Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "The transcriptional regulatory networks that specify and maintain human tissue diversity are largely uncharted. To gain insight into this circuitry, we used chromatin immunoprecipitation combined with promoter microarrays to identify systematically the genes occupied by the transcriptional regulators HNF1alpha, HNF4alpha, and HNF6, together with RNA polymerase II, in human liver and pancreatic islets. We identified tissue-specific regulatory circuits formed by HNF1alpha, HNF4alpha, and HNF6 with other transcription factors, revealing how these factors function as master regulators of hepatocyte and islet transcription. Our results suggest how misregulation of HNF4alpha can contribute to type 2 diabetes." provenance.
- _5 value "Inhibition of COX-2 caused apoptosis of the anergy-resistant lupus T cells by augmenting Fas signaling and markedly decreasing the survival molecule c-FLIP (cellular homolog of viral FLICE inhibitory protein)." provenance.
- _3 value "Aldosterone provoked expression of hypertrophic markers (NPPA, NPPB, and ACTA1) in rat cardiac myocytes by phosphorylation of protein kinase D (PKD) and expression of collagens (COL1A1, COL1A2, and COL3A1) and transforming growth factor-beta1 in rat cardiac fibroblasts by upregulation of phosphoinositide 3-kinase (PI3K)-p100delta. Inhibition of PKD and PI3K-p110delta abrogated the hypertrophic and profibrotic effects, respectively, as did the mineralocorticoid receptor (MR) antagonist spironolactone" provenance.
- _5 value "Aldosterone provoked expression of hypertrophic markers (NPPA, NPPB, and ACTA1) in rat cardiac myocytes by phosphorylation of protein kinase D (PKD) and expression of collagens (COL1A1, COL1A2, and COL3A1) and transforming growth factor-beta1 in rat cardiac fibroblasts by upregulation of phosphoinositide 3-kinase (PI3K)-p100delta. Inhibition of PKD and PI3K-p110delta abrogated the hypertrophic and profibrotic effects, respectively, as did the mineralocorticoid receptor (MR) antagonist spironolactone" provenance.
- _6 value "The biological actions of estrogens are mediated by estrogen binding to one of two specific estrogen receptors (ERs) ERalpha and ERbeta" provenance.
- _4 value "Furthermore, deletion studies revealed an activator protein-1 (AP-1) site in the ceruloplasmin promoter to be critical for optimal ceruloplasmin promoter activity." provenance.
- _8 value "Expression of CRMP-1 was higher in CTGF-transfected clones than in vector control cells, and its level decreased after cells were treated with anti-integrin alpha(v)beta3 and alpha(v)beta5 antibodies." provenance.
- _4 value "In A431 cells, epidermal growth factor induced striking p120 phosphorylation at Y228. Y228-phosphorylated p120 localized to adherens junctions and lamellipodia, and was significantly enhanced in cells around the colony periphery. " provenance.
- _3 value "Both RyR2 and SERCA mRNA level in L-thyroxin-induced cardiac hypertrophy was over-expressed and propranolol or verapamil inhibited the alteration." provenance.
- _3 value "Both RyR2 and SERCA mRNA level in L-thyroxin-induced cardiac hypertrophy was over-expressed and propranolol or verapamil inhibited the alteration." provenance.
- _3 value "A protein with a molecular mass of 27kDa was induced by hypoxia in a mouse brain capillary endothelial cell line and identified as triosephosphate isomerase (TPI)" provenance.
- _6 value "Modified assertion" provenance.
- _3 value "Exogenous activin A activated HSC and increased the expression of alpha-smooth muscle actin and collagen." provenance.
- _3 value "These data demonstrate for the first time that the angiogenic factor HARP can also negatively regulates the angiogenic activity of VEGF165." provenance.
- _7 value "We found that although both importin 7 and importin 8 could bind GR, only importin 7 could import GR. Under these conditions, full-length GR localized to nuclei in the presence but not absence of an unidentified component in cell extracts. Interestingly, importin 7, importin 8, and importin alpha bound GR even in the absence of hormone; thus, hormonal control of localization is exerted at a step downstream of import receptor binding." provenance.
- _7 value "We found that although both importin 7 and importin 8 could bind GR, only importin 7 could import GR. Under these conditions, full-length GR localized to nuclei in the presence but not absence of an unidentified component in cell extracts. Interestingly, importin 7, importin 8, and importin alpha bound GR even in the absence of hormone; thus, hormonal control of localization is exerted at a step downstream of import receptor binding." provenance.
- _7 value "We found that although both importin 7 and importin 8 could bind GR, only importin 7 could import GR. Under these conditions, full-length GR localized to nuclei in the presence but not absence of an unidentified component in cell extracts. Interestingly, importin 7, importin 8, and importin alpha bound GR even in the absence of hormone; thus, hormonal control of localization is exerted at a step downstream of import receptor binding." provenance.
- _3 value "Several other genes were induced principally by heat shock but less strongly (4- to 10-fold) than those described above....transcription factor GABPB2" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _6 value "Modified assertion" provenance.
- _3 value "The vascular endothelial growth factor (VEGF) family includes the related polypeptides VEGF-B, -C and -D, which contribute to endothelial and lymphatic vessel development." provenance.
- _5 value "From mutations file" provenance.
- _4 value "Serum response factor (SRF) activates genes involved in smooth muscle differentiation and proliferation by recruiting muscle-restricted cofactors, such as the transcriptional coactivator myocardin, and ternary complex factors (TCFs) of the ETS-domain family, respectively." provenance.
- _4 value "Treatment with candesartan, but not the combination of hydralazine and hydrochlorothiazide, significantly increased the expression of Cx37 and Cx40, although blood pressure decreased similarly." provenance.
- _4 value "Thrombin stimulated GIT1 tyrosine phosphorylation with a time course similar to FAK phosphorylation in a Rho kinase- and Src-dependent manner. " provenance.
- _5 value "Autocrine VEGF is important for breast carcinoma migration because it competes with semaphorin 3A for neuropilin-1 binding and thus overrides its migration suppressing activity." provenance.
- _4 value "In fact, our studies indicate that VEGF/neuropilin-1 autocrine signaling promotes the migration of breast carcinoma cells by increasing the expression of the chemokine receptor CXCR4 [19]. Our finding that VEGF regulates CXCR4 expression is relevant because stromal-derived factor-1, the ligand for this receptor, is present in tumor stroma and in tissues such as lymph and lung [36], which are the primary targets of invasive breast carcinoma cells, and CXCR4 inhibitors impair metastasis." provenance.
- _5 value "The ability of this integrin to activate PI3-K and, consequently, mTOR, results in stimulation of VEGF translation that has been linked to a6b4-mediated survival of carcinoma cells." provenance.
- _5 value "b-catenin can be oncogenically activated not only by direct mutation but also by inactivation of APC. Alterations of the APC gene occur in 80% of the human colon cancers. In the absence of APC, b-catenin cannot be phosphorylated by Gsk3b, and it consequently accumulates and translocates into the nucleus" provenance.
- _5 value "Blocking ILK activity with a kinase-deficient mutant ILK (ILK-KD) inhibits NF-kappaB activation and sensitizes HER2/neu-transformed cells to TNF-alpha-induced apoptosis. Stable expression of ILK-KD in HER2/neu-transformed cells suppressed Akt phosphorylation and the expression of IkappaB kinase alpha and beta (IKKalpha and beta) at both the protein and mRNA levels upregulation of IKKalpha and IKKbeta by the ILK/Akt pathway" provenance.
- _5 value "Blocking ILK activity with a kinase-deficient mutant ILK (ILK-KD) inhibits NF-kappaB activation and sensitizes HER2/neu-transformed cells to TNF-alpha-induced apoptosis. Stable expression of ILK-KD in HER2/neu-transformed cells suppressed Akt phosphorylation and the expression of IkappaB kinase alpha and beta (IKKalpha and beta) at both the protein and mRNA levels upregulation of IKKalpha and IKKbeta by the ILK/Akt pathway" provenance.
- _3 value "Ksp-cadherin induces homotypic and Ca2+-dependent cell-cell adhesion" provenance.
- _7 value "Here we show that activation of PKD in response to oxidative stress requires two sequential signaling events, i.e., phosphorylation of Tyr463 by Abl, which in turn promotes a second step, phosphorylation of the PKD activation loop (Ser738/Ser742). We show that this is mediated by PKCdelta (protein kinase Cdelta), a kinase that is activated by Src in response to oxidative stress." provenance.
- _5 value "Modified assertion" provenance.
- _6 value "Modified assertion" provenance.
- _2 value "Activated eosinophils play a critical role in asthma pathogenesis, and eosinophil cationic protein (ECP) is a useful indicator of inflammation" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: A. Largest fold increases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: B. Largest fold decreases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: B. Largest fold decreases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: B. Largest fold decreases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: B. Largest fold decreases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: B. Largest fold decreases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells: B. Largest fold decreases" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Table 1 Differentially expressed genes following camptothecin treatment of HeLa cells:C. Most significant changes" provenance.
- _3 value "Levels of SREBP cleavage-activating protein, a regulator of SREBP transcriptional activity, decreased after castration and increased significantly at androgen independence" provenance.
- _5 value "In this study, we demonstrate that Shb is phosphorylated in an Src-dependent manner upon vascular endothelial growth factor (VEGF) stimulation using porcine aortic endothelial cells expressing the human VEGF receptor 2 (VEGFR-2) (KDR)." provenance.
- _5 value "Modified assertion" provenance.
- _3 value "Studies in ERalpha and ERbeta knockout mice confirmed these different pathways, demonstrating that in the endometrium, estrogen-mediated Cx26 [and Cx43] gene induction, but not induction during decidualization, is dependent on functional ERalpha" provenance.
- _3 value "mediators of the inflammatory cascade such as prostaglandin F(2alpha) and interleukin-1beta are able to induce Cx26 expression through the ER-independent pathway." provenance.
- _4 value "Dissection of anti- and pro-apoptotic signalling events triggered by TLR4 identified the dsRNA responsive protein kinase PKR as a critical mediator of pathogen-induced macrophage apoptosis." provenance.
- _5 value "We report here that mice with renal-specific inactivation of HNF1beta develop polycystic kidney disease. We show that renal cyst formation is accompanied by a drastic defect in the transcriptional activation of Umod, Pkhd1 and Pkd2 genes In vivo chromatin immunoprecipitation experiments demonstrated that HNF1beta binds to several DNA elements in murine Umod, Pkhd1, Pkd2 and Tg737/Polaris genomic sequences" provenance.
- _5 value "We report here that mice with renal-specific inactivation of HNF1beta develop polycystic kidney disease. We show that renal cyst formation is accompanied by a drastic defect in the transcriptional activation of Umod, Pkhd1 and Pkd2 genes In vivo chromatin immunoprecipitation experiments demonstrated that HNF1beta binds to several DNA elements in murine Umod, Pkhd1, Pkd2 and Tg737/Polaris genomic sequences" provenance.
- _3 value "Inhibition of apoptosis, resulting from an increase in anti-apoptotic protein, plays a fundamental role in carcinogenesis. Because ICBP90 gene expression is deregulated in cancer cells, we studied its expression in Jurkat cells under apoptotic conditions to see whether ICBP90 is involved in the regulation of apoptosis. We found that ICBP90 expression and the percentage of living cells were dose-dependently decreased in PHA and ionophore A23187-stimulated Jurkat cells, but not in THP-1 cells. These results suggest that apoptosis is dependent upon ICBP90 expression downregulation and that ICBP90 exhibits anti-apoptotic properties." provenance.
- _3 value "RESULTS: Both treatment with progesterone alone and treatment with E(2) and progesterone combined significantly decreased IGF-I mRNA and protein expression in cultured leiomyoma cells" provenance.
- _5 value "the autophosphorylation of NDR2 protein kinase was stimulated in vitro by S100B, an EF-hand Ca(2+)-binding protein of the S100 family, suggesting that the two isoforms are regulated by the same mechanisms. Further we show a predominant cytoplasmic localization of ectopically expressed NDR2." provenance.
- _5 value "AVP not only recruited AQP2, but also AKAP18delta to the plasma membrane." provenance.
- _3 value "This event is initiated by activation of vasopressin V2 receptors, followed by an elevation of cAMP and the activation of protein kinase A (PKA)." provenance.
- _3 value "Furthermore, insulin stimulated adiponectin mRNA expression in adipocytes and augmented transactivation of the adiponectin promoter by ADD1/SREBP1c" provenance.
- _4 value "TABLE III - Functional categories of genes whose expression level are affected by knock-out of H1t and H1a (ko/wt) Hist1h1a upregulated" provenance.
- _4 value "TABLE III - Functional categories of genes whose expression level are affected by knock-out of H1t and H1a (ko/wt) Hist1h1a upregulated" provenance.
- _4 value "TABLE III - Functional categories of genes whose expression level are affected by knock-out of H1t and H1a (ko/wt) Hist1h1a upregulated" provenance.
- _4 value "TABLE III - Functional categories of genes whose expression level are affected by knock-out of H1t and H1a (ko/wt) Hist1h1a upregulated" provenance.
- _4 value "TABLE III - Functional categories of genes whose expression level are affected by knock-out of H1t and H1a (ko/wt) Hist1h1a upregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.