Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _4 value "Nicotine stimulated KDR tyrosine phosphorylation at Tyr996 to an extent similar to that brought about by VEGF (Figure 3c)." provenance.
- _5 value "Modified assertion" provenance.
- _4 value "SUMO-1 overexpression induces dramatic GR degradation" provenance.
- _4 value "Overexpressing cells (C17 or C48) degraded H(2)O(2) and t-butylhydroperoxide more rapidly and showed decreased sensitivity to oxidant stress as measured by (51)Cr release" provenance.
- _2 value "in rat pancreatic islets chronically exposed to high glucose or FFA, glucose- induced impairment of insulin secretion is associated with (and might be due to) altered mitochondrial function, which results in impaired glucose oxidation, overexpression of the UCP-2 protein, and a consequent decrease of ATP production." provenance.
- _3 value "in rat pancreatic islets chronically exposed to high glucose or FFA, glucose- induced impairment of insulin secretion is associated with (and might be due to) altered mitochondrial function, which results in impaired glucose oxidation, overexpression of the UCP-2 protein, and a consequent decrease of ATP production." provenance.
- _5 value "Modified assertion" provenance.
- _4 value "\"The TNF-alpha induced expression of Fas-ligand mRNA was seen as at 2 h, in the primary IEC ex vivo. The mRNA expression was significantly increased in the IEC (intestinal epithelial cells) in 12 h postinjection of TNF-alpha into mice (in vivo). The Fas-ligand protein expression was significantly increased in 6 h after the TNF-alpha treatment on primary IEC ex vivo, similarly it was also observed that the Fas-ligand protein expression was significantly increased in vivo (mice) after 12 h postinjection of TNF-alpha. \"" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _5 value "We report here that cell attachment leads to tyrosine phosphorylation of CrkII on Y221, and that CrkII-Y221F mutant demonstrates enhanced association with the Crk-binding partners C3G and paxillin. Despite this enhanced signaling complex formation, CrkII-Y221F fails to induce JNK and PAK activation, membrane ruffling and cell migration, suggesting that it is defective in activating Rac signaling. " provenance.
- _2 value "Moreover, we demonstrated that AT2 receptor stimulation inhibited insulin-induced Akt phosphorylation and that insulin-mediated antiapoptotic effect was also blocked by AT2 receptor activation." provenance.
- _4 value "We demonstrated that insulin-mediated insulin receptor substrate (IRS)-2-associated PI3K activity was inhibited by AT2 receptor stimulation," provenance.
- _7 value "We demonstrated that insulin-mediated insulin receptor substrate (IRS)-2-associated PI3K activity was inhibited by AT2 receptor stimulation," provenance.
- _3 value "The key regulatory enzymes directly associated with citrate production in the prostate cells are mitochondrial aspartate aminotransferase, pyruvate dehydrogenase, and mitochondrial aconitase. Testosterone and prolactin are involved in the regulation of the corresponding genes associated with these enzymes" provenance.
- _3 value "Downregulated genes at both time-points were: IL2RA, CMYC, NPM, DEK, AF4, FLI1, htlf, MNDA, BCR, IKAROS, BPI and NFAT4. Upregulated genes at both time-points were IL1B, CD14 and MCL1. CD55, CD58, IRF2, CREB1, ATF4, RAC1, TIAR, KIAA0053, BAT2, BTK, RCK, EV12B and EDN were downregulated at 24 h, while SPI1, MKK3, BTG1 and IL8 were upregulated. At 72 h the upregulated genes were IL1RA, IL2RG, CXCR4, SCYA1, SCYA3, SCYA4, SCYA5, SCYA22, ANX2, CD83 and UPAR" provenance.
- _3 value "Downregulated genes at both time-points were: IL2RA, CMYC, NPM, DEK, AF4, FLI1, htlf, MNDA, BCR, IKAROS, BPI and NFAT4. Upregulated genes at both time-points were IL1B, CD14 and MCL1. CD55, CD58, IRF2, CREB1, ATF4, RAC1, TIAR, KIAA0053, BAT2, BTK, RCK, EV12B and EDN were downregulated at 24 h, while SPI1, MKK3, BTG1 and IL8 were upregulated. At 72 h the upregulated genes were IL1RA, IL2RG, CXCR4, SCYA1, SCYA3, SCYA4, SCYA5, SCYA22, ANX2, CD83 and UPAR" provenance.
- _3 value "TPA-induced epidermal ODC activity and ODC mRNA expression." provenance.
- _5 value "TPA-induced epidermal ODC activity and ODC mRNA expression." provenance.
- _3 value "TPA-induced expression of cyclooxygenase-2" provenance.
- _2 value "Activin A inhibits hepatocellular DNA synthesis and induces cell death. Follistatin binds activin and sequesters it from the signaling pathway." provenance.
- _4 value "Overexpression of follistatin may represent a unique strategy of hepatic tumors to overcome the inhibitory action of a growth factor, activin, by decreasing its local bioavailability." provenance.
- _5 value "Jak1 phosphorylation was reduced in wildtype indivduals after Il13 treatement, implying that SHP-2 is responsible for this effect." provenance.
- _4 value "Stimulation with Il4 increased SHP-1 phosporylation; however, stimulation with Il13 increased SHP-2 phosphoryaltion" provenance.
- _4 value "Stimulation with Il4 increased SHP-1 phosporylation; however, stimulation with Il13 increased SHP-2 phosphoryaltion" provenance.
- _5 value "Stimulation with Il4 increased SHP-1 phosporylation; however, stimulation with Il13 increased SHP-2 phosphoryaltion" provenance.
- _5 value "Stimulation with Il4 increased SHP-1 phosporylation; however, stimulation with Il13 increased SHP-2 phosphoryaltion" provenance.
- _7 value "Stimulation with Il4 increased SHP-1 phosporylation; however, stimulation with Il13 increased SHP-2 phosphoryaltion" provenance.
- _4 value "Those individuals vearing the intracellular R551 variant of the Il4a and no other intracellular variant, and those bearing no intracellular variant were selected. Introduction- doesn't distinguish between variants! After binding of Il4 and Il13, activation of the receptor-associated kinases (Jak) takes place, followed by the direct activation of IRS1/2 and STAT6 (an Il4 specific transcription factor) and further signal transduction cascades (e.g. IRS1/2 iniates PI3 kinase)" provenance.
- _4 value "Those individuals vearing the intracellular R551 variant of the Il4a and no other intracellular variant, and those bearing no intracellular variant were selected. Introduction- doesn't distinguish between variants! After binding of Il4 and Il13, activation of the receptor-associated kinases (Jak) takes place, followed by the direct activation of IRS1/2 and STAT6 (an Il4 specific transcription factor) and further signal transduction cascades (e.g. IRS1/2 iniates PI3 kinase)" provenance.
- _5 value "Those individuals vearing the intracellular R551 variant of the Il4a and no other intracellular variant, and those bearing no intracellular variant were selected. Introduction- doesn't distinguish between variants! After binding of Il4 and Il13, activation of the receptor-associated kinases (Jak) takes place, followed by the direct activation of IRS1/2 and STAT6 (an Il4 specific transcription factor) and further signal transduction cascades (e.g. IRS1/2 iniates PI3 kinase)" provenance.
- _4 value "Treatment of cells with NGR-1 showed a 7 and 14 fold increase in JAK3 and TYK2 phosphorylation after 10 mins and rapidly decreased to their basal level, but when treated with 2C4, a specific antibody of HER-2 there was a total abrogation in this phosphorylation, indicating that HER2 receptor is required for NGR-1 induced activation of JAK3 and TYK2 phosphorylation." provenance.
- _5 value "Modified assertion" provenance.
- _5 value "Modified assertion" provenance.
- _4 value "AMP kinase (AMPK) activity was found to increase two- to three-fold in the deep red region of the quadriceps muscle within 5 min of the beginning of exercise and remained elevated for as long as the rat continued to run (Winder & Hardie, 1996). Evidence is accumulating for a role of AMPK in initiating the induction of some of the adaptations to endurance training, including the increase in muscle GLUT-4, hexokinase, uncoupling protein 3, and some of the mitochondrial oxidative enzymes (Winder & Hardie, 1996)." provenance.
- _2 value "Intriguingly, the type of exercise stimuli governs the intricate balance of which signalling pathways are turned on or off, thereby providing for a regulation of phenotypic outcomes. For example, aerobic exercise involving predominantly endurance type of work does not phosphorylate p70S6K (Sherwood et al. 1999), whereas high-resistance loading type of exercise does" provenance.
- _4 value "increase in AMPK activity during contraction increases NRF-1 (Bergeron et al. 2001; Murakami et al. 1998; Xia et al. 1997), a transcription factor, which, in turn, binds to the ALA synthase and mTFA gene promoters, resulting in increases in these proteins (Gordon et al. 2001) and consequently increases cytochrome c protein concentration and mitochondrial density (Hood, 2001)." provenance.
- _4 value "Dominant negative ASK1, MKK6, MKK4 and JNK1 potently inhibited EGCG-induced cell death" provenance.
- _3 value "We and others have found that the absence of dystrophin in cells of the Duchenne muscular dystrophy animal model, the mdx mouse, leads to elevated Ca(2+) influx and cytosolic Ca(2+) concentrations when exposed to stress" provenance.
- _4 value "Human lung myofibroblasts as effectors of the inflammatory process: the common receptor gamma chain is induced by Th2 cytokines, and CD40 ligand is induced by lipopolysaccharide, thrombin and TNF-alpha." provenance.
- _3 value "We found that TIP120B gene was induced in C2C12 myoblasts when these cells differentiated into myotubes, whereas TIP120A gene expression was down-regulated." provenance.
- _3 value "re, we show that HERG conductance markedly promotes H2O2-induced apoptosis of various tumor cells, whereas HERG expression facilitates the tumor cell proliferation caused by tumor necrosis factor (TNF) ligand (TNF-alpha)." provenance.
- _5 value "Trx-1 transfection also caused a significant increase in the protein products of hypoxia-responsive genes, including vascular endothelial growth factor (VEGF) and nitric oxide synthase 2 in a number of different cell lines (MCF-7 human breast and HT29 human colon carcinomas and WEHI7.2 mouse lymphoma cells) under both normoxic and hypoxic conditions." provenance.
- _7 value "Anti-GM-CSF elevated basal Erk1/2 activity, which is consistent with the profile for AP-1. Notably, however, maximal activation of Erk1/2 in response to LPS challenge was suppressed." provenance.
- _6 value "Consistent with in vitro models (21), LPS promoted expression of GM-CSF and TNF mRNA in vivo (Fig. 2C). Neutralizing GM-CSF significantly inhibited expression of both GM-CSF and TNF mRNA by 26 and 44% respectively," provenance.
- _6 value "Consistent with in vitro models (21), LPS promoted expression of GM-CSF and TNF mRNA in vivo (Fig. 2C). Neutralizing GM-CSF significantly inhibited expression of both GM-CSF and TNF mRNA by 26 and 44% respectively," provenance.
- _5 value "Importantly, prior treatment with U0126 completely abolished Erk activity and also potently suppressed GM-CSF release after LPS challenge," provenance.
- _7 value "Importantly, anti- GM-CSF reduced the activity of NFB by 30?40% during the maximal activation period" provenance.
- _4 value "LPS induced activation of Akt within 15 min, and this activation was abrogated by wortmannin. The degree of activation we observed in isolated trachea ex vivo was more intense than that we observed in whole lung but similar to levels reported previously for LPS-stimulated macrophages in vitro (29)." provenance.
- _4 value "LPS induced the DNA binding activity of nuclear NFB and AP-1, and maximal activity was maintained between 1 and 6 h." provenance.
- _4 value "LPS potently stimulated protease release in the BALF as assessed by clear regions corresponding to zones of degradation. Major bands of protease activity were identified at 90 kDa, corresponding to the molecular size of latent MMP9 (92 kDa) and a major band activity band corresponding to the active form of MMP9 (86 kDa)." provenance.
- _4 value "LPS potently stimulated protease release in the BALF as assessed by clear regions corresponding to zones of degradation. Major bands of protease activity were identified at 90 kDa, corresponding to the molecular size of latent MMP9 (92 kDa) and a major band activity band corresponding to the active form of MMP9 (86 kDa)." provenance.
- _5 value "We demonstrate that CXCR4-dependent stimulation of Lyn is associated with the activation of phosphatidylinositol 3-kinase (PI3-kinase)." provenance.
- _4 value "Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) mediate membrane fusion reactions in eukaryotic cells by assembling into complexes that link vesicle-associated SNAREs with SNAREs on target membranes (t-SNAREs). Many SNARE complexes contain two t-SNAREs that form a heterodimer, a putative intermediate in SNARE assembly. Individual t-SNAREs (e.g., syntaxin 1A) also regulate synaptic calcium channels and cystic fibrosis transmembrane conductance regulator (CFTR), the epithelial chloride channel that is defective in cystic fibrosis. Whether the regulation of ion channels by individual t-SNAREs is related to SNARE complex assembly and membrane fusion is unknown. Here we show that CFTR channels are coordinately regulated by two cognate t-SNAREs, SNAP-23 (synaptosome-associated protein of 23 kDa) and syntaxin 1A. SNAP-23 physically associates with CFTR by binding to its amino-terminal tail, a region that modulates channel gating. CFTR-mediated chloride currents are inhibited by introducing excess SNAP-23 into HT29-Cl.19A epithelial cells. Conversely, CFTR activity is stimulated by a SNAP-23 antibody that blocks the binding of this t-SNARE to the CFTR amino-terminal tail. The physical and functional interactions between SNAP-23 and CFTR depend on syntaxin 1A, which binds to both proteins. We conclude that CFTR channels are regulated by a t-SNARE complex that may tune CFTR activity to rates of membrane traffic in epithelial cells." provenance.
- _3 value "from full text - Box 2 | Bcl2 and the Rb/Arf/p53 network Inactivation of the retinoblastoma (Rb) pathway ? for example, by loss of cell-cycle inhibitor Ink4a, which can prevent cyclin-D?Cdk4 from phosphorylating Rb ? unleashes the transcription factor E2f1,which increases expression of Arf, a protein that is encoded by the same locus as Ink4a (REF. 136).Arf,which is also a transcriptional target of Myc, sequesters Mdm2, a negative regulator of p53. Raised p53 levels can either impose growth arrest, typically by inducing the Waf1 cell-cycle inhibitor, or promote apoptosis through targets such as Bax, Puma and Noxa. The apoptotic targets seem to also require the p53 relative p63 or p73 (REF. 152). Circles/ovals denote oncogene products; rectangles denote known or likely tumour suppressors. For more detail, see REFS 4?6,136.ATM, ataxia telengiectasia mutated; Chk2, checkpoint 2; NF-?B, nuclear factor-?B." provenance.
- _4 value "from full text - Box 2 | Bcl2 and the Rb/Arf/p53 network Inactivation of the retinoblastoma (Rb) pathway ? for example, by loss of cell-cycle inhibitor Ink4a, which can prevent cyclin-D?Cdk4 from phosphorylating Rb ? unleashes the transcription factor E2f1,which increases expression of Arf, a protein that is encoded by the same locus as Ink4a (REF. 136).Arf,which is also a transcriptional target of Myc, sequesters Mdm2, a negative regulator of p53. Raised p53 levels can either impose growth arrest, typically by inducing the Waf1 cell-cycle inhibitor, or promote apoptosis through targets such as Bax, Puma and Noxa. The apoptotic targets seem to also require the p53 relative p63 or p73 (REF. 152). Circles/ovals denote oncogene products; rectangles denote known or likely tumour suppressors. For more detail, see REFS 4?6,136.ATM, ataxia telengiectasia mutated; Chk2, checkpoint 2; NF-?B, nuclear factor-?B." provenance.
- _5 value "from full text - Box 2 | Bcl2 and the Rb/Arf/p53 network Inactivation of the retinoblastoma (Rb) pathway ? for example, by loss of cell-cycle inhibitor Ink4a, which can prevent cyclin-D?Cdk4 from phosphorylating Rb ? unleashes the transcription factor E2f1,which increases expression of Arf, a protein that is encoded by the same locus as Ink4a (REF. 136).Arf,which is also a transcriptional target of Myc, sequesters Mdm2, a negative regulator of p53. Raised p53 levels can either impose growth arrest, typically by inducing the Waf1 cell-cycle inhibitor, or promote apoptosis through targets such as Bax, Puma and Noxa. The apoptotic targets seem to also require the p53 relative p63 or p73 (REF. 152). Circles/ovals denote oncogene products; rectangles denote known or likely tumour suppressors. For more detail, see REFS 4?6,136.ATM, ataxia telengiectasia mutated; Chk2, checkpoint 2; NF-?B, nuclear factor-?B." provenance.
- _5 value "from full text - Box 2 | Bcl2 and the Rb/Arf/p53 network Inactivation of the retinoblastoma (Rb) pathway ? for example, by loss of cell-cycle inhibitor Ink4a, which can prevent cyclin-D?Cdk4 from phosphorylating Rb ? unleashes the transcription factor E2f1,which increases expression of Arf, a protein that is encoded by the same locus as Ink4a (REF. 136).Arf,which is also a transcriptional target of Myc, sequesters Mdm2, a negative regulator of p53. Raised p53 levels can either impose growth arrest, typically by inducing the Waf1 cell-cycle inhibitor, or promote apoptosis through targets such as Bax, Puma and Noxa. The apoptotic targets seem to also require the p53 relative p63 or p73 (REF. 152). Circles/ovals denote oncogene products; rectangles denote known or likely tumour suppressors. For more detail, see REFS 4?6,136.ATM, ataxia telengiectasia mutated; Chk2, checkpoint 2; NF-?B, nuclear factor-?B." provenance.
- _5 value "HIF-2alpha accumulation is associated with increased expression of the angiogenic factor TP." provenance.
- _4 value "By adding LPL to osteogenic induction medium, osteoblastic mineralization was inhibited in a dose-dependent manner. Interestingly, sortilin overexpression abolished the LPL-mediated suppression of osteogenic differentiation" provenance.
- _7 value "By adding LPL to osteogenic induction medium, osteoblastic mineralization was inhibited in a dose-dependent manner. Interestingly, sortilin overexpression abolished the LPL-mediated suppression of osteogenic differentiation" provenance.
- _4 value "Western blot analysis showed a rapid, fivefold increase, in GSTP1 protein levels after treatment with 25 microM forskolin, with a peak at 2 h post-treatment. The levels of phosphorylated CRE (Ser133) binding protein-1 (CREB-1) increased rapidly, sevenfold at 30 min, and reached 10-fold at 4 h following forskolin" provenance.
- _3 value "An analysis with high density oligonucleotide microarrays identified >100 glucose-regulated genes. We found among others immediately up-regulated genes encoding transcriptional regulators TIEG1, VDUP1, and HES1" provenance.
- _3 value "Ananalysis with high density oligonucleotide microarrays identified >100glucose-regulated genes. We found among others immediately up-regulated genes encoding transcriptional regulators TIEG1, VDUP1, and HES1, in addition to cooperatively regulated genes that are associated with cholesterol biosynthesisand cell cycle." provenance.
- _3 value "We found among others immediately up-regulated genes encoding transcriptional regulators TIEG1, VDUP1, and HES1, in addition to cooperatively regulated genes that are associated with cholesterol biosynthesis and cell cycle. The immediate up-regulation of Tieg1 and Vdup1 expression was dependent on glucose metabolism but not on protein synthesis, suggesting that the transcriptional regulators mediate the glucose-induced down-regulation of Per1 and Per2 expression" provenance.
- _3 value "glucose-induced down-regulation of Per1 and Per2 expression." provenance.
- _4 value "Immunoblotting with antiphosphopeptide antibodies specific for Thr(188/37) of C/EBPbeta (anti-P-C/EBPbeta) shows that GH rapidly and transiently promotes phosphorylation of mLAP and mLIP on the MAPK site. MEK inhibitors prevent this GH-promoted phosphorylation of LAP and LIP, suggesting that such phosphorylation depends on GH-activated MAPK signaling." provenance.
- _5 value "Changes in expression affected not only known p53 target genes, but also several unexpected genes such as Expi (Wdnm1), Cyp1b1, Gelsolin, Ramp2 and class I MHC genes." provenance.
- _5 value "Changes in expression affected not only known p53 target genes, but also several unexpected genes such as Expi (Wdnm1), Cyp1b1, Gelsolin, Ramp2 and class I MHC genes." provenance.
- _3 value "Treatment of adult rats for 14 days with flutamide (daily s.c. injection of 15 mg/Kg B.W.) resulted in increased expression of the four isoenzymes" provenance.
- _3 value "the expression of PKC isoenzymes (alpha, beta1, epsilon) increased in prostates from pubertal (35-days old) rats that are characterized by relatively low but extremely bioactive testosterone plasma levels" provenance.
- _3 value "PGE(2) (50 nm) attenuated LPS-induced mRNA and protein expression of chemokines including monocyte chemoattractant protein-1, interleukin-8, macrophage inflammatory protein-1alpha and -1beta, and interferon-inducible protein-10. PGE(2) also inhibited the tumor necrosis factor-alpha-, interferon-gamma-, and interleukin-1beta-mediated expression of these chemokines" provenance.
- _3 value "PGE(2) (50 nm) attenuated LPS-induced mRNA and protein expression of chemokines including monocyte chemoattractant protein-1, interleukin-8, macrophage inflammatory protein-1alpha and -1beta, and interferon-inducible protein-10. PGE(2) also inhibited the tumor necrosis factor-alpha-, interferon-gamma-, and interleukin-1beta-mediated expression of these chemokines" provenance.
- _3 value "PGE(2) (50 nm) attenuated LPS-induced mRNA and protein expression of chemokines including monocyte chemoattractant protein-1, interleukin-8, macrophage inflammatory protein-1alpha and -1beta, and interferon-inducible protein-10. PGE(2) also inhibited the tumor necrosis factor-alpha-, interferon-gamma-, and interleukin-1beta-mediated expression of these chemokines" provenance.
- _5 value "Functional promoter analysis revealed that PPAR-gamma ligands inhibited IL-1beta-induced transactivation of IL-6 gene via suppression of not only nuclear factor-kappaB but also C/EBP-DNA binding." provenance.
- _4 value "# sentences for pubmedID=12217406: # Ariadne: We further show that release of both MHC class II molecules and of the lysosomal enzyme cathepsin D is stimulated by lipopolysaccharide (LPS, 1 microg/ml, 48h). [MolTransport]" provenance.
- _5 value "Modified assertion" provenance.
- _4 value "CTGF also induced mesangial cell migration via a beta(3) integrin-dependent mechanism that was similarly sensitive to the inhibition of the p42/44 MAPK and PI3K pathways, and it promoted the adhesion of the mesangial cells to type I collagen via up-regulation of alpha(1) integrin. " provenance.
- _5 value "In addition, anti-beta(3) integrin antibodies attenuated the activation of both the p42/44 MAPK and protein kinase B and the increase in fibronectin levels. " provenance.
- _5 value "The inhibition of CTGF-induced p42/44 MAPK or phosphatidylinositol 3-kinase (PI3K)/protein kinase B pathway activities abrogated the induction of fibronectin expression." provenance.
- _4 value "The inhibition of CTGF-induced p42/44 MAPK or phosphatidylinositol 3-kinase (PI3K)/protein kinase B pathway activities abrogated the induction of fibronectin expression." provenance.
- _3 value "We report the crystal structure of calcineurin (CN) in complex with CyPA-CsA at 2.8-A resolution. The CyPA-CsA complex binds to a composite surface formed by the catalytic and regulatory subunits of CN, where the complex of FK506 and its binding protein FKBP also binds. While the majority of the CN residues involved in the binding are common for both immunophilin-immunosuppressant complexes, a significant number of the residues are distinct. Unlike FKBP-FK506, CyPA-CsA interacts with Arg-122 at the active site of CN, implying direct involvement of CyPA-CsA in the regulation of CN catalysis. The simultaneous interaction of CyPA with both the composite surface and the active site of CN suggests that the composite surface may serve as a substrate recognition site responsible for the narrow substrate specificity of CN. The comparison of CyPA-CsA-CN with FKBP-FK506-CN significantly contributes to understanding the molecular basis of regulation of CN activity by the immunophilin-immunosuppressant." provenance.
- _5 value "These gastrointestinal phenotypes are highly similar to the phenotypes exhibited by mice deficient in trefoil factor 1 (pS2/TFF1) and intestinal trefoil factor (ITF)/TFF3, respectively, and corresponded closely with the capacity of the two pathways to stimulate transcription of the genes encoding pS2/TFF1 and ITF/TFF3." provenance.
- _5 value "These gastrointestinal phenotypes are highly similar to the phenotypes exhibited by mice deficient in trefoil factor 1 (pS2/TFF1) and intestinal trefoil factor (ITF)/TFF3, respectively, and corresponded closely with the capacity of the two pathways to stimulate transcription of the genes encoding pS2/TFF1 and ITF/TFF3." provenance.
- _3 value "mice harboring the reciprocal mutation ablating STAT1/3 signaling (gp130(Delta STAT)), or deficient in IL-6-mediated gp130 signaling (IL-6(-/-) mice), showed impaired colonic mucosal wound healing." provenance.
- _3 value "mice harboring the reciprocal mutation ablating STAT1/3 signaling (gp130(Delta STAT)), or deficient in IL-6-mediated gp130 signaling (IL-6(-/-) mice), showed impaired colonic mucosal wound healing." provenance.
- _3 value "haploinsufficiency of the Foxo1 gene, encoding a forkhead transcription factor (forkhead box transcription factor O1), restores insulin sensitivity and rescues the diabetic phenotype in insulin-resistant mice by reducing hepatic expression of glucogenetic genes and increasing adipocyte expression of insulin-sensitizing genes." provenance.
- _4 value "100 representative genes with -fold change values greater than or equal to 2 that were dependent on NF-kappa B for maintaining their relative expression levels were selected from a primary WT (+TNFalpha ) versus Ikappa Balpha SR (+TNFalpha ) screen. Genes were grouped in categories based upon their physiological functions or properties. Gene accession numbers are in the far left column adjacent to their names and descriptions. In the first data column, -fold changes of genes identified in two independent primary microarray screens of WT MEFs compared with WT. MEFs constitutively expressing the Ikappa Balpha (SS32/36AA) superrepressor are provided. In data columns 2-4, the dependences of each of these genes on IKKalpha , NEMO/IKKgamma , and IKKbeta were determined in six independent microarray screens wherein WT MEFs were compared with mutant MEFs null for the individual IKK subunits. -Fold change values from duplicate screenings were listed together. Dependence on one or more signalsome subunits was stringently evaluated by adhering to two criteria: wild type MEF absolute calls of \"present\" (P) and \"increase\" (I) average difference calls. Each screen was performed with cells stimulated for 2 h with 10 ng/ml human TNFalpha . Genes that were dependent on basal NF-kappa B for their expression were identified by performing independent microarray screens in the absence of TNFalpha stimulation. Redundancy hits (corresponding to different oligonucleotide regions of the same gene) are noted in the gene description column. NC denotes a \"no change\" average difference call, indicating no significant dependence on that IKK subunit. Results of exposure to TNFalpha are presented in the indicated column as follows: - (no significant effect), +/- (~2-5-fold stimulation), and + (>10-fold stimulated). Two independent screens were conducted in all cases with similar results." provenance.
- _4 value "100 representative genes with -fold change values greater than or equal to 2 that were dependent on NF-kappa B for maintaining their relative expression levels were selected from a primary WT (+TNFalpha ) versus Ikappa Balpha SR (+TNFalpha ) screen. Genes were grouped in categories based upon their physiological functions or properties. Gene accession numbers are in the far left column adjacent to their names and descriptions. In the first data column, -fold changes of genes identified in two independent primary microarray screens of WT MEFs compared with WT. MEFs constitutively expressing the Ikappa Balpha (SS32/36AA) superrepressor are provided. In data columns 2-4, the dependences of each of these genes on IKKalpha , NEMO/IKKgamma , and IKKbeta were determined in six independent microarray screens wherein WT MEFs were compared with mutant MEFs null for the individual IKK subunits. -Fold change values from duplicate screenings were listed together. Dependence on one or more signalsome subunits was stringently evaluated by adhering to two criteria: wild type MEF absolute calls of \"present\" (P) and \"increase\" (I) average difference calls. Each screen was performed with cells stimulated for 2 h with 10 ng/ml human TNFalpha . Genes that were dependent on basal NF-kappa B for their expression were identified by performing independent microarray screens in the absence of TNFalpha stimulation. Redundancy hits (corresponding to different oligonucleotide regions of the same gene) are noted in the gene description column. NC denotes a \"no change\" average difference call, indicating no significant dependence on that IKK subunit. Results of exposure to TNFalpha are presented in the indicated column as follows: - (no significant effect), +/- (~2-5-fold stimulation), and + (>10-fold stimulated). Two independent screens were conducted in all cases with similar results." provenance.
- _4 value "100 representative genes with -fold change values greater than or equal to 2 that were dependent on NF-kappa B for maintaining their relative expression levels were selected from a primary WT (+TNFalpha ) versus Ikappa Balpha SR (+TNFalpha ) screen. Genes were grouped in categories based upon their physiological functions or properties. Gene accession numbers are in the far left column adjacent to their names and descriptions. In the first data column, -fold changes of genes identified in two independent primary microarray screens of WT MEFs compared with WT. MEFs constitutively expressing the Ikappa Balpha (SS32/36AA) superrepressor are provided. In data columns 2-4, the dependences of each of these genes on IKKalpha , NEMO/IKKgamma , and IKKbeta were determined in six independent microarray screens wherein WT MEFs were compared with mutant MEFs null for the individual IKK subunits. -Fold change values from duplicate screenings were listed together. Dependence on one or more signalsome subunits was stringently evaluated by adhering to two criteria: wild type MEF absolute calls of \"present\" (P) and \"increase\" (I) average difference calls. Each screen was performed with cells stimulated for 2 h with 10 ng/ml human TNFalpha . Genes that were dependent on basal NF-kappa B for their expression were identified by performing independent microarray screens in the absence of TNFalpha stimulation. Redundancy hits (corresponding to different oligonucleotide regions of the same gene) are noted in the gene description column. NC denotes a \"no change\" average difference call, indicating no significant dependence on that IKK subunit. Results of exposure to TNFalpha are presented in the indicated column as follows: - (no significant effect), +/- (~2-5-fold stimulation), and + (>10-fold stimulated). Two independent screens were conducted in all cases with similar results." provenance.
- _4 value "100 representative genes with -fold change values greater than or equal to 2 that were dependent on NF-kappa B for maintaining their relative expression levels were selected from a primary WT (+TNFalpha ) versus Ikappa Balpha SR (+TNFalpha ) screen. Genes were grouped in categories based upon their physiological functions or properties. Gene accession numbers are in the far left column adjacent to their names and descriptions. In the first data column, -fold changes of genes identified in two independent primary microarray screens of WT MEFs compared with WT. MEFs constitutively expressing the Ikappa Balpha (SS32/36AA) superrepressor are provided. In data columns 2-4, the dependences of each of these genes on IKKalpha , NEMO/IKKgamma , and IKKbeta were determined in six independent microarray screens wherein WT MEFs were compared with mutant MEFs null for the individual IKK subunits. -Fold change values from duplicate screenings were listed together. Dependence on one or more signalsome subunits was stringently evaluated by adhering to two criteria: wild type MEF absolute calls of \"present\" (P) and \"increase\" (I) average difference calls. Each screen was performed with cells stimulated for 2 h with 10 ng/ml human TNFalpha . Genes that were dependent on basal NF-kappa B for their expression were identified by performing independent microarray screens in the absence of TNFalpha stimulation. Redundancy hits (corresponding to different oligonucleotide regions of the same gene) are noted in the gene description column. NC denotes a \"no change\" average difference call, indicating no significant dependence on that IKK subunit. Results of exposure to TNFalpha are presented in the indicated column as follows: - (no significant effect), +/- (~2-5-fold stimulation), and + (>10-fold stimulated). Two independent screens were conducted in all cases with similar results." provenance.
- _3 value "induction of a neuronal phenotype by nerve growth factor (NGF) is accompanied by a marked increase in GAP-43 levels" provenance.
- _5 value "PLAB showed similar concentration-dependent effects for the activation of PPAR alpha, gamma and delta isoforms in CV-1 and H4IIEC3 cells. O-Deacetylation of PLAB (PLAC) or esterification of the free carboxy group of PLAB with beta-D-O-glucopyranoside (PLAG) markedly reduced or abolished the activation of these PPAR isoforms." provenance.
- _6 value "Nuclear receptor corepressor (N-CoR) and silencing mediator of retinoid and thyroid receptor (SMRT) are both corepressors of numerous transcription factors, including steroid hormone receptors." provenance.
- _5 value "Repressor of tamoxifen transcriptional activity (RTA) has recently been defined as a potent repressor of tamoxifen-mediated ERa transcriptional activity as well as an agonist of the ERa, the glucocorticoid receptor, and the PR" provenance.
- _4 value "Since the ER plays a major role in breast cancer development and the PR is a target of estrogen, the changes of the expression level of E6-AP might interfere with the normal functioning of the ER and the PR. Hence, E6-AP may participate in the formation and progression of breast tumors." provenance.
- _7 value "The growing family of nuclear receptor coactivators has recently acquired a unique member, steroid receptor RNA activator (SRA) [22]. Differing from the other coactivators, SRA functions as a RNA transcript instead of as a protein. SRA specifically coactivates the transcriptional activity of steroid receptors, including the PR, the ER, the glucocorticoid receptor, and the androgen receptor." provenance.
- _5 value "The role of BRCA1 in cancer development is unclear. In addition to its ability to coactivate p53 and to modulate p300/CBP expression, BRCA1 is also a ligand-independent corepressor for the ER, the androgen receptor and the PR [35]. If BRCA1 is mutated, all of these pathways will be more or less impaired." provenance.
- _5 value "The steroid receptor coactivator (SRC) family is composed of three distinct but structurally and functionally related members: SRC-1 (nuclear receptor coactivator 1), SRC-2 (transcription intermediary factor 2/glucocorticoid receptor- interacting protein 1/nuclear receptor coactivator 2), and SRC-3 (p300/CREB-binding protein [CBP] cointegrator- associated protein/receptor-associated coactivator 3/activator of thyroid and retinoid receptors/amplified in breast cancer 1/thyroid receptor activator molecule 1). All three members of the SRC family interact with the PR and enhance its transcriptional activation in a ligand-dependent manner" provenance.
- _5 value "there are a few other proteins that have been demonstrated to upregulate the transcriptional activity of the PR. Chromatin highmobility group protein 1, chromatin high-mobility group protein 2, TIP60 (Tat-interacting protein), proline-rich nuclear receptor coregulatory protein 1, proline-rich nuclear receptor coregulatory protein 2, Cdc25B, and GT198 all function as PR coactivators," provenance.
- _6 value "there are a few other proteins that have been demonstrated to upregulate the transcriptional activity of the PR. Chromatin highmobility group protein 1, chromatin high-mobility group protein 2, TIP60 (Tat-interacting protein), proline-rich nuclear receptor coregulatory protein 1, proline-rich nuclear receptor coregulatory protein 2, Cdc25B, and GT198 all function as PR coactivators," provenance.