Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _4 value "The blockade of p38 with the pharmacologic inhibitor SB203580 abrogated IL-8 production by cell stretching" provenance.
- _6 value "With the lipid surface, activated protein C dose-dependently reduced thrombin generation. Similarly, when endothelial cells provided the only surface for thrombin generation, activated protein C dose-dependently decreased thrombin generation significantly." provenance.
- _3 value "We also demonstrate that (i) insulin-stimulation of adipocytes and (ii) integrin ligation of endothelial cells can both induce the tyrosine phosphorylation of caveolin-2" provenance.
- _4 value "In initial experiments, we found that Wnt-3A protein elevates the levels of ?-catenin 5?10 fold (Figure 4); and that a transiently transfected TCF reporter construct is activated 3?4 fold (not shown). (from full text)" provenance.
- _4 value "Exposure of MCF-7 cells to insulin, insulin-like growth factor 1 (IGF-1) or epidermal growth factor (EGF) can lead to the phosphorylation of ETS-2, Akt and ERK1/2." provenance.
- _4 value "Exposure of MCF-7 cells to insulin, insulin-like growth factor 1 (IGF-1) or epidermal growth factor (EGF) can lead to the phosphorylation of ETS-2, Akt and ERK1/2." provenance.
- _3 value "Exposure of MCF-7 cells to insulin, insulin-like growth factor 1 (IGF-1) or epidermal growth factor (EGF) can lead to the phosphorylation of ETS-2, Akt and ERK1/2." provenance.
- _6 value "Interestingly, overexpression of PTEN in MCF-7 leads to blockade of insulin-stimulated, but not EGF-stimulated, phosphorylation of ERK, accompanied by dramatic decreases in ETS-2 phosphorylation." provenance.
- _5 value "overexpression of wild-type PTEN in the MCF-7 breast cancer line results in phosphatase activity-dependent decreases in the phosphorylation of ETS-2 PTEN blocks insulin-stimulated ETS-2 phosphorylation Our observations, therefore, suggest that PTEN blocks insulin-stimulated ETS-2 phosphorylation through inhibition of the ERK members of the MAP kinase family" provenance.
- _5 value "overexpression of wild-type PTEN in the MCF-7 breast cancer line results in phosphatase activity-dependent decreases in the phosphorylation of ETS-2 PTEN blocks insulin-stimulated ETS-2 phosphorylation Our observations, therefore, suggest that PTEN blocks insulin-stimulated ETS-2 phosphorylation through inhibition of the ERK members of the MAP kinase family" provenance.
- _6 value "overexpression of wild-type PTEN in the MCF-7 breast cancer line results in phosphatase activity-dependent decreases in the phosphorylation of ETS-2 PTEN blocks insulin-stimulated ETS-2 phosphorylation Our observations, therefore, suggest that PTEN blocks insulin-stimulated ETS-2 phosphorylation through inhibition of the ERK members of the MAP kinase family" provenance.
- _6 value "overexpression of wild-type PTEN in the MCF-7 breast cancer line results in phosphatase activity-dependent decreases in the phosphorylation of ETS-2 PTEN blocks insulin-stimulated ETS-2 phosphorylation Our observations, therefore, suggest that PTEN blocks insulin-stimulated ETS-2 phosphorylation through inhibition of the ERK members of the MAP kinase family" provenance.
- _5 value "In primary rat neuronal and HT22 cells, FGF1 promoted a time-dependent inactivation of GSK3beta by phosphorylation at serine 9. Blocking FGF1 receptors with heparinase reduced this effect. The effects of FGF1 on GSK3beta were dependent on phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) because inhibitors of this pathway or infection with dominant negative Akt adenovirus blocked inactivation. Furthermore, treatment of neuronal cells with FGF1 resulted in ERK-independent Akt phosphorylation" provenance.
- _3 value "Moreover, ubiquilin has the ability to attenuate CHOP induction by hypoxia." provenance.
- _3 value "ubiquilin is also up-regulated in response to hypoxia in glial cells with a time course similar to that of PDI induction." provenance.
- _6 value "Modified assertion" provenance.
- _3 value "Expression array analysis identified nine genes that demonstrated a >2-fold decrease in expression in both RCC cell lines after restoration of WT pVHL. Three of the nine genes (VEGF, PAI-1, and LRP1) had been reported previously as pVHL targets and are known to be hypoxia-inducible." provenance.
- _3 value "Expression array analysis identified nine genes that demonstrated a >2-fold decrease in expression in both RCC cell lines after restoration of WT pVHL. Three of the nine genes (VEGF, PAI-1, and LRP1) had been reported previously as pVHL targets and are known to be hypoxia-inducible." provenance.
- _3 value "Using the Differential Display Polymerase Chain Reaction and 5' Rapid Amplification of cDNA Ends protocols, we isolated overlapping cDNAs encoding a 3.0-kb-long mRNA, Wound Inducible Transcript, 3.0 (wit 3.0). In situ hybridization demonstrated that wit 3.0 was primarily expressed by the fibroblasts associated with tooth extraction wound-healing." provenance.
- _6 value "Beta-catenin is a transcriptional activator that is regulated by glycogen synthase kinase-3 (GSK-3). GSK-3 is constitutively active in unstimulated cells where it phosphorylates beta-catenin, targeting beta-catenin for rapid degradation. Receptor-induced inhibition of GSK-3 allows beta-catenin to accumulate in the cytoplasm and then translocate to the nucleus where it promotes the transcription of genes such as c-myc and cyclin D1. Wnt hormones, the best known regulators of beta-catenin, inhibit GSK-3 via the Disheveled protein. However, GSK-3 is also inhibited when it is phosphorylated by Akt, a downstream target of phosphatidylinositol 3-kinase (PI3K). We have previously shown that B cell Ag receptor (BCR) signaling leads to activation of PI3K and Akt as well as inhibition of GSK-3. Therefore, we hypothesized that BCR engagement would induce the accumulation of beta-catenin via a PI3K/Akt/GSK-3 pathway. We now show that BCR ligation causes an increase in the level of beta-catenin in the nuclear fraction of B cells as well as an increase in beta-catenin-dependent transcription. Direct inhibition of GSK-3 by LiCl also increased beta-catenin levels in B cells. This suggests that GSK-3 keeps beta-catenin levels low in unstimulated B cells and that BCR-induced inhibition of GSK-3 allows the accumulation of beta-catenin. Surprisingly, we found that the BCR-induced phosphorylation of GSK-3 on its negative regulatory sites, as well as the subsequent up-regulation of beta-catenin, was not mediated by Akt but by the phospholipase C-dependent activation of protein kinase C. Thus, the BCR regulates beta-catenin levels via a phospholipase C/protein kinase C/GSK-3 pathway." provenance.
- _6 value "Beta-catenin is a transcriptional activator that is regulated by glycogen synthase kinase-3 (GSK-3). GSK-3 is constitutively active in unstimulated cells where it phosphorylates beta-catenin, targeting beta-catenin for rapid degradation. Receptor-induced inhibition of GSK-3 allows beta-catenin to accumulate in the cytoplasm and then translocate to the nucleus where it promotes the transcription of genes such as c-myc and cyclin D1. Wnt hormones, the best known regulators of beta-catenin, inhibit GSK-3 via the Disheveled protein. However, GSK-3 is also inhibited when it is phosphorylated by Akt, a downstream target of phosphatidylinositol 3-kinase (PI3K). We have previously shown that B cell Ag receptor (BCR) signaling leads to activation of PI3K and Akt as well as inhibition of GSK-3. Therefore, we hypothesized that BCR engagement would induce the accumulation of beta-catenin via a PI3K/Akt/GSK-3 pathway. We now show that BCR ligation causes an increase in the level of beta-catenin in the nuclear fraction of B cells as well as an increase in beta-catenin-dependent transcription. Direct inhibition of GSK-3 by LiCl also increased beta-catenin levels in B cells. This suggests that GSK-3 keeps beta-catenin levels low in unstimulated B cells and that BCR-induced inhibition of GSK-3 allows the accumulation of beta-catenin. Surprisingly, we found that the BCR-induced phosphorylation of GSK-3 on its negative regulatory sites, as well as the subsequent up-regulation of beta-catenin, was not mediated by Akt but by the phospholipase C-dependent activation of protein kinase C. Thus, the BCR regulates beta-catenin levels via a phospholipase C/protein kinase C/GSK-3 pathway." provenance.
- _6 value "Ariadne: Thus, Bcl6 binds to the IL-4 silencer region in Th1 cells and may deacetylate histones of the chromosomal region to repress expression of those cytokine genes by recruiting the SMRT and histone deacetylase complex." provenance.
- _2 value "These results thus confirm the neuroprotective effect of Bcl-xL against ischemic brain injury and provide the first evidence that the PTD can be used to efficiently transduce a biologically active neuroprotectant in experimental cerebral ischemia." provenance.
- _4 value "When CNP(50 nM) was added to NGF(25 ng/ml)-treated cells, CNP was able to completely abolish the NGF-induced increase in proliferation. CNP also completely inhibited the increase in apoptosis of NST-positive cells in response to NGF. This suggests that in the absence of additional factors, many of the cells induced by NGF to proliferate undergo apoptosis, and that CNP was able to both inhibit this proliferation and save NGF-treated cells from subsequent apoptosis. Cnp signal through its receptor Npr2." provenance.
- _5 value "In cell transfection assays, JDP-2 substantially increased hormone-dependent PR-mediated transactivation and worked primarily by stimulating AF-1 activity." provenance.
- _5 value "The progesterone receptor (PR) contains two transcription activation function (AF) domains, constitutive AF-1 in the N terminus and AF-2 in the C terminus. AF-2 activity is mediated by a hormone-dependent interaction with a family of steroid receptor coactivators (SRCs). SRC-1 can also stimulate AF-1 activity through a secondary domain that interacts simultaneously with the primary AF-2 interaction site." provenance.
- _4 value "Cux/CDP homozygous mutant mice displayed increased expression of SI mRNA during early postnatal development." provenance.
- _4 value "Both glucosamine and high glucose stimulated the in vitro kinase activity of immunoprecipitated PKC-betaI and -delta." provenance.
- _5 value "Cotransfected dominant negative PKC-betaI and -delta completely blocked the induction of PAI-1 promoter transcription by both sugars, whereas only dominant negative PKC-betaI interfered with Sp1-GAL4 activation." provenance.
- _5 value "In an alternate pathway, inhibition of IL-1 receptor-associated kinase-1 (IRAK) with AS ODN to IRAK reduced IL-18-induced expression of nuclear factor kappaB (NFkappaB). Finally, IL-18-induced cell surface VCAM-1 expression was inhibited by treatment with AS ODNs to c-Src, IRAK, PI3-kinase, and ERK1/2" provenance.
- _4 value "In an alternate pathway, inhibition of IL-1 receptor-associated kinase-1 (IRAK) with AS ODN to IRAK reduced IL-18-induced expression of nuclear factor kappaB (NFkappaB). Finally, IL-18-induced cell surface VCAM-1 expression was inhibited by treatment with AS ODNs to c-Src, IRAK, PI3-kinase, and ERK1/2" provenance.
- _5 value "Modified assertion" provenance.
- _5 value "From Full Paper Introduction PKB is involved in numerous cell processes...this includes supression of apoptosis, at least in part through its ability to phosphorylate the pro-apoptotic protein BAD." provenance.
- _5 value "Furthermore, ATP-citrate lyase was phosphorylated in vitro by recombinant protein kinase B on the same site. Taken together, these results demonstrate that serine 454 of ATP-citrate lyase is a novel and major in vivo substrate for protein kinase B." provenance.
- _5 value "Furthermore, ATP-citrate lyase was phosphorylated in vitro by recombinant protein kinase B on the same site. Taken together, these results demonstrate that serine 454 of ATP-citrate lyase is a novel and major in vivo substrate for protein kinase B." provenance.
- _3 value "We show that peroxiredoxins I and II are present in the cytoplasm of pancreatic islet cells as well as in insulinoma cell lines beta TC6-F7 and INS-1. Peroxiredoxins I and II were up-regulated by all stress agents used." provenance.
- _3 value "NO acts as a strong repressor of CTGF expression in cultured rat MC." provenance.
- _5 value "The induction of the inducible NO-synthase by TNF-alpha, IL-1beta and LPS provoked a transient down-regulation of CTGF mRNA, an effect that could be partially overcome by pretreatment with the NOS-inhibitor Nomega-nitro-l-arginine methyl ester." provenance.
- _5 value "Il6 activates STAT1 and STAT5 in addition to STAT3" provenance.
- _5 value "Il6 activates STAT1 and STAT5 in addition to STAT3" provenance.
- _6 value "JAK1, JAK2, and Tky-2 are activated and are tyrosine-phosphorylated in response to Il6, CNTF, LIF, and OSM" provenance.
- _5 value "Socs1 a negative regulatory molecule of Il6 signaling on the basis of its binding to JAK Socs1 directly interacts with JAK1 and JAK2 and thus inhibits their catalytic activity" provenance.
- _7 value "Socs1 a negative regulatory molecule of Il6 signaling on the basis of its binding to JAK Socs1 directly interacts with JAK1 and JAK2 and thus inhibits their catalytic activity" provenance.
- _7 value "binding of Il6 to Il6R induces homodimerization ofgp130, activating JAK associated with gp130 at Box1.......Our group and others found that JAK1, JAK2, and Tky-2 are activated and are tyrosine-phosphorylated in response to IL-6, CNTF, LIF, and OSM [14]" provenance.
- _4 value "in Il6 signal cascade, the SHP2 interaction site of gp130 has also been shown to be a Socs3 contact site so that Socs3 may compete for the SHP2-gp130 interaction site" provenance.
- _5 value "nonreceptor tyrosine kinases, such as Btk, Tec, Fes, and Hck are activated through the Il6R receptor" provenance.
- _3 value "ATF6 is an endoplasmic reticulum (ER) stress-regulated transmembrane transcription factor that activates the transcription of ER molecular chaperones. Upon ER stress, ATF6 translocates from the ER to the Golgi where it is processed to its active form. We have found that the ER chaperone BiP/GRP78 binds ATF6 and dissociates in response to ER stress. Loss of BiP binding correlates with the translocation of ATF6 to the Golgi, which was slowed in cells overexpressing BiP. Two Golgi localization signals (GLSs) were identified in ATF6. Removal of BiP binding sites from ATF6, while retaining a GLS, resulted in its constitutive translocation to the Golgi. These results suggest that BiP retains ATF6 in the ER by inhibiting its GLSs and that dissociation of BiP during ER stress allows ATF6 to be transported to the Golgi." provenance.
- _4 value "ATF6 is an endoplasmic reticulum (ER) stress-regulated transmembrane transcription factor that activates the transcription of ER molecular chaperones. Upon ER stress, ATF6 translocates from the ER to the Golgi where it is processed to its active form. We have found that the ER chaperone BiP/GRP78 binds ATF6 and dissociates in response to ER stress. Loss of BiP binding correlates with the translocation of ATF6 to the Golgi, which was slowed in cells overexpressing BiP. Two Golgi localization signals (GLSs) were identified in ATF6. Removal of BiP binding sites from ATF6, while retaining a GLS, resulted in its constitutive translocation to the Golgi. These results suggest that BiP retains ATF6 in the ER by inhibiting its GLSs and that dissociation of BiP during ER stress allows ATF6 to be transported to the Golgi." provenance.
- _6 value "Upon ER stress, ATF6 translocates from the ER to the Golgi where it is processed to its active form." provenance.
- _4 value "The p53 tumor suppressor is inhibited and destabilized by Mdm2. c-Abl is important for p53 activation under stress conditions. In response to DNA damage, c-Abl protects p53 by neutralizing the inhibitory effects of Mdm2. Hdm2 (human Mdm2) phosphorylation at Tyr394. Substitution of Tyr394 by Phe394 enhances the ability of Mdm2 to promote p53 degradation and to inhibit its transcriptional and apoptotic activities. Our results suggest that phosphorylation of Mdm2 by c-Abl impairs the inhibition of p53 by Mdm2, hence defining a novel mechanism by which c-Abl activates p53. Mutation studies revealed that N-terminal and C-terminal of mdm2 are both important for binding c-Abl." provenance.
- _5 value "Modified assertion" provenance.
- _3 value "The captured complex V displayed ATP hydrolysis activity" provenance.
- _3 value "The captured complex V displayed ATP hydrolysis activity" provenance.
- _5 value "Modified assertion" provenance.
- _5 value "Modified assertion" provenance.
- _6 value "Modified assertion" provenance.
- _6 value "OSM caused ligand-independent activation of the AR in DU-145 cells. In the presence of OSM, hydroxyflutamide behaved as an AR agonist. Bicalutamide down-regulated AR activation caused by OSM only at a concentration of 1 microM." provenance.
- _5 value "OSM caused ligand-independent activation of the AR in DU-145 cells. In the presence of OSM, hydroxyflutamide behaved as an AR agonist. Bicalutamide down-regulated AR activation caused by OSM only at a concentration of 1 microM." provenance.
- _4 value "Among the MMPs, MMP-1, -3, -7, and -13 processed CTGF of the complex into the major NH(2)- and COOH-terminal fragments, whereas VEGF(165) was completely resistant to the MMPs." provenance.
- _5 value "Modified assertion" provenance.
- _3 value "# Ariadne: Leptin was found to specifically repress RNA levels and enzymatic activity of hepatic stearoyl-CoA desaturase-1 (SCD-1), which catalyzes the biosynthesis of monounsaturated fatty acids. [MolSynthesis]" provenance.
- _4 value "It was proposed that NE affects proteolysis indirectly by decreasing cell ATP from activation of uncoupling protein-1 (UCP1)-dependent mitochondrial respiration. This was tested by comparing the effects of NE and fatty acids (which directly activate UCP1)" provenance.
- _4 value "Altered translational activation resulted in defective processing of protamine 2 and severe defects in sperm morphogenesis" provenance.
- _3 value "E2 stimulation of S118 phosphorylation was observed within 10 min of its addition" provenance.
- _3 value "We show here the transient activation of the small GTPase Rac, followed by a rise in reactive oxygen species (ROS), as necessary early steps in a signal transduction cascade that lead to NFkappaB activation and collagenase-1 (CL-1)/matrix metalloproteinase-1 production after integrin-mediated cell shape changes." provenance.
- _3 value "This protein has a potential role in protecting the NADPH oxidase by inactivating H(2)O(2) or altering signaling pathways affected by H(2)O(2)." provenance.
- _5 value "We conclude that MK can act as a growth, survival, and angiogenic factor during tumorigenesis and signals through the ALK receptor." provenance.
- _4 value "# GeneRif: demonstrate that ectopic MAP4 promotes outgrowth of extended MTs during beta1-integrin-induced cell spreading" provenance.
- _3 value "Flavopiridol induces apoptosis and suppresses Drg1 expression on SN-38-treated Hct116 cells." provenance.
- _5 value "Hyaluronan-CD44 binding stimulated Ras-Mek1-Mapk pathway, which inturn stimulated MMP-2 secretion in a time and dose dependent manner." provenance.
- _2 value "the invasiveness of QG90 was clearly activated by HA treatment. " provenance.
- _2 value "an inhibition of insulin receptor (IR) mRNA levels and insulin binding by aldosterone this inhibition of the insulin response by aldosterone is mediated by a downregulation of the levels of mineralocorticoid receptors (MRs) (50% decrease) and their mRNA (50% decrease)" provenance.
- _4 value "Cardiac ankyrin repeat protein (CARP), glutathione peroxidase (Gpx1), and genes which participate in the formation of extracellular matrix including decorin, TSC-36, Magp2, Osf2, and SPARC are upregulated in CSQ mouse hearts at 7 and 13 weeks of age compared to those of non-transgenic littermates." provenance.
- _6 value "These effects of high glucose were blocked by antioxidants (taurine and tiron), inhibitors of mitochondrial electron transport chain complex I (rotenone) and II (thenoyltrifluoroacetone), an inhibitor of glycolysis-derived pyruvate transport into mitochondria (alpha-cyano-4-hydroxycinnamic acid), an uncoupler of oxidative phosphorylation (carbonyl cyanide m-chlorophenylhydrazone), a manganese superoxide dismutase mimetic, catalase, and a specific inhibitor of p38 MAPK (SB 203580)," provenance.
- _5 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _6 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _6 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _4 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _6 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _4 value "In this study, cAMP-elevating agents such as isoproterenol, prostaglandin E(2), CGS-21680 (an adenosine A(2a) receptor agonist), the type IV phosphodiesterase inhibitor RO 20-1724, the adenylate cyclase activator forskolin, and the Gs-protein activator cholera toxin all inhibited LT biosynthesis and 5-LO translocation to the nucleus in cytokine-primed human PMN" provenance.
- _6 value "In this study, cAMP-elevating agents such as isoproterenol, prostaglandin E(2), CGS-21680 (an adenosine A(2a) receptor agonist), the type IV phosphodiesterase inhibitor RO 20-1724, the adenylate cyclase activator forskolin, and the Gs-protein activator cholera toxin all inhibited LT biosynthesis and 5-LO translocation to the nucleus in cytokine-primed human PMN" provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Pretreatment of HCAECs with simvastatin or atorvastatin (1 and 10 microM) reduced ox-LDL-induced expression of LOX-1 as well as adhesion molecules" provenance.
- _3 value "Pretreatment of HCAECs with simvastatin or atorvastatin (1 and 10 microM) reduced ox-LDL-induced expression of LOX-1 as well as adhesion molecules" provenance.
- _3 value "We observed that ox-LDL (40 microg/ml) treatment up-regulated the expression of E- and P-selectins, VCAM-1 and ICAM-1 in HCAECs." provenance.
- _3 value "We observed that ox-LDL (40 microg/ml) treatment up-regulated the expression of E- and P-selectins, VCAM-1 and ICAM-1 in HCAECs." provenance.
- _3 value "Table 1." provenance.
- _3 value "Table 1." provenance.
- _4 value "It is known that LPS stimulation leads to increased activation of three subgroups of MAPKs, i.e., ERK, JNK, and p38, in murine macrophages and human monocytes (38, 39)." provenance.
- _6 value "cells expressing myrAkt maintained higher levels of transferrin receptor on the cell surface in the absence of IL3 than control cells these results indicate that transferrin receptor surface expression is regulated by IL3 and that myrAkt can support growth factor-independent transferrin receptor expression." provenance.
- _9 value "these results suggest that Akt-mediated increases in transporter and receptor surface expression in the absence of IL3 are dependent on mTOR activity." provenance.
- _5 value "These observations indicate that phosphorylation of Ser 362 and Ser 374 prime c-Fos for additional growth factor-regulated phosphorylation... ERK phosphorylates Thr 325 and Thr 331 in primed c-Fos. [Figure 2c shows the experimental results, done with ERK 1/2.]" provenance.
- _5 value "These observations indicate that phosphorylation of Ser 362 and Ser 374 prime c-Fos for additional growth factor-regulated phosphorylation... ERK phosphorylates Thr 325 and Thr 331 in primed c-Fos. [Figure 2c shows the experimental results, done with ERK 1/2.]" provenance.
- _6 value "Here we demonstrate that Tiam1, a Rac-specific GEF, preferentially associates with activated GTP-bound Ras through a Ras-binding domain. Furthermore, activated Ras and Tiam1 cooperate to cause synergistic formation of Rac-GTP in a PI(3)K-independent manner. Thus, Tiam1 can function as an effector that directly mediates Ras activation of Rac." provenance.
- _3 value "FSH, through its second messengers (increase in intracellular cAMP and intracellular calcium), downregulated the glypican-1 mRNA expression in Sertoli cells from 20-day-old rats." provenance.
- _3 value "FSH, through its second messengers (increase in intracellular cAMP and intracellular calcium), downregulated the glypican-1 mRNA expression in Sertoli cells from 20-day-old rats." provenance.
- _2 value "ATP application significantly increased the number of cells expressing MHC and the number of myotubes formed in 24 hours" provenance.
- _4 value "Furthermore, we demonstrate that ATP application results in a significant and rapid increase in the phosphorylation of MAPKs, particularly p38, and that inhibition of p38 activity can prevent the effect of ATP on cell number." provenance.
- _4 value "P2rx5 is present on satellite cells and that activation of a p2x receptor inhibits proliferation, stimulates expression of markers of muscle cell differentiation, including myogenin, p21, and myosin heavy chain, and increases the rate of myotube formation" provenance.