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• _3 value "Below are the contents of a table from the paper" provenance.
• _3 value "Below are the contents of a table from the paper" provenance.
• _3 value "Below are the contents of a table from the paper" provenance.
• _2 value "Below are the contents of a table from the paper" provenance.
• _3 value "Below are the contents of a table from the paper" provenance.
• _3 value "Below are the contents of a table from the paper" provenance.
• _3 value "Below are the contents of a table from the paper" provenance.
• _3 value "Below are the contents of a table from the paper" provenance.
• _5 value "A number of ubiquitin-like proteins have been discovered recently that are attached to lysine residues of target proteins in a way analogous to that of ubiquitylation. Among them, SUMO-1, which is highly conserved from yeast to humans, has been shown to modify a number of proteins such as RanGAP1 (Matunis et al., 1996; Mahajan et al., 1997), the two nuclear body PML and SP100 proteins (Sternsdorf et al., 1997; Kamitani et al., 1998; Muller et al., 1998), p53 (Gostissa et al., 1999; Rodriguez et al., 1999; Muller et al., 2000), IkappaBalpha (Desterro et al., 1998) and a growing number of other proteins including viral proteins (for reviews see Melchior, 2000; Muller et al., 2001; Seeler and Dejean, 2001). Unlike ubiquitylation, sumoylation does not appear to promote protein degradation but rather was shown to be involved in mediating protein/protein interactions, subcellular compartmentalization and protein stability. Conjugation of SUMO-1 requires the E1-activating heterodimer Aos1/Uba2 and the single E2-conjugating Ubc9 enzyme. Very recently, two distinct families of SUMO E3 ligases have been identified. In yeast, the majority of SUMO conjugation requires the Siz1 and Siz2 proteins (Johnson and Gupta, 2001; Takahashi et al., 2001). The mammalian proteins to which Siz1 and Siz2 are most closely related are the PIAS (protein inhibitor of activated STAT) proteins, and PIAS1 and PIASy were shown to catalyse sumoylation of p53 and LEF-1, respectively (Kahyo et al., 2001; Sachdev et al., 2001; reviewed in Hochstrasser, 2001)." provenance.
• _5 value "Insulin stimulates malic enzyme (ME)-chloramphenicol acetyltransferase (CAT) and collagenase-1-CAT fusion gene expression in H4IIE cells through identical activator protein-1 (AP-1) motifs." provenance.
• _4 value "Insulin stimulates malic enzyme (ME)-chloramphenicol acetyltransferase (CAT) and collagenase-1-CAT fusion gene expression in H4IIE cells through identical activator protein-1 (AP-1) motifs." provenance.
• _4 value "Insulin stimulates malic enzyme (ME)-chloramphenicol acetyltransferase (CAT) and collagenase-1-CAT fusion gene expression in H4IIE cells through identical activator protein-1 (AP-1) motifs." provenance.
• _4 value "Insulin stimulates malic enzyme (ME)-chloramphenicol acetyltransferase (CAT) and collagenase-1-CAT fusion gene expression in H4IIE cells through identical activator protein-1 (AP-1) motifs." provenance.
• _5 value "In human circulating monocytes, inhibition of PDE4 by rolipram markedly suppresses TNF- synthesis and release in response to LPS; ... LPS stimulation of macrophages induces a large increase in TNF- mRNA by increasing gene transcription via activation of the transcriptional factors NF-B (13-15), c-jun, and c-fos (16). ... A study investigating the control of TNF- synthesis by using reporter constructs has demonstrated that this AU-rich element and the flanking sequences are sufficient to mediate a more than 200-fold increase in the LPS-dependent synthesis of the reporter protein. This element is involved in both the control of mRNA degradation and its translation This increase is not due to a change in cytoplasmic mRNA concentration but rather to a reversal of the translation repression in response to LPS ...The consequent increase in PDE activity leads to a decrease in cAMP, thus removing the cAMP constraint and allowing a full induction of TNF- mRNA and protein synthesis. The induction of PDE4B should then be viewed as a positive feedback loop that contributes to a full activation of the cytokine responses." provenance.
• _4 value "In human circulating monocytes, inhibition of PDE4 by rolipram markedly suppresses TNF- synthesis and release in response to LPS; ... LPS stimulation of macrophages induces a large increase in TNF- mRNA by increasing gene transcription via activation of the transcriptional factors NF-B (13-15), c-jun, and c-fos (16). ... A study investigating the control of TNF- synthesis by using reporter constructs has demonstrated that this AU-rich element and the flanking sequences are sufficient to mediate a more than 200-fold increase in the LPS-dependent synthesis of the reporter protein. This element is involved in both the control of mRNA degradation and its translation This increase is not due to a change in cytoplasmic mRNA concentration but rather to a reversal of the translation repression in response to LPS ...The consequent increase in PDE activity leads to a decrease in cAMP, thus removing the cAMP constraint and allowing a full induction of TNF- mRNA and protein synthesis. The induction of PDE4B should then be viewed as a positive feedback loop that contributes to a full activation of the cytokine responses." provenance.
• _4 value "In human circulating monocytes, inhibition of PDE4 by rolipram markedly suppresses TNF- synthesis and release in response to LPS; ... LPS stimulation of macrophages induces a large increase in TNF- mRNA by increasing gene transcription via activation of the transcriptional factors NF-B (13-15), c-jun, and c-fos (16). ... A study investigating the control of TNF- synthesis by using reporter constructs has demonstrated that this AU-rich element and the flanking sequences are sufficient to mediate a more than 200-fold increase in the LPS-dependent synthesis of the reporter protein. This element is involved in both the control of mRNA degradation and its translation This increase is not due to a change in cytoplasmic mRNA concentration but rather to a reversal of the translation repression in response to LPS ...The consequent increase in PDE activity leads to a decrease in cAMP, thus removing the cAMP constraint and allowing a full induction of TNF- mRNA and protein synthesis. The induction of PDE4B should then be viewed as a positive feedback loop that contributes to a full activation of the cytokine responses." provenance.
• _6 value "LPS induction of tumor necrosis factor-alpha secretion by circulating leukocytes was decreased by approximately 90% in mice deficient in PDE4B but not in mice lacking PDE4D" provenance.
• _4 value "LPS induction of tumor necrosis factor-alpha secretion by circulating leukocytes was decreased by approximately 90% in mice deficient in PDE4B but not in mice lacking PDE4D" provenance.
• _5 value "PhosphoElm data from PMID 15212693" provenance.
• _5 value "Modified assertion" provenance.
• _4 value "Oncogene cooperation by Tbx3 correlates with an ability of Tbx3 to suppress the induction of p19ARF and p53 that is typically caused by overexpression Myc and Ras, and to protect against Myc-induced apoptosis." provenance.
• _4 value "Oncogene cooperation by Tbx3 correlates with an ability of Tbx3 to suppress the induction of p19ARF and p53 that is typically caused by overexpression Myc and Ras, and to protect against Myc-induced apoptosis." provenance.
• _7 value "Oncogene cooperation by Tbx3 correlates with an ability of Tbx3 to suppress the induction of p19ARF and p53 that is typically caused by overexpression Myc and Ras, and to protect against Myc-induced apoptosis." provenance.
• _4 value "In order to investigate the physiological role of acetoacetyl-CoA synthetase (acetoacetate-CoA ligase, EC 6.2.1.16), a cytosolic acetoacetate-activating enzyme, effects of streptozotocin (STZ)-induced diabetes on the enzyme activity was investigated in rats. At 72 hr of the STZ administration (80 mg/kg body weight, injected intravenously), hepatic enzyme specific activity decreased to 23% of its initial activity" provenance.
• _4 value "Activated STAT5 increases the mRNA and protein levels of A1 and pim-1 through Bcr-Abl signaling pathway." provenance.
• _5 value "Northern analysis of the apoptosis-associated genes Gadd34 and Gadd45 verified their higher expression in JNK2AS-treated cells (Fig. 4C)Citation , and the mRNA levels of Gadd153, another gene whose expression is often up-regulated by conditions that induce Gadd34 and Gadd45, were also elevated. The induction of the Gadd genes suggested that JNK2AS-treated cells were under stress and prompted us to examine the expression of two other stress-regulated genes: (a) Grp78, a molecular chaperone involved in protein folding; and (b) the cyclin-dependent kinase inhibitor p21Cip1/Waf1, which we had found previously to be up-regulated in other JNK2AS-treated cells (17 , 18) . Both genes were markedly up-regulated in JNK2AS-treated cells (Fig. 4C)Citation , suggesting that depletion of JNK2 in PC3 cells facilitates the induction of several independent stress-signaling pathways. Activation of the JNK pathway is important for the phosphorylation and activation of protein components of AP-1 transcription factor complexes (1, 2, 3, 4 , 5, 6, 7 , 28) , suggesting that genes regulated by AP-1-dependent transcription could be negatively affected by JNKAS treatment. Indeed, we detected reduced expression of several AP-1-regulated genes, including lamin A-C (29) , and integrin b-4 (Ref. 30 ; Fig. 4DCitation ). Among other genes whose lower expression after JNK2AS treatment was verified by Northern blotting were HMG-I(Y), a protein highly expressed in prostate cancer (31) and recently identified as a myc-regulated oncogene (32) , Lsm5 (33) , transcobalamin, and DSS1 (Ref. 34 ; Fig. 4Citation D, and data not shown). Importantly, although most JNK2AS-altered genes appeared to be specific for treatment with this oligonucleotide, some gene expression changes were also seen in the JNK1AS- and JNKScr-treated groups, indicating that a more global response to the uptake of oligonucleotides (Fig. 4E)Citation was elicited. Within this group were two IFN-inducible genes, ISGF-3 and ISG15, suggesting that application of phosphorothioate oligonucleotides could induce IFN-dependent responses." provenance.
• _5 value "Northern analysis of the apoptosis-associated genes Gadd34 and Gadd45 verified their higher expression in JNK2AS-treated cells (Fig. 4C)Citation , and the mRNA levels of Gadd153, another gene whose expression is often up-regulated by conditions that induce Gadd34 and Gadd45, were also elevated. The induction of the Gadd genes suggested that JNK2AS-treated cells were under stress and prompted us to examine the expression of two other stress-regulated genes: (a) Grp78, a molecular chaperone involved in protein folding; and (b) the cyclin-dependent kinase inhibitor p21Cip1/Waf1, which we had found previously to be up-regulated in other JNK2AS-treated cells (17 , 18) . Both genes were markedly up-regulated in JNK2AS-treated cells (Fig. 4C)Citation , suggesting that depletion of JNK2 in PC3 cells facilitates the induction of several independent stress-signaling pathways. Activation of the JNK pathway is important for the phosphorylation and activation of protein components of AP-1 transcription factor complexes (1, 2, 3, 4 , 5, 6, 7 , 28) , suggesting that genes regulated by AP-1-dependent transcription could be negatively affected by JNKAS treatment. Indeed, we detected reduced expression of several AP-1-regulated genes, including lamin A-C (29) , and integrin b-4 (Ref. 30 ; Fig. 4DCitation ). Among other genes whose lower expression after JNK2AS treatment was verified by Northern blotting were HMG-I(Y), a protein highly expressed in prostate cancer (31) and recently identified as a myc-regulated oncogene (32) , Lsm5 (33) , transcobalamin, and DSS1 (Ref. 34 ; Fig. 4Citation D, and data not shown). Importantly, although most JNK2AS-altered genes appeared to be specific for treatment with this oligonucleotide, some gene expression changes were also seen in the JNK1AS- and JNKScr-treated groups, indicating that a more global response to the uptake of oligonucleotides (Fig. 4E)Citation was elicited. Within this group were two IFN-inducible genes, ISGF-3 and ISG15, suggesting that application of phosphorothioate oligonucleotides could induce IFN-dependent responses." provenance.
• _5 value "Northern analysis of the apoptosis-associated genes Gadd34 and Gadd45 verified their higher expression in JNK2AS-treated cells (Fig. 4C)Citation , and the mRNA levels of Gadd153, another gene whose expression is often up-regulated by conditions that induce Gadd34 and Gadd45, were also elevated. The induction of the Gadd genes suggested that JNK2AS-treated cells were under stress and prompted us to examine the expression of two other stress-regulated genes: (a) Grp78, a molecular chaperone involved in protein folding; and (b) the cyclin-dependent kinase inhibitor p21Cip1/Waf1, which we had found previously to be up-regulated in other JNK2AS-treated cells (17 , 18) . Both genes were markedly up-regulated in JNK2AS-treated cells (Fig. 4C)Citation , suggesting that depletion of JNK2 in PC3 cells facilitates the induction of several independent stress-signaling pathways. Activation of the JNK pathway is important for the phosphorylation and activation of protein components of AP-1 transcription factor complexes (1, 2, 3, 4 , 5, 6, 7 , 28) , suggesting that genes regulated by AP-1-dependent transcription could be negatively affected by JNKAS treatment. Indeed, we detected reduced expression of several AP-1-regulated genes, including lamin A-C (29) , and integrin b-4 (Ref. 30 ; Fig. 4DCitation ). Among other genes whose lower expression after JNK2AS treatment was verified by Northern blotting were HMG-I(Y), a protein highly expressed in prostate cancer (31) and recently identified as a myc-regulated oncogene (32) , Lsm5 (33) , transcobalamin, and DSS1 (Ref. 34 ; Fig. 4Citation D, and data not shown). Importantly, although most JNK2AS-altered genes appeared to be specific for treatment with this oligonucleotide, some gene expression changes were also seen in the JNK1AS- and JNKScr-treated groups, indicating that a more global response to the uptake of oligonucleotides (Fig. 4E)Citation was elicited. Within this group were two IFN-inducible genes, ISGF-3 and ISG15, suggesting that application of phosphorothioate oligonucleotides could induce IFN-dependent responses." provenance.
• _5 value "Northern analysis of the apoptosis-associated genes Gadd34 and Gadd45 verified their higher expression in JNK2AS-treated cells (Fig. 4C)Citation , and the mRNA levels of Gadd153, another gene whose expression is often up-regulated by conditions that induce Gadd34 and Gadd45, were also elevated. The induction of the Gadd genes suggested that JNK2AS-treated cells were under stress and prompted us to examine the expression of two other stress-regulated genes: (a) Grp78, a molecular chaperone involved in protein folding; and (b) the cyclin-dependent kinase inhibitor p21Cip1/Waf1, which we had found previously to be up-regulated in other JNK2AS-treated cells (17 , 18) . Both genes were markedly up-regulated in JNK2AS-treated cells (Fig. 4C)Citation , suggesting that depletion of JNK2 in PC3 cells facilitates the induction of several independent stress-signaling pathways. Activation of the JNK pathway is important for the phosphorylation and activation of protein components of AP-1 transcription factor complexes (1, 2, 3, 4 , 5, 6, 7 , 28) , suggesting that genes regulated by AP-1-dependent transcription could be negatively affected by JNKAS treatment. Indeed, we detected reduced expression of several AP-1-regulated genes, including lamin A-C (29) , and integrin b-4 (Ref. 30 ; Fig. 4DCitation ). Among other genes whose lower expression after JNK2AS treatment was verified by Northern blotting were HMG-I(Y), a protein highly expressed in prostate cancer (31) and recently identified as a myc-regulated oncogene (32) , Lsm5 (33) , transcobalamin, and DSS1 (Ref. 34 ; Fig. 4Citation D, and data not shown). Importantly, although most JNK2AS-altered genes appeared to be specific for treatment with this oligonucleotide, some gene expression changes were also seen in the JNK1AS- and JNKScr-treated groups, indicating that a more global response to the uptake of oligonucleotides (Fig. 4E)Citation was elicited. Within this group were two IFN-inducible genes, ISGF-3 and ISG15, suggesting that application of phosphorothioate oligonucleotides could induce IFN-dependent responses." provenance.
• _5 value "We have recently identified ICAT, a beta-catenin-interacting protein that interferes with the interaction between beta-catenin and TCF-4, thereby negatively regulating Wnt signaling." provenance.
• _3 value "Here we show parathyroid, thyroid, and kidney CASR mRNA levels increased 2-fold at 15 h after intraperitoneal injection of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in rats." provenance.
• _8 value "EphrinB2 not only increased the phosphorylation of EphB2 and EphB4 in a time-dependent manner but also increased recruitment of p120-Ras-GTPase-activating protein (p120-RasGAP) to EphB2 and EphB4. Accordingly, ephrinB2 inhibited VEGF- and Ang1-induced Ras-MAPK activities, whereas ephrinB2 did not alter VEGF-induced Flk phosphorylation or Ang1-induced Tie2 phosphorylation. " provenance.
• _7 value "In addition, PRMT2 enhanced PR, PPARgamma, and RARalpha-mediated transactivation." provenance.
• _5 value "LMX1B transcription factor, which regulates the expression of key glomerular type IV collagen genes COL4A3 and COL4A4" provenance.
• _5 value "Together, these results show that AVP induces myogenic differentiation through the transcriptional activation of MEF2, a mechanism that is critical for myogenesis." provenance.
• _3 value "The levels of CYP1A1, CYP1A2, CYP1B1, ALDH3, and ALDH6 mRNA increased after exposure to omeprazole" provenance.
• _3 value "The levels of CYP1A1, CYP1A2, CYP1B1, ALDH3, and ALDH6 mRNA increased after exposure to omeprazole" provenance.
• _3 value "Okadaic acid was found to induce ALA synthase mRNA in a concentration-dependent fashion in both Huh-7 and HepG2 cells" provenance.
• _5 value "Although Akt also phosphorylated p27(Kip1) at Ser(10) and Thr(187), these two sites were not involved in the binding to 14-3-3 proteins." provenance.
• _5 value "Further analysis revealed that 14-3-3 proteins bound to p27(Kip1) through Thr(198) only when it was phosphorylated by Akt. Although Akt also phosphorylated p27(Kip1) at Ser(10) and Thr(187), these two sites were not involved in the binding to 14-3-3 proteins. p27(Kip1) phosphorylated at Thr(198) exists only in the cytoplasm" provenance.
• _5 value "Inhibition of serine/threonine kinase Akt signaling by some pharmacological agents or by PTEN induces G(1) arrest, in part by up-regulating p27(Kip1)" provenance.
• _5 value "Modified assertion" provenance.
• _5 value "Table 1 Apparent inhibitory constants (KI,app in M) for IAPs against selected human caspases" provenance.
• _5 value "Table 1 Apparent inhibitory constants (KI,app in M) for IAPs against selected human caspases" provenance.
• _5 value "Table 1 Apparent inhibitory constants (KI,app in M) for IAPs against selected human caspases" provenance.
• _5 value "The BIRs are essential for the anti-apoptotic properties of the IAPs, and in several cases this has been directly attributed to the binding and inhibition of caspases, a family of cysteine proteases with a substrate preference for aspartic acid that are essential for the apoptotic process" provenance.
• _8 value "a dimeric Smac/DIABLO molecule is required for binding to BIR2, but not to BIR3, which indicates significant differences in the affinity or mechanism by which Smac/DIABLO binds to these domains Figure 5: Association of IAPs with signalling complexes." provenance.
• _5 value "Cancer arises from a stepwise accumulation of genetic changes that liberates neoplastic cells from the homeostatic mechanisms that govern normal cell proliferation. In humans, at least four to six mutations are required to reach this state, but fewer seem to be required in mice. By rationalizing the shared and unique elements of human and mouse models of cancer, we should be able to identify the molecular circuits that function differently in humans and mice, and use this knowledge to improve existing models of cancer." provenance.
• _2 value "Cancer arises from a stepwise accumulation of genetic changes that liberates neoplastic cells from the homeostatic mechanisms that govern normal cell proliferation. In humans, at least four to six mutations are required to reach this state, but fewer seem to be required in mice. By rationalizing the shared and unique elements of human and mouse models of cancer, we should be able to identify the molecular circuits that function differently in humans and mice, and use this knowledge to improve existing models of cancer." provenance.
• _6 value "Cancer arises from a stepwise accumulation of genetic changes that liberates neoplastic cells from the homeostatic mechanisms that govern normal cell proliferation. In humans, at least four to six mutations are required to reach this state, but fewer seem to be required in mice. By rationalizing the shared and unique elements of human and mouse models of cancer, we should be able to identify the molecular circuits that function differently in humans and mice, and use this knowledge to improve existing models of cancer." provenance.
• _3 value "The present results indicate that peripheral inflammation not only initially activates but also later up-regulates soluble guanylate cyclase expression" provenance.
• _4 value "LAT is a raft-associated transmembrane adaptor molecule which recruits several signaling molecules, including PKC/AKT regulating proteins like PLCg1, SLP76 and PI3K upon T-cell activation" provenance.
• _4 value "LAT is a raft-associated transmembrane adaptor molecule which recruits several signaling molecules, including PKC/AKT regulating proteins like PLCg1, SLP76 and PI3K upon T-cell activation" provenance.
• _4 value "PTEN, which inhibits AKT activation, is an essential mediator of the CD95 response and a repressor of autoimmunity" provenance.
• _4 value "Pro-death Bcl-2 family members are sequestered in the cytoplasm until activated, at which time they complex with Bcl-2 or Bcl-xL and inhibit their function" provenance.
• _3 value "aPKC family members known to antagonize apoptosis" provenance.
• _5 value "besides AKT activation, PI3K products also influence other PH domain-containing signaling molecules, as the Tec family of tyrosine kinases, the guanine nucleotide exchange factor (GEF) Vav-1 and the serine/threonine kinase PDK1" provenance.
• _6 value "changes in the mitochondria leading to release of cytochrome C into the cytoplasm occurs, a prerequisite for the formation of the apoptosome, consisting of cytochrome C, Apaf-1 adapter protein, dATP and the aspartyl-directed protease caspase 9" provenance.
• _5 value "An analysis of the intracellular domains of RON/STK and Tyro3 reveal a common multi-substrate binding site, which can recruit common signaling molecules such as growth factor receptor bound 2 (Grb2) and phosphatidylinositol 3-kinase (PI3-K)." provenance.
• _3 value "Significant progress has been made in defining pathways that mediate the formation of the mammalian heart. Little is known, however, about the genetic program that directs the differentiation of cardiac myocytes from their precursor cells. A major hindrance to this kind of investigation has been the absence of an appropriate cell culture model of cardiac myocyte differentiation. Recently, a subline of P19 cells (P19CL6) was derived that, following dimethyl sulfoxide (DMSO) treatment, differentiate efficiently over 10 days into spontaneously beating cardiac myocytes. We demonstrate that these cells are indeed cardiac myocytes as they express cell type-specific markers and exhibit electrophysiological properties indicative of cardiac myocytes. The requirement for DMSO stimulation in this paradigm was shown to be limited to the first 4 days, suggesting that critical events in the differentiation process occur over this interval. To uncover relationships among known genes and identify novel genes that mediate cardiac myocyte differentiation, a detailed time course of changes in global gene expression was carried out using cDNA microarrays. In addition to the activation of genes encoding cardiac transcription factors and structural proteins, increases were noted in the expression of multiple known genes and expressed sequence tags (ESTs). Analysis of the former suggested the involvement of a variety of signaling pathways in cardiac myocyte differentiation. The 16 ESTs whose expression was increased during the early, stimulus-dependent phase of cardiac myocyte differentiation may be novel regulators of this process. Thus this first report of large-scale changes in gene expression during cardiac myocyte differentiation has delineated relationships among the expression patterns of known genes and identified a number of novel genes that merit further study." provenance.
• _3 value "Significant progress has been made in defining pathways that mediate the formation of the mammalian heart. Little is known, however, about the genetic program that directs the differentiation of cardiac myocytes from their precursor cells. A major hindrance to this kind of investigation has been the absence of an appropriate cell culture model of cardiac myocyte differentiation. Recently, a subline of P19 cells (P19CL6) was derived that, following dimethyl sulfoxide (DMSO) treatment, differentiate efficiently over 10 days into spontaneously beating cardiac myocytes. We demonstrate that these cells are indeed cardiac myocytes as they express cell type-specific markers and exhibit electrophysiological properties indicative of cardiac myocytes. The requirement for DMSO stimulation in this paradigm was shown to be limited to the first 4 days, suggesting that critical events in the differentiation process occur over this interval. To uncover relationships among known genes and identify novel genes that mediate cardiac myocyte differentiation, a detailed time course of changes in global gene expression was carried out using cDNA microarrays. In addition to the activation of genes encoding cardiac transcription factors and structural proteins, increases were noted in the expression of multiple known genes and expressed sequence tags (ESTs). Analysis of the former suggested the involvement of a variety of signaling pathways in cardiac myocyte differentiation. The 16 ESTs whose expression was increased during the early, stimulus-dependent phase of cardiac myocyte differentiation may be novel regulators of this process. Thus this first report of large-scale changes in gene expression during cardiac myocyte differentiation has delineated relationships among the expression patterns of known genes and identified a number of novel genes that merit further study." provenance.
• _3 value "Significant progress has been made in defining pathways that mediate the formation of the mammalian heart. Little is known, however, about the genetic program that directs the differentiation of cardiac myocytes from their precursor cells. A major hindrance to this kind of investigation has been the absence of an appropriate cell culture model of cardiac myocyte differentiation. Recently, a subline of P19 cells (P19CL6) was derived that, following dimethyl sulfoxide (DMSO) treatment, differentiate efficiently over 10 days into spontaneously beating cardiac myocytes. We demonstrate that these cells are indeed cardiac myocytes as they express cell type-specific markers and exhibit electrophysiological properties indicative of cardiac myocytes. The requirement for DMSO stimulation in this paradigm was shown to be limited to the first 4 days, suggesting that critical events in the differentiation process occur over this interval. To uncover relationships among known genes and identify novel genes that mediate cardiac myocyte differentiation, a detailed time course of changes in global gene expression was carried out using cDNA microarrays. In addition to the activation of genes encoding cardiac transcription factors and structural proteins, increases were noted in the expression of multiple known genes and expressed sequence tags (ESTs). Analysis of the former suggested the involvement of a variety of signaling pathways in cardiac myocyte differentiation. The 16 ESTs whose expression was increased during the early, stimulus-dependent phase of cardiac myocyte differentiation may be novel regulators of this process. Thus this first report of large-scale changes in gene expression during cardiac myocyte differentiation has delineated relationships among the expression patterns of known genes and identified a number of novel genes that merit further study." provenance.
• _3 value "Table 1 List of oestrogen-activated genes." provenance.
• _3 value "Table 1 List of oestrogen-activated genes." provenance.
• _3 value "Table 1 List of oestrogen-activated genes." provenance.
• _6 value "gp130 either homodimerizes in response to IL6 and IL11 or forms heterodimers with the leukemia inhibitory factor, LIF, receptor, LIFR in response to LIF, oncostatin M, ciliary neurotrophic factor, CNTF, cardiotrophin-1 or cardiotrophin-like cytokine resulting in the onset of cytoplasmic tyrosine phosphorylation cascades" provenance.
• _5 value "BACKGROUND: In vitro-derived human mast cells exhibit different properties, depending in part on the source of progenitor cells. Most investigations have used fetal liver, cord blood or peripheral blood. Few have used adult bone marrow. OBJECTIVE: Human mast cells derived in vitro from the CD34(+) progenitors in bone marrow and cord blood that had been cultured with recombinant human stem cell factor (rhSCF) and recombinant human interleukin-6 (rhIL-6) were compared. METHODS AND RESULTS: After 12 weeks of culture, nearly all of the cells were mast cells, and nearly all of these had cytoplasmic granules containing both tryptase and chymase (MCTC type), stained metachromatically with acidic toluidine blue, and expressed CD117 on the cell surface. Both tryptase protein and mRNA were detected by two weeks of culture. Chymase mRNA and protein were detected at 4 weeks but not at 2 weeks of culture. Different forms of tryptase (both total and ?-tryptase) in HBMMC were measured by sandwich ELISA" provenance.
• _9 value "Whereas ILPIP moderately activates JNK family members when expressed alone, it strongly enhances XIAP-mediated activation of JNK1, JNK2, and JNK3" provenance.
• _5 value "AKT2 interacts with and phosphorylates I kappa B kinase alpha ()" provenance.
• _5 value "As shown in Fig. 4C, IKKalpha was highly phosphorylated in cells expressing constitutively active AKT2 but not in the cells transfected with pcDNA3 and dominant-negative AKT2. Collectively, these data indicate that IKKalpha is an AKT2 physiological substrate." provenance.
• _5 value "Constitutively active AKT2 alone was able to induce NFkB activity to a level comparable with UV- or TNFalpha-treated cells transfected with wildtype AKT2. These data show that PI3K/AKT2 mediates both stress- and TNFalpha-activated NFbB pathway." provenance.
• _5 value "For this reason we examined the effects of stress on AKT2 activation in two ovarian epithelial cancer cell lines, A2780 cells, which were transiently transfected with HA-AKT2, and OVCAR3 cells, which express high levels of endogenous AKT2 (7). The cells were exposed to UV-C, heat shock (45 �C), 0.4 M NaCl, or 20 ng/ml TNFalpha. IGF1- stimulated cells were used as controls. As assessed by in vitro kinase and Western blot analyses of AKT2 immunoprecipitates, all the stimuli substantially increased AKT2 activity in both A2780 and OVCAR3 cells (Figs. 1, A and B)." provenance.
• _5 value "For this reason we examined the effects of stress on AKT2 activation in two ovarian epithelial cancer cell lines, A2780 cells, which were transiently transfected with HA-AKT2, and OVCAR3 cells, which express high levels of endogenous AKT2 (7). The cells were exposed to UV-C, heat shock (45 �C), 0.4 M NaCl, or 20 ng/ml TNFalpha. IGF1- stimulated cells were used as controls. As assessed by in vitro kinase and Western blot analyses of AKT2 immunoprecipitates, all the stimuli substantially increased AKT2 activity in both A2780 and OVCAR3 cells (Figs. 1, A and B)." provenance.
• _5 value "Moreover, inhibition of AKT2 activity by expression of dominant-negative AKT2 increased the percentage of apoptotic cells in the UVand TNFalpha-treated populations by~2-fold." provenance.
• _3 value "expression of constitutively active AKT2 inhibits programmed cell death in response to UV and TNFalpha -induced apoptosis by induction of stress kinases and provide the first evidence that AKT inhibits stress kinase JNK through activation of the NF kappa B pathway" provenance.
• _5 value "Modified assertion" provenance.
• _4 value "ER stress activates ASK 1 through formation of an IRE1-TRAF2-ASK1 complex" provenance.
• _5 value "Modified assertion" provenance.
• _4 value "In these studies, we used a phosphorylation state-specific antibody to show that VEGF promotes dephosphorylation of eNOS at serine residue 116 in cultured endothelial cells." provenance.
• _5 value "PhosphoElm data from PMID 15212693" provenance.
• _7 value "Upon attachment to fibronectin, ECV 304 cells transfected with dn Cdc42 or dn Rac1 mutants exhibited the phosphorylated form of FAK. FAK phosphorylated at Tyr397 appeared within 60 minutes and was detected even in the presence of dn Cdc42 or dn Rac1, indicating that these integrin-induced signaling components are still activated by attachment when Cdc42 and Rac1 are blocked." provenance.
• _5 value "We conclude that histone deacetylation contributes to the repression of cyclin B1 expression in G(0) and G(1), and that this mechanism requires, in part, the E-box." provenance.
• _5 value "SGKL is activated via its lipid-binding domain (phox homology domain) in response to PI3K signaling." provenance.
• _6 value "An increase in c-Jun phosphorylation by ERK was also found to accompany the increased AP-1 activity as detected by Western blot." provenance.
• _3 value "Dietary cholesterol stimulates CYP7A1 transcription via activation of oxysterol receptor, LXR alpha, whereas bile acids repress transcription through FXR-mediated induction of SHP protein. " provenance.
• _4 value "Modified assertion" provenance.
• _4 value "Modified assertion" provenance.
• _5 value "Induction of murine H-rev107 gene expression by growth arrest and histone acetylation" provenance.
• _3 value "Furthermore, co-transfection of the methyl-CpG binding proteins, MeCP2 and MBD2, inhibited H-rev107 promoter activity up to 70% in SL2 cells when the promoter was methylated." provenance.
• _5 value "Consistent with this possibility, Tat binds to p300 ( 76-78 ), which in turn associates to cyclin E-Cdk2 to activate NFkappaB/rel transcription factors ( 79 )." provenance.
• _4 value "SP-A induced a significant CD25 expression ( p < 0.01, n = 3) that was 70% of the LPS response (Fig. 2 )." provenance.
• _7 value "In vitro treatment of activated T cells with curcumin inhibited IL-12-induced tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT3 and STAT4 transcription factors. " provenance.
• _7 value "In vitro treatment of activated T cells with curcumin inhibited IL-12-induced tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT3 and STAT4 transcription factors. " provenance.
• _7 value "In vitro treatment of activated T cells with curcumin inhibited IL-12-induced tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT3 and STAT4 transcription factors. " provenance.
• _4 value "Fig. A simplified diagram illustrating the role of the renin-angiotensin -aldosterone system in sodium and volume homeostasis" provenance.
• _3 value "Another cluster indicated genes that were commonly down-regulated by all three stimuli and included HSF2, NF-kappa B p65, ICE, IGF-II and FGF-7, MMP2, MMP14, and presenilin 2." provenance.
• _3 value "Another cluster indicated genes that were commonly down-regulated by all three stimuli and included HSF2, NF-kappa B p65, ICE, IGF-II and FGF-7, MMP2, MMP14, and presenilin 2." provenance.
• _3 value "Time-course studies identified early, intermediate, and late genes that were commonly up-regulated by all three stimuli. These genes included: phosphodiesterase 1C, cAMP-dependent protein kinase, iNOS, beta-NGF, proenkephalin B and orphanin, corticotrophin-releasing factor (CRF) R, estrogen R, PAI2, and protease inhibitor 17, NFkB p105, c-fos, fos-B, basic transcription factors, and cytoskeleton and motility proteins." provenance.
• _4 value "HUVECs were grown in 24-well plates with 0.5 ml of culture medium for 3 days with or without bFGF or VEGF. Basic FGF dramatically down regulated the production of MCP-1." provenance.
• _3 value "Monocyte transendothelial migration induced by C5a and chemokines (MCP-1, SDF-1 alpha, RANTES, MIP-1 alpha) was also suppressed (by 50 to 75%) on bFGF-stimulated HUVECs." provenance.

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