORDS ) |
16422 | HMG-I binds to GATA motifs : implications for an HPFH syndrome . | <protein>HMG-I</protein> binds to <dna>GATA motifs</dna> : implications for an HPFH syndrome . |
16423 | We have examined binding of the nuclear protein HMG-I to the human gamma-globin promoter . | We have examined binding of the <protein>nuclear protein</protein> <protein>HMG-I</protein> to the <dna>human gamma-globin promoter</dna> . |
16424 | We find that HMG-I binds preferentially to the more 3 ' of a pair of GATA motifs in the gamma-globin promoter ; this paired motif is bound by the erythroid factor GATA-1 . | We find that <protein>HMG-I</protein> binds preferentially to the more 3 ' of a pair of <dna>GATA motifs</dna> in the <dna>gamma-globin promoter</dna> ; this paired motif is bound by the <protein>erythroid factor GATA-1</protein> . |
16425 | A naturally occurring mutation ( -175 T-C ) in the area bound by HMG-I results in overexpression of gamma-globin in adult red blood cells ( HPFH ) and up-regulation of the gamma-globin promoter in in vitro expression assays ; HMG-I does not bind to this mutant sequence . | A naturally occurring mutation ( -175 T-C ) in the area bound by <protein>HMG-I</protein> results in overexpression of <protein>gamma-globin</protein> in <cell_type>adult red blood cells</cell_type> ( <cell_type>HPFH</cell_type> ) and up-regulation of the <dna>gamma-globin promoter</dna> in in vitro expression assays ;... |
16426 | A survey of GATA motifs from other globin cis-elements demonstrates HMG-I binding to most of them . | A survey of <dna>GATA motifs</dna> from other <dna>globin cis-elements</dna> demonstrates <protein>HMG-I</protein> binding to most of them . |
16427 | These findings implicate HMG-I in the HPFH phenotype ; we speculate that it may participate in the formation of multiprotein complexes that regulate globin gene expression . | These findings implicate <protein>HMG-I</protein> in the <cell_type>HPFH</cell_type> phenotype ; we speculate that it may participate in the formation of <protein>multiprotein complexes</protein> that regulate globin gene expression . |
16428 | Constitutive activation of different Jak tyrosine kinases in human T cell leukemia virus type 1 ( HTLV-1 ) tax protein or virus-transformed cells . | Constitutive activation of different <protein>Jak tyrosine kinases</protein> in <protein>human T cell leukemia virus type 1 ( HTLV-1 ) tax protein</protein> or <cell_line>virus-transformed cells</cell_line> . |
16429 | HTLV-1 infection causes an adult T cell leukemia in humans . | HTLV-1 infection causes an adult T cell leukemia in humans . |
16430 | The viral encoded protein tax , is thought to play an important role in oncogenesis . | The <protein>viral encoded protein</protein> <protein>tax</protein> , is thought to play an important role in oncogenesis . |
16431 | Our previous data obtained from a tax transgenic mouse model revealed that tax transforms mouse fibroblasts but not thymocytes , despite comparable levels of tax expression in both tissues . | Our previous data obtained from a <protein>tax</protein> transgenic mouse model revealed that <protein>tax</protein> transforms <cell_type>mouse fibroblasts</cell_type> but not <cell_type>thymocytes</cell_type> , despite comparable levels of <protein>tax</protein> expression in both tissues . |
16432 | Constitutive tyrosine phosphorylation of a 130-kD protein ( s ) was observed in the tax transformed fibroblast B line and in HTLV-1 transformed human lymphoid lines , but not in thymocytes from Thy-tax transgenic mice . | Constitutive tyrosine phosphorylation of a <protein>130-kD protein</protein> ( s ) was observed in the <protein>tax</protein> <cell_line>transformed fibroblast B line</cell_line> and in <cell_line>HTLV-1 transformed human lymphoid lines</cell_line> , but not in <cell_type>thymocytes</cell_type> from Thy-tax transgenic ... |
16433 | Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of Jak kinase specific antibodies , identified p130 as Jak2 in the tax transformed mouse fibroblastic cell line and Jak3 in HTLV-1 transformed human T cell lines . | Phosphotyrosine immunoprecipitation followed by Western blot analysis with a set of <protein>Jak kinase specific antibodies</protein> , identified p130 as <protein>Jak2</protein> in the <protein>tax</protein> transformed <cell_line>mouse fibroblastic cell line</cell_line> and <protein>Jak3</protein> in <cell_line>HTLV-... |
16434 | Phosphorylation of Jak2 in tax transformed cells resulted from high expression of IL-6 . | Phosphorylation of <protein>Jak2</protein> in <cell_line>tax transformed cells</cell_line> resulted from high expression of IL-6 . |
16435 | Tyrosine phosphorylation of this protein could also be induced in Balb/c3T3 cells using a supernatant from the B line , which was associated with induction of cell proliferation . | Tyrosine phosphorylation of this protein could also be induced in <cell_line>Balb/c3T3 cells</cell_line> using a supernatant from the <cell_line>B line</cell_line> , which was associated with induction of cell proliferation . |
16436 | Both phosphorylation and proliferation were inhibited by IL-6 neutralizing antibodies . | Both phosphorylation and proliferation were inhibited by <protein>IL-6 neutralizing antibodies</protein> . |
16437 | Constitutive phosphorylation of Jak kinases may facilitate tumor growth in both HTLV-1 infected human T cells and the transgenic mouse model . | Constitutive phosphorylation of <protein>Jak kinases</protein> may facilitate tumor growth in both <cell_type>HTLV-1 infected human T cells</cell_type> and the transgenic mouse model . |
16438 | Regulation of c-jun mRNA expression by hydroxyurea in human K562 cells during erythroid differentiation [ published erratum appears in Biochim Biophys Acta 1995 Dec 27 ; 1264 ( 3 ) : 409 ] | Regulation of <rna>c-jun mRNA</rna> expression by hydroxyurea in <cell_line>human K562 cells</cell_line> during erythroid differentiation [ published erratum appears in Biochim Biophys Acta 1995 Dec 27 ; 1264 ( 3 ) : 409 ] |
16439 | Hydroxyurea ( HU ) is an antitumor agent which also induces hemoglobinization during erythroid differentiation . | Hydroxyurea ( HU ) is an antitumor agent which also induces hemoglobinization during erythroid differentiation . |
16440 | In addition , HU stimulates the synthesis of fetal hemoglobin in sickle cell anemia patients . | In addition , HU stimulates the synthesis of <protein>fetal hemoglobin</protein> in sickle cell anemia patients . |
16441 | To further understand its mechanism of action , we investigated the effects of HU on regulation of c-jun expression prior to the onset of erythroid differentiation of K562 cells . | To further understand its mechanism of action , we investigated the effects of HU on regulation of <dna>c-jun</dna> expression prior to the onset of erythroid differentiation of <cell_line>K562 cells</cell_line> . |
16442 | HU induced a dose-dependent stimulation of c-jun synthesis . | HU induced a dose-dependent stimulation of <dna>c-jun</dna> synthesis . |
16443 | The levels of c-jun mRNA was elevated 4 to 7.5-fold by HU within 2 h . | The levels of <rna>c-jun mRNA</rna> was elevated 4 to 7.5-fold by HU within 2 h . |
16444 | This was followed by a gradual decline to the basal level by 24 h . | This was followed by a gradual decline to the basal level by 24 h . |
16445 | Both nuclear run-on and actinomycin D pulse experiments strongly indicate that HU regulates c-jun mRNA expression by increasing the rate of synthesis as well as stabilizing the c-jun mRNA . | Both nuclear run-on and actinomycin D pulse experiments strongly indicate that HU regulates <rna>c-jun mRNA</rna> expression by increasing the rate of synthesis as well as stabilizing the <rna>c-jun mRNA</rna> . |
16446 | In addition , the level of jun protein was elevated by 2 to 5-fold within 4 h in HU treated cells . | In addition , the level of <protein>jun protein</protein> was elevated by 2 to 5-fold within 4 h in <cell_line>HU treated cells</cell_line> . |
16447 | Furthermore , concentrations of HU below 250 microM slightly increased the 5X AP-1 /CAT activity . | Furthermore , concentrations of HU below 250 microM slightly increased the 5X <protein>AP-1</protein> <protein>/CAT</protein> activity . |
16448 | These results strongly suggest that HU induces both transcriptional and post-transcription regulation of c-jun during erythroid differentiation . | These results strongly suggest that HU induces both transcriptional and post-transcription regulation of <dna>c-jun</dna> during erythroid differentiation . |
16449 | In vivo and in vitro effects of glucocorticoids on lymphocyte proliferation in man : relationship to glucocorticoid receptors . | In vivo and in vitro effects of glucocorticoids on lymphocyte proliferation in man : relationship to <protein>glucocorticoid receptors</protein> . |
16450 | Interrelations between the hypothalamic-pituitary-adrenal system ( HPA ) and the immune system represent a well-documented biological phenomenon . | Interrelations between the hypothalamic-pituitary-adrenal system ( HPA ) and the immune system represent a well-documented biological phenomenon . |
16451 | While in vitro administration of glucocorticoids may inhibit concanavalin A ( Con A ) - and phytohemagglutinin ( PHA ) -induced T-cell proliferation , pokeweed mitogen ( PWM ) -driven B-cell mitogenesis is relatively resistant to glucocorticoids . | While in vitro administration of glucocorticoids may inhibit concanavalin A ( Con A ) - and phytohemagglutinin ( PHA ) -induced T-cell proliferation , <protein>pokeweed mitogen</protein> ( <protein>PWM</protein> ) -driven B-cell mitogenesis is relatively resistant to glucocorticoids . |
16452 | To further explore the link between the HPA and the immune system in relation to glucocorticoid receptor function , dose-response curves were obtained for Con A -and PHA -induced T-cell mitogenesis , PWM -generated B-cell mitogenesis and spontaneous lymphocyte proliferation in 13 healthy controls . | To further explore the link between the HPA and the immune system in relation to <protein>glucocorticoid receptor</protein> function , dose-response curves were obtained for Con A -and <protein>PHA</protein> -induced T-cell mitogenesis , <protein>PWM</protein> -generated B-cell mitogenesis and spontaneous lymphocyte pr... |
16453 | Glucocorticoid effects were assessed in vivo by depletion of endogenous glucocorticoids after oral administration of 1.5 g metyrapone ( MET ) and subsequent glucocorticoid replacement , and in vitro by incubation of the cells with different doses of dexamethasone ( DEX ) . | Glucocorticoid effects were assessed in vivo by depletion of endogenous glucocorticoids after oral administration of 1.5 g metyrapone ( MET ) and subsequent glucocorticoid replacement , and in vitro by incubation of the cells with different doses of dexamethasone ( DEX ) . |
16454 | There was a significant decrease in PWM -induced B-cell mitogenesis and a more pronounced effect of DEX administered in vitro on spontaneous lymphocyte proliferation after MET treatment when compared with the DEX plus MET pretreated condition in vivo . | There was a significant decrease in <protein>PWM</protein> -induced B-cell mitogenesis and a more pronounced effect of DEX administered in vitro on spontaneous lymphocyte proliferation after MET treatment when compared with the DEX plus MET pretreated condition in vivo . |
16455 | These data suggest that the inhibition of spontaneous lymphocyte proliferation by glucocorticoids in vitro is related to glucocorticoid receptor function . | These data suggest that the inhibition of spontaneous lymphocyte proliferation by glucocorticoids in vitro is related to <protein>glucocorticoid receptor</protein> function . |
16456 | The decrease in PWM -generated B-cell proliferation following cortisol depletion by MET may be seen in connection with impaired glucocorticoid-mediated induction of interleukin-1 receptor synthesis . | The decrease in <protein>PWM</protein> -generated B-cell proliferation following cortisol depletion by MET may be seen in connection with impaired glucocorticoid-mediated induction of <protein>interleukin-1 receptor</protein> synthesis . |
16457 | Transcription specific differences visualized by fluorescence in situ hybridization pattern on interphase nuclei of different cell types . | Transcription specific differences visualized by fluorescence in situ hybridization pattern on interphase nuclei of different cell types . |
16458 | Application of a `` formamide free '' and thus `` material preserving '' in situ hybridization technique using the cDNA of the myf3 gene revealed the following results : Human rhabdomyosarcoma cells , characterized by a high expression of myf3 show intensive hybridization signals in their interphase . | Application of a `` formamide free '' and thus `` material preserving '' in situ hybridization technique using the <dna>cDNA</dna> of the <dna>myf3 gene</dna> revealed the following results : <cell_type>Human rhabdomyosarcoma cells</cell_type> , characterized by a high expression of <dna>myf3</dna> show intensive hybri... |
16459 | RNase treatment prior to hybridization considerably reduces the size of this signals . | <protein>RNase</protein> treatment prior to hybridization considerably reduces the size of this signals . |
16460 | In comparison , isolated nuclei of human lymphocytes in which no need for the expression of this gene exists , show barely hybridization signals . | In comparison , isolated nuclei of <cell_type>human lymphocytes</cell_type> in which no need for the expression of this gene exists , show barely hybridization signals . |
16461 | Correspondingly , RNase treatment had no effect on hybridization pattern at all . | Correspondingly , <protein>RNase</protein> treatment had no effect on hybridization pattern at all . |
16462 | In conclusion an increased transcription efficiency of a cell type specific gene is accompanied by a higher hybridization accessibility in the corresponding cell nuclei . | In conclusion an increased transcription efficiency of a cell type specific gene is accompanied by a higher hybridization accessibility in the corresponding cell nuclei . |
16463 | Oncogenicity of human papillomavirus- or adenovirus-transformed cells correlates with resistance to lysis by natural killer cells . | Oncogenicity of <cell_line>human papillomavirus- or adenovirus-transformed cells</cell_line> correlates with resistance to lysis by <cell_type>natural killer cells</cell_type> . |
16464 | The reasons for the dissimilar oncogenicities of human adenoviruses and human papillomaviruses ( HPV ) in humans are unknown but may relate to differences in the capacities of the E1A and E7 proteins to target cells for rejection by the host natural killer ( NK ) cell response . | The reasons for the dissimilar oncogenicities of human adenoviruses and human papillomaviruses ( HPV ) in humans are unknown but may relate to differences in the capacities of the <protein>E1A</protein> and <protein>E7 proteins</protein> to <cell_type>target cells</cell_type> for rejection by the <cell_type>host natura... |
16465 | As one test of this hypothesis , we compared the abilities of E1A -and E7 -expressing human fibroblastic or keratinocyte-derived human cells to be selectively killed by either unstimulated or interferon ( IFN ) -activated NK cells . | As one test of this hypothesis , we compared the abilities of <protein>E1A</protein> -and <protein>E7</protein> -expressing <cell_line>human fibroblastic or keratinocyte-derived human cells</cell_line> to be selectively killed by either <cell_type>unstimulated</cell_type> or <cell_line>interferon ( IFN ) -activated NK ... |
16466 | Cells expressing the E1A oncoprotein were selectively killed by unstimulated NK cells , while the same parental cells but expressing the HPV type 16 ( HPV-16 ) or HPV-18 E7 oncoprotein were resistant to NK cell lysis . | Cells expressing the <protein>E1A oncoprotein</protein> were selectively killed by <cell_line>unstimulated NK cells</cell_line> , while the same <cell_type>parental cells</cell_type> but expressing the HPV type 16 ( HPV-16 ) or HPV-18 <protein>E7 oncoprotein</protein> were resistant to NK cell lysis . |
16467 | The ability of IFN-activated NK cells to selectively kill virally transformed cells depends on IFN 's ability to induce resistance to NK cell lysis in normal ( i.e. , non-viral oncogene-expressing ) but not virally transformed cells . | The ability of <cell_line>IFN-activated NK cells</cell_line> to selectively kill virally transformed cells depends on <protein>IFN</protein> 's ability to induce resistance to NK cell lysis in normal ( i.e. , <cell_line>non-viral oncogene-expressing</cell_line> ) but not <cell_line>virally transformed cells</cell_line>... |
16468 | E1A blocked IFN 's induction of cytolytic resistance , resulting in the selective lysis of adenovirus-transformed cells by IFN-activated NK cells . | <protein>E1A</protein> blocked <protein>IFN</protein> 's induction of cytolytic resistance , resulting in the selective lysis of <cell_line>adenovirus-transformed cells</cell_line> by <cell_line>IFN-activated NK cells</cell_line> . |
16469 | The extent of IFN -induced NK cell killing of E1A-expressing cells was proportional to the level of E1A expression and correlated with the ability of E1A to block IFN -stimulated gene expression in target cells . | The extent of <protein>IFN</protein> -induced NK cell killing of <cell_line>E1A-expressing cells</cell_line> was proportional to the level of <protein>E1A</protein> expression and correlated with the ability of <protein>E1A</protein> to block <protein>IFN</protein> -stimulated gene expression in <cell_type>target cells... |
16470 | In contrast , E7 blocked neither IFN -stimulated gene expression nor IFN 's induction of cytolytic resistance , thereby precluding the selective lysis of HPV-transformed cells by IFN-activated NK cells . | In contrast , <protein>E7</protein> blocked neither <protein>IFN</protein> -stimulated gene expression nor <protein>IFN</protein> 's induction of cytolytic resistance , thereby precluding the selective lysis of <cell_line>HPV-transformed cells</cell_line> by <cell_line>IFN-activated NK cells</cell_line> . |
16471 | In conclusion , E1A expression marks cells for destruction by the host NK cell response , whereas the E7 oncoprotein lacks this activity . | In conclusion , <protein>E1A</protein> expression marks cells for destruction by the host <cell_type>NK cell</cell_type> response , whereas the <protein>E7 oncoprotein</protein> lacks this activity . |
16472 | Regulation of IkB alpha phosphorylation by PKC- and Ca ( 2+ ) -dependent signal transduction pathways . | Regulation of <protein>IkB alpha</protein> phosphorylation by PKC- and Ca ( 2+ ) -dependent signal transduction pathways . |
16473 | The Ca ( 2+ ) -dependent phosphatase calcineurin , a target of FK506 and CsA , synergizes with PKC -induced activation of nuclear factor ( NF ) -kappa B in T cell lines . | The <protein>Ca ( 2+ ) -dependent phosphatase</protein> <protein>calcineurin</protein> , a target of FK506 and CsA , synergizes with <protein>PKC</protein> -induced activation of <protein>nuclear factor ( NF ) -kappa B</protein> in <cell_line>T cell lines</cell_line> . |
16474 | We have investigated whether this synergy is present in other cell types and the mechanism ( s ) by which these two pathways lead to NF-kappa B activation . | We have investigated whether this synergy is present in other cell types and the mechanism ( s ) by which these two pathways lead to <protein>NF-kappa B</protein> activation . |
16475 | While this synergy is present in other cell types , in the monocytic cell line U937 calcineurin is also sufficient to activate NF-kappa B . | While this synergy is present in other cell types , in the <cell_line>monocytic cell line U937</cell_line> <protein>calcineurin</protein> is also sufficient to activate <protein>NF-kappa B</protein> . |
16476 | Having previously shown that Ca ( 2+ ) - and PKC-dependent pathways synergize by accelerating the degradation of IkB alpha , we focused on the regulation of IkB alpha phosphorylation . | Having previously shown that Ca ( 2+ ) - and PKC-dependent pathways synergize by accelerating the degradation of <protein>IkB alpha</protein> , we focused on the regulation of <protein>IkB alpha</protein> phosphorylation . |
16477 | While PKC -dependent pathways sequentially result in the phosphorylation and in an incomplete degradation of IkB alpha in T cell lines , co-activation of Ca ( 2+ ) -dependent pathways accelerates the rate of IkB alpha phosphorylation and results in its complete degradation . | While <protein>PKC</protein> -dependent pathways sequentially result in the phosphorylation and in an incomplete degradation of <protein>IkB alpha</protein> in <cell_line>T cell lines</cell_line> , co-activation of Ca ( 2+ ) -dependent pathways accelerates the rate of <protein>IkB alpha</protein> phosphorylation and re... |
16478 | Activation of Ca ( 2+ ) -dependent pathways alone do not result in the phosphorylation and/or degradation of IkB alpha in Jurkat T or in U937 cells . | Activation of Ca ( 2+ ) -dependent pathways alone do not result in the phosphorylation and/or degradation of <protein>IkB alpha</protein> in <cell_line>Jurkat T</cell_line> or in <cell_line>U937 cells</cell_line> . |
16479 | Treatment of T cells with the selective PKC inhibitor GF109203X abrogates the PMA-induced IkB alpha phosphorylation/degradation irrespective of activation of Ca ( 2+ ) -dependent pathways , but not the phosphorylation and degradation of IkB alpha induced by TNF-alpha , a PKC -independent stimulus . | Treatment of <cell_type>T cells</cell_type> with the selective <protein>PKC</protein> inhibitor GF109203X abrogates the PMA-induced <protein>IkB alpha</protein> phosphorylation/degradation irrespective of activation of Ca ( 2+ ) -dependent pathways , but not the phosphorylation and degradation of <protein>IkB alpha</pr... |
16480 | Contrary to the interaction with PKC , Ca ( 2+ ) -dependent pathways synergize with TNF-alpha not at the level of IkB alpha phosphorylation , but at the level of its degradation . | Contrary to the interaction with <protein>PKC</protein> , Ca ( 2+ ) -dependent pathways synergize with <protein>TNF-alpha</protein> not at the level of <protein>IkB alpha</protein> phosphorylation , but at the level of its degradation . |
16481 | These results indicate that Ca ( 2+ ) -dependent pathways , including the phosphatase calcineurin , participate in the regulation of NF-kappa B in a cell specific fashion and synergize with PKC -dependent and -independent pathways at the level of IkB alpha phosphorylation and degradation . | These results indicate that Ca ( 2+ ) -dependent pathways , including the <protein>phosphatase</protein> <protein>calcineurin</protein> , participate in the regulation of <protein>NF-kappa B</protein> in a cell specific fashion and synergize with <protein>PKC</protein> -dependent and -independent pathways at the level ... |
16482 | Vitamin E therapy of acute CCl4-induced hepatic injury in mice is associated with inhibition of nuclear factor kappa B binding . | Vitamin E therapy of acute CCl4-induced hepatic injury in mice is associated with inhibition of <protein>nuclear factor kappa B</protein> binding . |
16483 | Oxidative stress , with reactive oxygen intermediate formation , may represent a common mechanism by which liver injury is induced by diverse etiologies . | Oxidative stress , with reactive oxygen intermediate formation , may represent a common mechanism by which liver injury is induced by diverse etiologies . |
16484 | Oxidative stress enhances nuclear factor kappa B ( NF-kappa B ) activity , and NF-kappa B activity has been shown to enhance the expression of cytotoxic cytokines . | Oxidative stress enhances <protein>nuclear factor kappa B</protein> ( <protein>NF-kappa B</protein> ) activity , and <protein>NF-kappa B</protein> activity has been shown to enhance the expression of <protein>cytotoxic cytokines</protein> . |
16485 | Acute hepatic injury caused by reactive oxygen intermediate production was induced by an intraperitoneal injection of CCl4 in mice . | Acute hepatic injury caused by reactive oxygen intermediate production was induced by an intraperitoneal injection of CCl4 in mice . |
16486 | This injury was significantly inhibited by intravenous pretreatment of the mice with a water-soluble emulsion of alpha-tocopherol . | This injury was significantly inhibited by intravenous pretreatment of the mice with a water-soluble emulsion of alpha-tocopherol . |
16487 | Alpha-tocopherol treatment of the mice given the CCl4 also reduced the NF-kappa B binding to levels approaching those found in normal mice . | Alpha-tocopherol treatment of the mice given the CCl4 also reduced the <protein>NF-kappa B</protein> binding to levels approaching those found in normal mice . |
16488 | In vitro treatment of a monocyte/macrophage cell line with CCl4 led to enhanced NF-kappa B binding and an increase in tumor necrosis factor-alpha ( TNF-alpha ) messenger RNA levels . | In vitro treatment of a monocyte/macrophage cell line with CCl4 led to enhanced <protein>NF-kappa B</protein> binding and an increase in <rna>tumor necrosis factor-alpha ( TNF-alpha ) messenger RNA</rna> levels . |
16489 | Liver specimens taken from patients with acute fulminant hepatitis had markedly increased NF-kappa B binding activity in comparison with the binding of normal livers . | Liver specimens taken from patients with acute fulminant hepatitis had markedly increased <protein>NF-kappa B</protein> binding activity in comparison with the binding of normal livers . |
16490 | These data demonstrate that abolishing acute hepatic injury with alpha-tocopherol , a free radical scavenger , also eliminated increased NF-kappa B binding . | These data demonstrate that abolishing acute hepatic injury with alpha-tocopherol , a free radical scavenger , also eliminated increased <protein>NF-kappa B</protein> binding . |
16491 | It is tempting to speculate that enhanced NF-kappa B expression caused by free radical production/oxidative stress may modulate liver injury , perhaps through an effect on cytotoxic cytokine synthesis . | It is tempting to speculate that enhanced <protein>NF-kappa B</protein> expression caused by free radical production/oxidative stress may modulate liver injury , perhaps through an effect on <protein>cytotoxic cytokine</protein> synthesis . |
16492 | Immunosuppression by glucocorticoids : inhibition of NF-kappa B activity through induction of I kappa B synthesis [ see comments ] | Immunosuppression by glucocorticoids : inhibition of <protein>NF-kappa B</protein> activity through induction of <protein>I kappa B</protein> synthesis [ see comments ] |
16493 | Glucocorticoids are among the most potent anti-inflammatory and immunosuppressive agents . | Glucocorticoids are among the most potent anti-inflammatory and immunosuppressive agents . |
16494 | They inhibit synthesis of almost all known cytokines and of several cell surface molecules required for immune function , but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B ( NF-kappa B ) activation in mice and cultured cell... | They inhibit synthesis of almost all known <protein>cytokines</protein> and of several <protein>cell surface molecules</protein> required for immune function , but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of <protein>nuclear factor kappa B</pro... |
16495 | This inhibition is mediated by induction of the I kappa B alpha inhibitory protein , which traps activated NF-kappa B in inactive cytoplasmic complexes . | This inhibition is mediated by induction of the <protein>I kappa B</protein> alpha inhibitory protein , which traps activated <protein>NF-kappa B</protein> in <protein>inactive cytoplasmic complexes</protein> . |
16496 | Because NF-kappa B activates many immunoregulatory genes in response to pro-inflammatory stimuli , the inhibition of its activity can be a major component of the anti-inflammatory activity of glucocorticoids . | Because <protein>NF-kappa B</protein> activates many <dna>immunoregulatory genes</dna> in response to pro-inflammatory stimuli , the inhibition of its activity can be a major component of the anti-inflammatory activity of glucocorticoids . |
16497 | Transcriptional repression of the interleukin-2 gene by vitamin D3 : direct inhibition of NFATp/AP-1 complex formation by a nuclear hormone receptor . | Transcriptional repression of the <dna>interleukin-2 gene</dna> by vitamin D3 : direct inhibition of <protein>NFATp/AP-1 complex</protein> formation by a <protein>nuclear hormone receptor</protein> . |
16498 | T-lymphocyte proliferation is suppressed by 1 , 25-dihydroxyvitamin D3 [ 1 , 25 ( OH ) 2D3 ] , the active metabolite of vitamin D3 , and is associated with a decrease in interleukin 2 ( IL-2 ) , gamma interferon , and granulocyte-macrophage colony-stimulating factor mRNA levels . | T-lymphocyte proliferation is suppressed by 1 , 25-dihydroxyvitamin D3 [ 1 , 25 ( OH ) 2D3 ] , the active metabolite of vitamin D3 , and is associated with a decrease in interleukin 2 ( IL-2 ) , gamma interferon , and granulocyte-macrophage colony-stimulating factor mRNA levels . |
16499 | We report here that 1 , 25 ( OH ) 2D3-mediated repression in Jurkat cells is cycloheximide resistant , suggesting that it is a direct transcriptional repressive effect on IL-2 expression by the vitamin D3 receptor ( VDR ) . | We report here that 1 , 25 ( OH ) 2D3-mediated repression in <cell_line>Jurkat cells</cell_line> is cycloheximide resistant , suggesting that it is a direct transcriptional repressive effect on <protein>IL-2</protein> expression by the <protein>vitamin D3 receptor</protein> ( <protein>VDR</protein> ) . |
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