Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _5 value "Table I: Genes regulated by progesterone" provenance.
- _5 value "Table I: Genes regulated by progesterone" provenance.
- _3 value "The P2Y(1) receptor protein is shown to be restricted to the neuromuscular junctions and colocalized with AChRs in adult muscle (chicken, Xenopus, and rat) but not in the chick embryo. Denervation or crush of the motor nerve (in chicken or rat) caused up to 90% decrease in the muscle P2Y(1) transcript, which was restored on regeneration, whereas the AChR mRNA greatly increased" provenance.
- _5 value "We demonstrate that purified SCG10 can be phosphorylated by two subclasses of mitogen-activated protein (MAP) kinases, c-Jun N-terminal/stress-activated protein kinase (JNK/SAPK) and p38 MAP kinase. Moreover, SCG10 was found to bind tightly and specifically to JNK3/SAPKbeta. JNK3/SAPKbeta phosphorylation occurs at Ser-62 and Ser-73, residues that result in reduced microtubule-destabilizing activity for SCG10" provenance.
- _4 value "Two different constructs of LRP5 were made in which the cytoplasmic tail (LRP5deltaC) or the transmembrane domain and cytoplasmic tail (LRP5deltaTM) were deleted. The two dominant-negative forms decreased ALP activity induced by Wnt3a in both C3H10T1/2 and ST2 cells strongly suggesting that LRP5 modulates the inducing effect of Wnt3a. It was also seen that LRP5deltaC and LRP5deltaTM significantly inhibited the induction of ALP by BMP2 in ST2 AND C3H10T1/2 cells. Moreover, ST2 cells that were stably expressing LRP5deltaC(LRP5deltaC-ST2) were less able to express ALP in response to either Wnt3a or BMP2, compared to ST2 cells stably expressing wild-type LRP5 (LRP5-ST2)." provenance.
- _2 value "In addition, stable, inducible expression of PLZF in U937 cells inhibited the ability of 1,25(OH)(2)D(3) to induce surface expression of the monocytic marker CD14 and morphologic changes associated with differentiation" provenance.
- _4 value "In addition, stable, inducible expression of PLZF in U937 cells inhibited the ability of 1,25(OH)(2)D(3) to induce surface expression of the monocytic marker CD14 and morphologic changes associated with differentiation" provenance.
- _4 value "DNA microarray analysis of 6538 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity alpha were significantly up-regulated, whereas IL-1beta was significantly down-regulated in PC3 cells expressing TARP" provenance.
- _4 value "DNA microarray analysis of 6538 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity alpha were significantly up-regulated, whereas IL-1beta was significantly down-regulated in PC3 cells expressing TARP" provenance.
- _3 value "TARP expression is up-regulated by testosterone in LNCaP cells that express a functional androgen receptor" provenance.
- _4 value "cDNA microarray analysis of 6538 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity alpha were significantly up-regulated, whereas IL-1beta was significantly down-regulated in PC3 cells expressing TARP" provenance.
- _4 value "cDNA microarray analysis of 6538 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity alpha were significantly up-regulated, whereas IL-1beta was significantly down-regulated in PC3 cells expressing TARP" provenance.
- _4 value "cDNA microarray analysis of 6538 genes revealed that caveolin 1, caveolin 2, amphiregulin, and melanoma growth stimulatory activity alpha were significantly up-regulated, whereas IL-1beta was significantly down-regulated in PC3 cells expressing TARP" provenance.
- _4 value "Consistent with our prediction, IL-4 pretreatment decreases both basal and RANKL-stimulated mRNA levels of Ikappa Balpha , ICAM-1, and TLR-2 (Fig. 7B), all of which are transcriptionally activated by NF-kappa B (28-30)." provenance.
- _6 value "Because RNF4 interacts also with the androgen receptor (AR) functioning as a coactivator..." provenance.
- _4 value "Finally, we show that the repression of endogenous PATZ expression by antisense expression plasmids in LNCaP cells results in a stronger androgen response." provenance.
- _4 value "Troglitazone significantly reduced the activities of glyoxalase I and II; this inhibitory effect was concentration-dependent and time-dependent and was associated with reduced mRNA contents and increased AGEs formation" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _4 value "TGF-beta2 inhibited phosphorylation of p27 in actively cycling cells" provenance.
- _3 value "mGBP-2 induced a faster growth rate, with the highest expressing clones showing approximately a 50% reduction in doubling time." provenance.
- _4 value "Here, we demonstrate that Flt-1-mediated antiproliferative activity can be blocked completely by the dominant negative mutant of CDC42 (CDC42-17N) and partially by a Rac1 dominant negative mutant (Rac1-17N) but is not affected by a RhoA dominant negative mutant (RhoA-19N). Both CDC42-17N and Rac1-17N increase the intracellular Ca(2+) mobilization in response to VPF/VEGF but have no effect on KDR and MAPK phosphorylation." provenance.
- _7 value "Here, we demonstrate that Flt-1-mediated antiproliferative activity can be blocked completely by the dominant negative mutant of CDC42 (CDC42-17N) and partially by a Rac1 dominant negative mutant (Rac1-17N) but is not affected by a RhoA dominant negative mutant (RhoA-19N). Both CDC42-17N and Rac1-17N increase the intracellular Ca(2+) mobilization in response to VPF/VEGF but have no effect on KDR and MAPK phosphorylation." provenance.
- _6 value "Recently, it has been shown that KDR is responsible for VPF/VEGF-stimulated endothelial cell (EC) proliferation and migration, whereas Flt-1 activation down-modulates KDR-mediated EC proliferation. Although KDR-mediated EC proliferation and migration have been extensively studied, much less is known about Flt-1-mediated antiproliferation. Here, we demonstrate that Flt-1-mediated antiproliferative activity can be blocked completely by the dominant negative mutant of CDC42 (CDC42-17N) and partially by a Rac1 dominant negative mutant (Rac1-17N) but is not affected by a RhoA dominant negative mutant (RhoA-19N)." provenance.
- _6 value "Using the chimeric-receptor EGLT in which the extracellular domain of epidermal growth factor receptor was fused to the transmembrane and intracellular domains of Flt-1, we also demonstrate that CDC42 and Rac1 are activated by EGLT. Previously, we showed that phosphatidylinositol 3-kinase is required for Flt-1-mediated antiproliferative activity, but phospholipase C is not required." provenance.
- _4 value "Pretreatment of cells with the p38MAPK-specific inhibitor SB202190 downregulates the induction of SOCS3-mRNA expression by IL-6." provenance.
- _5 value "activation of p38MAPK by IL-6" provenance.
- _4 value "Not available" provenance.
- _3 value "Each of the drugs increased triacylglyceride synthesis, cellular triacylglyceride content, and expression of fatty acid synthase by reporter gene and Northern blot analysis." provenance.
- _4 value "We evaluated the effects of the hydroxymethylglutaryl coenzyme A reductase inhibitors (HMGRI) atorvastatin, lovastatin, and simvastatin on lipid homeostasis in HepG2 cells." provenance.
- _4 value "We evaluated the effects of the hydroxymethylglutaryl coenzyme A reductase inhibitors (HMGRI) atorvastatin, lovastatin, and simvastatin on lipid homeostasis in HepG2 cells." provenance.
- _5 value "Modified assertion" provenance.
- _6 value "Modified assertion" provenance.
- _6 value "Nuclear Receptor: PPARA Ligand: Fatty acid, fibrate CYP Enzyme: ^CYP4A1, ^CYP4A3 Cytosolic binding protein: ^L-FABP ABC transporter: ^ABCD2, ABCD3, ^ABCB4" provenance.
- _6 value "Nuclear Receptor: PPARG Ligand: Fatty acid, Eicosanoid, Thiazolidinedione CYP Enzyme: ^CYP4B1 Cytosolic binding protein: ^ALBP, ^H-FABP ABC transporter: ?" provenance.
- _4 value "In conclusion, we have identified YB-1 as a protein that interacts with a TGF-beta response element in the distal region of the collagen alpha 1(I) gene. YB-1 protein activates the collagen promoter and translocates into the nucleus during TGF-beta addition to fibroblasts, suggesting a role for this protein in TGF-beta signaling." provenance.
- _3 value "Our results showed that estrogen stimulated Akt activation, as indicated by phosphorylation at Ser(473) of the oncoprotein, in ER-negative breast cancer cells. Activation of Akt by estrogen in these cells was time and dose dependent and could be blocked by inhibitors of phosphatidylinositol 3'-kinase and Src kinase but not by estrogen antagonists." provenance.
- _4 value "FACL4 and COX-2 synergistically inhibit apoptosis by reducing the intracellular level of free arachidonic acid. Here, we report that expression of FACL4 is significantly increased in colon adenocarcinoma" provenance.
- _2 value "Mitochondrial DNA (mtDNA) content decreased in an age-dependent manner and may be one of the causal factors in age-related type 2 diabetes." provenance.
- _6 value "In skeletal muscle, voltage-dependent potentiation of L-type Ca(2+) channel (Ca(V)1.1) activity requires phosphorylation by cyclic AMP-dependent protein kinase (PKA) anchored via an A kinase-anchoring protein (AKAP15)." provenance.
- _7 value "We found that Pak directly associates with Raf-1 under both physiological and overexpressed conditions. The association is greatly stimulated by 4beta-12-O-tetradecanoylphorbol-13-acetate and nocodazole and by expression of the active mutants of Rac and Ras." provenance.
- _3 value "Insulin (10(-7) mol/L) also increased GPI-PLD mRNA levels in rat islets and betaTC6-F7 cells 2- to 4-fold commensurate with an increase in GPI-PLD biosynthesis." provenance.
- _3 value "Islet GPI-PLD mRNA was increased 5-fold while liver mRNA and serum GPI-PLD levels were reduced 30% in ob/ob mice" provenance.
- _3 value "The progesterone concentration of Mssp-/- mice was decrease to 6.5% of that of wild-type mice at E2.5." provenance.
- _3 value "increase in glucose transport in response to 30 microU/ml insulin was about twofold greater in rat epitrochlearis muscles that had been made hypoxic or treated with AICAR 3.5 h previously than in untreated control muscles" provenance.
- _4 value "These results clearly indicate that increasing hepatic fructose 2,6-bisphosphate overcomes the impairment of insulin in suppressing hepatic glucose production, and it provides a potential therapy for type 2 diabetes." provenance.
- _5 value "TRAF6 activates the extracellular signal?regulated kinases (ERK) 1 and 2 as well as p38 mitogen-activated protein kinase (MAPK),11,118?125" provenance.
- _3 value "lipid lowering limits the expression of CD40L in experimental atheroma" provenance.
- _5 value "recent studies revealed that Cox-2 enhances basic fibroblast growth factor?induced angiogenesis through induction of VEGF76 and participates in VEGFmediated angiogenesis.77,78" provenance.
- _5 value "from full text - Figure 2" provenance.
- _5 value "Recently, it was shown that repression of AP-1-mediated transactivation of the collagenase 3 promoter by the ligand-activated glucocorticoid receptor occurs after AP-1 DNA binding (79). The glucocorticoid receptor-interacting coactivator GRIP1 was important for AP-1 repression, and it was proposed that GRIP1 confers activation and repression of target genes in a context-dependent manner." provenance.
- _4 value "In spinal cord tissue and spleenocytes of mice, MBP-stimulated the production of IL12p40." provenance.
- _5 value "In splenocytes of mice Mbp activated p65." provenance.
- _3 value "MSU crystals induced phosphorylation of p70s6k and the Src kinases c-Src, Lyn, Hck, and Fyn." provenance.
- _6 value "Transfection of the native Src inhibitor, C-terminal Src kinase (Csk), also suppressed crystal-induced c-Src, ERK1/2, and IkappaBalpha phosphorylation and IL-8 expression." provenance.
- _3 value "Expression in MCF7 cells of a dominant negative form of Erk5 resulted in a significant decrease in NRG-induced proliferation of MCF7 cells." provenance.
- _5 value "GT198 potently stimulated transcription mediated by estrogen receptor alpha and beta, thyroid hormone receptor beta1, androgen receptor, glucocorticoid receptor, and progesterone receptor." provenance.
- _6 value "Modified assertion" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _7 value "In response to signal activation, the phosphorylation state of S392 is reduced, allowing the KSR1 complex to colocalize with activated Ras and Raf-1 at the plasma membrane, thereby facilitating the phosphorylation reactions required for the activation of MEK and MAPK." provenance.
- _5 value "ERK1/ERK2 was found to phosphorylate the architectural transcription factor UBF at amino acids 117 and 201 within HMG boxes 1 and 2, preventing interaction with DNA" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _3 value "Ca2+ induced the HAT activities of both CBP and P/CAF in HaCaT cells." provenance.
- _3 value "Ca2+ induced the HAT activities of both CBP and P/CAF in HaCaT cells." provenance.
- _5 value "However, ectopic expression of RhoB, but not the closely related family member RhoA, resulted in a 5-fold decrease of T beta R-II promoter activity. Furthermore, ectopic expression of RhoB, but not RhoA, resulted in a significant decrease of T beta R-II protein expression and resistance of tumor cells to TGF-beta-mediated cell growth inhibition. Consequently, transcription assays using an AP1 reporter showed that AP1-mediated transcription is down-regulated by RhoB. Altogether, these results identify a mechanism by which RhoB antagonizes TGF-beta action through transcriptional down-regulation of AP1 in T beta R-II promoter." provenance.
- _6 value "However, ectopic expression of RhoB, but not the closely related family member RhoA, resulted in a 5-fold decrease of T beta R-II promoter activity. Furthermore, ectopic expression of RhoB, but not RhoA, resulted in a significant decrease of T beta R-II protein expression and resistance of tumor cells to TGF-beta-mediated cell growth inhibition. Consequently, transcription assays using an AP1 reporter showed that AP1-mediated transcription is down-regulated by RhoB. Altogether, these results identify a mechanism by which RhoB antagonizes TGF-beta action through transcriptional down-regulation of AP1 in T beta R-II promoter." provenance.
- _5 value "However, ectopic expression of RhoB, but not the closely related family member RhoA, resulted in a 5-fold decrease of T beta R-II promoter activity. Furthermore, ectopic expression of RhoB, but not RhoA, resulted in a significant decrease of T beta R-II protein expression and resistance of tumor cells to TGF-beta-mediated cell growth inhibition. Consequently, transcription assays using an AP1 reporter showed that AP1-mediated transcription is down-regulated by RhoB. Altogether, these results identify a mechanism by which RhoB antagonizes TGF-beta action through transcriptional down-regulation of AP1 in T beta R-II promoter." provenance.
- _4 value "However, ectopic expression of RhoB, but not the closely related family member RhoA, resulted in a 5-fold decrease of T beta R-II promoter activity. Furthermore, ectopic expression of RhoB, but not RhoA, resulted in a significant decrease of T beta R-II protein expression and resistance of tumor cells to TGF-beta-mediated cell growth inhibition. Consequently, transcription assays using an AP1 reporter showed that AP1-mediated transcription is down-regulated by RhoB. Altogether, these results identify a mechanism by which RhoB antagonizes TGF-beta action through transcriptional down-regulation of AP1 in T beta R-II promoter." provenance.
- _4 value "AGC kinases that are downstream of PI(3)K include serum- and glucocorticoid- regulated kinase and the atypical PKCs, PKC-z and -l. Akt and/or the atypical PKCs seem to be required for insulin stimulated glucose transport.." provenance.
- _4 value "Akt has been suggested to be important in transmission of the insulin signal, by phosphorylation of the enzyme GSK-3 (see below), the forkhead transcription factors and cAMP response element-binding protein38,39 Other AGC kinases that are downstream of PI(3)K include serum- and glucocorticoid- regulated kinase and the atypical PKCs, PKC-z and -l42. Akt and/or the atypical PKCs seem to be required for insulinstimulated glucose transport." provenance.
- _6 value "Akt phosphorylates and inactivates GSK-3, decreasing the rate of phosphorylation of glycogen synthase, thus increasing its activity state59. Insulin does not activate PP1 globally, but rather specifically targets discrete pools of the phosphatase, primarily increasing PP1 activity localized at the glycogen particle. The compartmentalized activation of PP1 by insulin is due to glycogen-targeting subunits, which serve as 'molecular scaffolds', bringing together the enzyme directly with its substrates glycogen synthase and phosphorylase in a macromolecular complex," provenance.
- _5 value "At least nine intracellular substrates of the insulin/IGF-I receptor kinases have been identified (Fig. 2). Four of these belong to the family of insulin-receptor substrate (IRS) proteins9. Other substrates include Gab-1, p60dok, Cbl, APS and isoforms of Shc10." provenance.
- _2 value "Both obesity and lipoatrophy also cause insulin resistance and predisposition to type 2 diabetes, demonstrating that adipose tissue is crucial in regulating metabolism beyond its ability to take up glucose4. Although insulin does not stimulate glucose uptake in liver, it blocks glycogenolysis and gluconeogenesis, and stimulates glycogen synthesis, thus regulating fasting glucose levels." provenance.
- _6 value "Expression of dominant-interfering CAP mutants that cannot bind to Cbl or flotillin inhibit Cbl translocation and insulin-stimulated glucose uptake." provenance.
- _3 value "Expression of tumour-necrosis factor-a (TNF-a) is increased in fat of obese rodents and humans, and has been shown to produce serine phosphorylation of IRS-1, resulting in reduced insulin receptor kinase activity and insulin resistance19." provenance.
- _3 value "IRS-1-knockout mice exhibit generalized pre- and post-natal growth retardation, as well as insulin resistance in peripheral tissues and impaired glucose tolerance11,12. IRS-2-knockout mice also exhibit insulin resistance in both peripheral tissues and liver," provenance.
- _3 value "IRS-1-knockout mice exhibit generalized pre- and post-natal growth retardation, as well as insulin resistance in peripheral tissues and impaired glucose tolerance11,12. IRS-2-knockout mice also exhibit insulin resistance in both peripheral tissues and liver," provenance.
- _4 value "Inhibitors of class Ia PI(3)K, or transfections with dominant negative constructs of the enzyme, block most metabolic actions of insulin, including stimulation of glucose transport, glycogen and lipid synthesis." provenance.
- _5 value "Insulin Stimulated phosphorylation cascade This pathway involves the tyrosine phosphorylation of IRS proteins and/or Shc, which in turn interact with the adapter protein Grb2, recruiting the Son-of-sevenless (SOS) exchange protein to the plasma membrane for activation of Ras. The activation of Ras also requires stimulation of the tyrosine phosphatase SHP2, through its interaction with receptor substrates such as Gab-1 or IRS1/2. Activated ERK can translocate into the nucleus, where it catalyses the phosphorylation of transcription factors such as p62TCF, Blockade of the pathway with dominant negative mutants or pharmacological inhibitors prevents the stimulation of cell growth by insulin, but has no effect on the metabolic actions of the hormone54. Insulin increases synthesis and blocks the degradation of proteins through activation of mTOR. The stimulation of this protein kinase involves PI(3)K activation, although another signal may also be required56. mTOR can control the mammalian translation machinery by direct phosphorylation and activation of p70 ribosomal S6 kinase (p70rsk)57, as well as phosphorylation of the initiation factor 4E for eukaryotic translation (eIF-4E) inhibitor, PHAS1 or 4E-binding protein 1 (ref. 58). P70rsk activates ribosome biosynthesis by phosphorylating the ribosomal S6 protein, producing increased translation of mRNAs with a 58-terminal oligopyrimidine tract. P70rsk also requires a second PtdIns(3,4,5)P3-dependent phosphorylation, presumably catalysed by PDK1. Phosphorylation of PHAS-1 by mTOR results in its dissociation from eIF-2, allowing capdependent translation of mRNAs with a highly structured 58-untranslated region. Although the mechanism of activation of mTOR remains unclear, it seems to require the presence of amino acids in the media for full activation by growth factors, and thus may also represent a nutrient sensor55. Glucose and lipid regulation Regulation of glycogen synthesis Insulin stimulates glycogen accumulation through a coordinated increase in glucose transport and glycogen synthesis. The hormone activates glycogen synthase by promoting its dephosphorylation, through the inhibition of kinases such as PKA or GSK-3 (ref. 59), and activation of protein phosphatase 1 (PP1)60." provenance.
- _6 value "Insulin Stimulated phosphorylation cascade This pathway involves the tyrosine phosphorylation of IRS proteins and/or Shc, which in turn interact with the adapter protein Grb2, recruiting the Son-of-sevenless (SOS) exchange protein to the plasma membrane for activation of Ras. The activation of Ras also requires stimulation of the tyrosine phosphatase SHP2, through its interaction with receptor substrates such as Gab-1 or IRS1/2. Activated ERK can translocate into the nucleus, where it catalyses the phosphorylation of transcription factors such as p62TCF, Blockade of the pathway with dominant negative mutants or pharmacological inhibitors prevents the stimulation of cell growth by insulin, but has no effect on the metabolic actions of the hormone54. Insulin increases synthesis and blocks the degradation of proteins through activation of mTOR. The stimulation of this protein kinase involves PI(3)K activation, although another signal may also be required56. mTOR can control the mammalian translation machinery by direct phosphorylation and activation of p70 ribosomal S6 kinase (p70rsk)57, as well as phosphorylation of the initiation factor 4E for eukaryotic translation (eIF-4E) inhibitor, PHAS1 or 4E-binding protein 1 (ref. 58). P70rsk activates ribosome biosynthesis by phosphorylating the ribosomal S6 protein, producing increased translation of mRNAs with a 58-terminal oligopyrimidine tract. P70rsk also requires a second PtdIns(3,4,5)P3-dependent phosphorylation, presumably catalysed by PDK1. Phosphorylation of PHAS-1 by mTOR results in its dissociation from eIF-2, allowing capdependent translation of mRNAs with a highly structured 58-untranslated region. Although the mechanism of activation of mTOR remains unclear, it seems to require the presence of amino acids in the media for full activation by growth factors, and thus may also represent a nutrient sensor55. Glucose and lipid regulation Regulation of glycogen synthesis Insulin stimulates glycogen accumulation through a coordinated increase in glucose transport and glycogen synthesis. The hormone activates glycogen synthase by promoting its dephosphorylation, through the inhibition of kinases such as PKA or GSK-3 (ref. 59), and activation of protein phosphatase 1 (PP1)60." provenance.
- _4 value "Insulin also profoundly inhibits lipolysis in adipocytes, primarily through inhibition of the enzyme hormone sensitive lipase71. This enzyme is acutely regulated by control of its phosphorylation state, which is activated by PKA-dependent phosphorylation, and inhibited as a result of a combination of kinase inhibition and phosphatase activation. Insulin inhibits the activity of the lipase primarily through reductions in cAMP levels, owing to the activation of a cAMP-specific phosphodiesterase in fat cells72." provenance.
- _5 value "Insulin also profoundly inhibits lipolysis in adipocytes, primarily through inhibition of the enzyme hormone sensitive lipase71. This enzyme is acutely regulated by control of its phosphorylation state, which is activated by PKA-dependent phosphorylation, and inhibited as a result of a combination of kinase inhibition and phosphatase activation. Insulin inhibits the activity of the lipase primarily through reductions in cAMP levels, owing to the activation of a cAMP-specific phosphodiesterase in fat cells72." provenance.
- _3 value "Insulin can also influence glucose metabolism indirectly by changes in free fatty acids generated from visceral fat, the so called 'single gateway' hypothesis64. Because visceral fat is less sensitive to insulin than subcutaneous fat, even after a meal there is little suppression of lipolysis by the hormone in this fat depot. The resulting direct flux of fatty acids derived from these fat cells through the portal vein to the liver can stimulate glucose production, thus providing a signal for both insulin action and insulin resistance in the liver It [insulin] inhibits the transcription of the gene encoding phosphoenolpyruvate carboxylase, the rate-limiting step in gluconeogenesis66. The hormone also decreases transcription of the genes encoding fructose-1,6-bisphosphatase and glucose-6- phosphatase, and increases transcription of glycolytic enzymes such as glucokinase and pyruvate kinase, and lipogenic enzymes such as fatty acid synthase and acetyl-CoA carboxylase." provenance.
- _3 value "Insulin can also influence glucose metabolism indirectly by changes in free fatty acids generated from visceral fat, the so called 'single gateway' hypothesis64. Because visceral fat is less sensitive to insulin than subcutaneous fat, even after a meal there is little suppression of lipolysis by the hormone in this fat depot. The resulting direct flux of fatty acids derived from these fat cells through the portal vein to the liver can stimulate glucose production, thus providing a signal for both insulin action and insulin resistance in the liver It [insulin] inhibits the transcription of the gene encoding phosphoenolpyruvate carboxylase, the rate-limiting step in gluconeogenesis66. The hormone also decreases transcription of the genes encoding fructose-1,6-bisphosphatase and glucose-6- phosphatase, and increases transcription of glycolytic enzymes such as glucokinase and pyruvate kinase, and lipogenic enzymes such as fatty acid synthase and acetyl-CoA carboxylase." provenance.
- _3 value "Insulin can also influence glucose metabolism indirectly by changes in free fatty acids generated from visceral fat, the so called 'single gateway' hypothesis64. Because visceral fat is less sensitive to insulin than subcutaneous fat, even after a meal there is little suppression of lipolysis by the hormone in this fat depot. The resulting direct flux of fatty acids derived from these fat cells through the portal vein to the liver can stimulate glucose production, thus providing a signal for both insulin action and insulin resistance in the liver It [insulin] inhibits the transcription of the gene encoding phosphoenolpyruvate carboxylase, the rate-limiting step in gluconeogenesis66. The hormone also decreases transcription of the genes encoding fructose-1,6-bisphosphatase and glucose-6- phosphatase, and increases transcription of glycolytic enzymes such as glucokinase and pyruvate kinase, and lipogenic enzymes such as fatty acid synthase and acetyl-CoA carboxylase." provenance.
- _3 value "Insulin can also influence glucose metabolism indirectly by changes in free fatty acids generated from visceral fat, the so called 'single gateway' hypothesis64. Because visceral fat is less sensitive to insulin than subcutaneous fat, even after a meal there is little suppression of lipolysis by the hormone in this fat depot. The resulting direct flux of fatty acids derived from these fat cells through the portal vein to the liver can stimulate glucose production, thus providing a signal for both insulin action and insulin resistance in the liver It [insulin] inhibits the transcription of the gene encoding phosphoenolpyruvate carboxylase, the rate-limiting step in gluconeogenesis66. The hormone also decreases transcription of the genes encoding fructose-1,6-bisphosphatase and glucose-6- phosphatase, and increases transcription of glycolytic enzymes such as glucokinase and pyruvate kinase, and lipogenic enzymes such as fatty acid synthase and acetyl-CoA carboxylase." provenance.
- _7 value "The activation of Ras also requires stimulation of the tyrosine phosphatase SHP2, through its interaction with receptor substrates such as Gab-1 or IRS1/2. Gab1 appears to interact with the SH2 containing tyrosine phosphatase SHP2," provenance.
- _4 value "The hormone (insulin) activates glycogen synthase by promoting its dephosphorylation, through the inhibition of kinases such as PKA or GSK-3 (ref. 59), and activation of protein phosphatase 1 (PP1)60. Insulin does not activate PP1 globally, but rather specifically targets discrete pools of the phosphatase, primarily increasing PP1 activity localized at the glycogen particle" provenance.
- _3 value "Osmolality of the mammalian renal medulla is high because of the operation of the urinary concentrating mechanism. To understand molecular events during the early phase of cellular adaptation to hypertonicity, we performed comprehensive searches for genes induced in response to hypertonicity using a cell line (mIMCD3) derived from the inner medullary collecting duct of mouse kidney. PCR-based subtractive hybridization of cDNA pools and cDNA microarray analysis were used. We report 12 genes whose mRNA expression is significantly increased within 4 h after exposure to hypertonicity. The increase in mRNA expression was the result of increased transcription. Many are either stress response genes or growth regulatory genes, supporting the notion that hypertonicity evokes the stress response and growth regulation in cells. Experiments using inhibitors revealed that mitogen-activated protein kinases were commonly involved in signaling for the induction of genes by hypertonicity. Tyrosine kinases and phosphatidylinositol 3-kinase also play a significant role. Signaling pathways for stimulation of transcription appeared quite diverse in that each gene was sensitive to different combinations of inhibitors." provenance.
- _3 value "Osmolality of the mammalian renal medulla is high because of the operation of the urinary concentrating mechanism. To understand molecular events during the early phase of cellular adaptation to hypertonicity, we performed comprehensive searches for genes induced in response to hypertonicity using a cell line (mIMCD3) derived from the inner medullary collecting duct of mouse kidney. PCR-based subtractive hybridization of cDNA pools and cDNA microarray analysis were used. We report 12 genes whose mRNA expression is significantly increased within 4 h after exposure to hypertonicity. The increase in mRNA expression was the result of increased transcription. Many are either stress response genes or growth regulatory genes, supporting the notion that hypertonicity evokes the stress response and growth regulation in cells. Experiments using inhibitors revealed that mitogen-activated protein kinases were commonly involved in signaling for the induction of genes by hypertonicity. Tyrosine kinases and phosphatidylinositol 3-kinase also play a significant role. Signaling pathways for stimulation of transcription appeared quite diverse in that each gene was sensitive to different combinations of inhibitors." provenance.
- _3 value "Osmolality of the mammalian renal medulla is high because of the operation of the urinary concentrating mechanism. To understand molecular events during the early phase of cellular adaptation to hypertonicity, we performed comprehensive searches for genes induced in response to hypertonicity using a cell line (mIMCD3) derived from the inner medullary collecting duct of mouse kidney. PCR-based subtractive hybridization of cDNA pools and cDNA microarray analysis were used. We report 12 genes whose mRNA expression is significantly increased within 4 h after exposure to hypertonicity. The increase in mRNA expression was the result of increased transcription. Many are either stress response genes or growth regulatory genes, supporting the notion that hypertonicity evokes the stress response and growth regulation in cells. Experiments using inhibitors revealed that mitogen-activated protein kinases were commonly involved in signaling for the induction of genes by hypertonicity. Tyrosine kinases and phosphatidylinositol 3-kinase also play a significant role. Signaling pathways for stimulation of transcription appeared quite diverse in that each gene was sensitive to different combinations of inhibitors." provenance.
- _3 value "Osmolality of the mammalian renal medulla is high because of the operation of the urinary concentrating mechanism. To understand molecular events during the early phase of cellular adaptation to hypertonicity, we performed comprehensive searches for genes induced in response to hypertonicity using a cell line (mIMCD3) derived from the inner medullary collecting duct of mouse kidney. PCR-based subtractive hybridization of cDNA pools and cDNA microarray analysis were used. We report 12 genes whose mRNA expression is significantly increased within 4 h after exposure to hypertonicity. The increase in mRNA expression was the result of increased transcription. Many are either stress response genes or growth regulatory genes, supporting the notion that hypertonicity evokes the stress response and growth regulation in cells. Experiments using inhibitors revealed that mitogen-activated protein kinases were commonly involved in signaling for the induction of genes by hypertonicity. Tyrosine kinases and phosphatidylinositol 3-kinase also play a significant role. Signaling pathways for stimulation of transcription appeared quite diverse in that each gene was sensitive to different combinations of inhibitors." provenance.
- _3 value "Osmolality of the mammalian renal medulla is high because of the operation of the urinary concentrating mechanism. To understand molecular events during the early phase of cellular adaptation to hypertonicity, we performed comprehensive searches for genes induced in response to hypertonicity using a cell line (mIMCD3) derived from the inner medullary collecting duct of mouse kidney. PCR-based subtractive hybridization of cDNA pools and cDNA microarray analysis were used. We report 12 genes whose mRNA expression is significantly increased within 4 h after exposure to hypertonicity. The increase in mRNA expression was the result of increased transcription. Many are either stress response genes or growth regulatory genes, supporting the notion that hypertonicity evokes the stress response and growth regulation in cells. Experiments using inhibitors revealed that mitogen-activated protein kinases were commonly involved in signaling for the induction of genes by hypertonicity. Tyrosine kinases and phosphatidylinositol 3-kinase also play a significant role. Signaling pathways for stimulation of transcription appeared quite diverse in that each gene was sensitive to different combinations of inhibitors." provenance.
- _4 value "Upon addition of TNF-alpha there was a concomitant increase in the monocyte activation marker, CD14." provenance.
- _4 value "Impaired HSP gene expression (HSP68, 105, 27, 40, 70 Official gene names: Hspa1a, Hsph1, Hspb2, Dnajb1, Hspab1) and decreased IkappaB protein (official gene name: NFKBIA) in APAP-treated COX-2-/+ male mice." provenance.
- _3 value "Treatment of 0.1 nM R1881, a mitogenic dose of Androgen, induces the cell cycle regulatory proteins Cyclin A, Cyclin B1, CDK1 and CDK2 expression." provenance.
- _3 value "Furthermore, basal TLR-4 mRNA expression by human monocyte-derived macrophages was upregulated by ox-LDL in vitro." provenance.
- _6 value "Modified assertion" provenance.
- _4 value "Modified assertion" provenance.
- _3 value "Th1 cells produce IFN-gamma and TNF-beta, which promote cell-mediated immunity, while Th2 cells secrete IL-4, IL-5, IL-6, IL-9, IL-10, and IL-13, which favor humoral responses" provenance.
- _4 value "in the presence of insulin, stimulation with CCK-8 led to a dramatic accumulation of cyclin D1, comparable to that induced by EGF and insulin. Addition of CCK-8 in the presence of EGF also induced a marked increase in the level of cyclin D1. As shown in Figure 8, addition of CCK- 8 to Swiss 3T3 CCKBRGFP cells also promoted a striking increase in the level of cyclin D3 in the presence of insulin or EGF. Accordingly, addition of CCK-8 in combination with either insulin or EGF also induce a striking accumulation of cyclin E." provenance.