Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _7 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _7 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _6 value "These proteins signal by stimulating formation of specific heteromeric complexes of type I and type II serine/threonine kinase receptors. The type II receptors are encoded by five known mammalian genes, bind to ligands, and phosphorylate and activate the type I receptors, of which there are seven mammalian members (Fig. 1)." provenance.
- _7 value "inhibitory Smads (I-Smads: Smad6 and Smad7), which are induced by TGF-b family members. The latter exert a negative feedback effect by competing with RSmads for receptor interaction and by marking the receptors for degradation." provenance.
- _5 value "Katz et al. (2000) presented evidence that overexpression of mammalian tensin activates both the JNK (601158) and p38 MAPK (600289) pathways. Tensin-mediated JNK activation was independent of the activities of Rac (602048) and Cdc42 (116952), but did depend on Sek (601335)." provenance.
- _5 value "title := \"Insulin-stimulated phosphorylation of lipin mediated by the mammalian target of rapamycin.\" Incubating adipocytes with insulin decreased the electrophoretic mobility and stimulated the phosphorylation of both Ser and Thr residues in lipin. The effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase, and by rapamycin, a specific inhibitor of the mammalian target of rapamcyin (mTOR)." provenance.
- _5 value "ASK1, a MAP kinase kinase kinase mediating the TNF-alpha signal has been identified as a thioredoxin binding protein. Thioredoxin shows an inhibitory effect on the TNF-alpha induced activation of ASK1" provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _4 value "HEF1 production increases levels of mRNA transcripts encoding proteins that are associated with motility, cell transformation and invasiveness, including several metalloproteinases, MLCK, p160ROCK and ErbB2. Upregulation of such proteins suggests mechanisms through which misregulation of HEF1 may be involved in cancer progression." provenance.
- _3 value "Hyperoxia-induced mRNA levels of NAD(P)H:quinone oxidoreductase 1 (NQO1), glutathione-S-transferase (GST)-Ya and -Yc subunits, UDP glycosyl transferase (UGT), glutathione peroxidase-2 (GPx2), and heme oxygenase-1 (HO-1) were significantly lower in Nrf2-/- mice compared with Nrf2+/+ mice." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _5 value "Furthermore, we found that Opn expression was upregulated by DNA damage-induced Tp53 activity and by adenovirus-mediated transfer of the human TP53 gene. In addition, a luciferase assay showed that the Opn gene has a functional Tp53-responsive element in its promoter region, and a chromatin immunoprecipitation assay confirmed interaction between the Opn promoter and Tp53 protein in vivo." provenance.
- _7 value "# Ariadne: Dermo-1 interacted directly with MEF2 and selectively repressed the MEF2 transactivation domain. [Regulation]" provenance.
- _3 value "The results demonstrate a central role for the laminin alpha4 chain in microvessel growth ...and may play a role in angiogenesis" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _6 value "After activating Ras using EGF, the GTP-bound form of Ras was precipitated with GST-RBD (GST-Raf containing Ras binding domain). Precipitated Ras was detected using the HA-antibody. As shown in Fig. 5D, in the presence of EGF, the amount of GTP-bound Ras increased over that of the control. Levels of the GTP-bound Ras significantly decreased in cells expressing DIP1/2; however, DIP1/2m failed to stimulate Ras GTPase in cells treated with EGF." provenance.
- _6 value "After activating Ras using EGF, the GTP-bound form of Ras was precipitated with GST-RBD (GST-Raf containing Ras binding domain). Precipitated Ras was detected using the HA-antibody. As shown in Fig. 5D, in the presence of EGF, the amount of GTP-bound Ras increased over that of the control. Levels of the GTP-bound Ras significantly decreased in cells expressing DIP1/2; however, DIP1/2m failed to stimulate Ras GTPase in cells treated with EGF." provenance.
- _4 value "he expression of pulmonary CYP2E1 mRNA and protein have been established in several studies 17, 19, 21, 29, 37, 42, 43. CYP2E1 is an interesting CYP form because it is the most active CYP enzyme in forming oxygen radicals, causing tissue injury 44" provenance.
- _8 value "Uba3 directly interacts with ligand-occupied ERalpha and ERbeta Transient transfection of Uba3 in mammalian cells inhibited ER-mediated transactivation in a time-dependent fashion" provenance.
- _4 value "Modified assertion" provenance.
- _6 value "Here, we show that cdk5 directly phosphorylates c-Jun N-terminal kinase 3 (JNK3) on Thr131 and inhibits its kinase activity, leading to reduced c-Jun phosphorylation" provenance.
- _5 value "NF1/X repressed PDGF-A promoter-dependent transcription and endogenous mRNA expression," provenance.
- _6 value "This increase in C/EBP beta activity occurs through transcriptional and posttranslational regulation, and the latter is mediated by activation of p90 ribosomal S6 kinase (RSK)" provenance.
- _5 value "A substantial body of literature indicates that endothelial COX-2 activity is upregulated by a number of cytokines and mitogenic stimuli, including Interleukin-1 alpha and beta (IL-l alpha and beta), tumour necrosis factor alpha (TNFa), transforming growth factor beta (TGFbeta), phorbol ester, lipolysaccharide (LPS) and interferon gamma (IFNy) I2 13." provenance.
- _4 value "A substantial body of literature indicates that endothelial COX-2 activity is upregulated by a number of cytokines and mitogenic stimuli, including Interleukin-1 alpha and beta (IL-l alpha and beta), tumour necrosis factor alpha (TNFa), transforming growth factor beta (TGFbeta), phorbol ester, lipolysaccharide (LPS) and interferon gamma (IFNy) I2 13." provenance.
- _5 value "Modified assertion" provenance.
- _6 value "Phosphorylation of PDE3A and activation of PDE3A and PDE4 were blocked by the PKA inhibitors [protein kinase inhibitor (PKI) and H-89]" provenance.
- _3 value "Genes induced by retinoic acid" provenance.
- _5 value "Here we demonstrate that insulin induces an increase in the plasma membrane abundance of SAT2 in a phosphatidylinositol 3-kinase-dependent manner" provenance.
- _3 value "nicotine induces basic fibroblast growth factor and platelet-derived growth factor release in endothelial cells and increases proliferation.7,8" provenance.
- _4 value "Treatment of cells with CD40L and IFN-gamma induced both protein and mRNA expression of MCP-1. MCP-1 protein expression induced by CD40L and IFN-gamma, was significantly inhibited by highly specific ERK1/2 inhibitor U0126 when treated for 24 hours. This suggests that CD40L and IFN-gamma induced MCP-1 expression is MAPK dependent. CD40L alone also induced MCP-1 expression, but co-treatment of CD40L and IFN-gamma potentiated the effect." provenance.
- _3 value "PTX, like exogenous db-cAMP, inhibited in a dose-dependent manner the basal and TNF-alpha-modulated IEC18 cell proliferation; this effect was partly prevented by PKI." provenance.
- _7 value "Mig-6 as a novel negative feedback regulator of the epidermal growth factor receptor (EGFR) and potential tumor suppressor." provenance.
- _8 value "Mig-6 overexpression results in reduced activation of the mitogenactivated protein kinase ERK2 in response to EGF," provenance.
- _5 value "Insulin stimulates the tyrosine phosphorylation of caveolin... Investigation of this pathway revealed the phosphorylation of another insulin receptor substrate, the proto-oncogene c-Cbl... The phosphorylation of Cbl requires the presence of another protein that recruits Cbl to the insulin receptor, which is likely to be the adaptor protein APS (adaptor protein containing PH and SH2 domains)." provenance.
- _5 value "insulin receptor is a tyrosine kinase that catalyzes the phosphorylation of several intracellular substrates, including the insulin receptor substrate (IRS) proteins, GAB-1, Shc, APS, p60(DOK), SIRPS, and c-Cbl" provenance.
- _5 value "Table 1 - Gene regulated by overexpressing HOXD3 in A549 lung cancer cell lines by more than 1.6 fold." provenance.
- _5 value "Table 1 - Gene regulated by overexpressing HOXD3 in A549 lung cancer cell lines by more than 1.6 fold." provenance.
- _4 value "The cells treated HGF showed significant increased and phosphorylation at tyrosine of Met, a HGF receptor. The level of tyrosine phosphorylation of Met in SP1 cells was dramatically reduced in cells within 60 min after detachment and is restored within 15 min of incubation with HGF. Met was constitutively phosphorylated at tyrosine residues in SP1 cells adhering to, and spreading on, FN substratum and shows a further increase after addition of HGF. Tyrosine phosphorylation of Met in carcinoma cells was augmented by cell adhesion and spreading on fibronectin substratum. In contrast, detached serum-starved cells exhibited reduced tyrosine phosphorylation of Met and undergo apoptotic cell death within 18 to 24 h." provenance.
- _8 value "As shown in Fig. 5, A and B, ZIN, but not ZIN-(365?488), inhibited TNF- and IL1-induced NF-KB activation in a dose-dependent manner." provenance.
- _4 value "Cells expressing Wnt3a shows the induction of Wnt5b." provenance.
- _6 value "Modified assertion" provenance.
- _4 value "The natural PPAR{gamma} ligand 15d-PGJ2 as well as three different synthetic PPAR{gamma} ligands (BRL49653, troglitazone, and ciglitazone) effectively repressed this induction of MHC-II by IFN-{gamma} (Figure 2a) in a dose-dependent manner (Figure 2b), " provenance.
- _4 value "Cell-specific prostaglandin synthases convert PGH2 into a series of prostaglandins, including PGI2, PGF2alpha, PGD2 and PGE2 (Fig. 1). Fig. 1 Legend - Pathway of prostaglandin production. Arachidonic acid is liberated from membranes by phospholipase A2. The cyclooxygenase enzymes (COX-1 and COX-2) produce prostaglandin H2 (PGH2) from arachidonic acid. PGH2 is acted upon by prostaglandin synthases to produce PGI2, PGD2, PGE2 and PGF2alpha. PGD2 is metabolized to 15-deoxy-12,14-PGJ2 (15-d-PGJ2). " provenance.
- _6 value "Once in the cytoplasm, FKHRL1 remains phosphorylated and bound to 14-3-3, thereby preventing nuclear reimport." provenance.
- _5 value "Table 1. E2f responsive genes upregulated 4-fold or higher by the IE86 protein (cytomegalovirus). FROM FULL TEXT: An increase in the level of steady-state RNA from E2F-responsive genes was detected by Northern blot analysis in Ad-IE86 transduced cells but not in Ad-GFP transduced cells (Fig. 4). E2F-responsive genes such as A-myb, cdk-2, RR2, MCM4, and Cdc7 were not included in Table 1 because these genes were up-regulated 4-fold or higher in one microarray but not in both microarrays (data not shown). JParker, 05282008" provenance.
- _6 value "Modified assertion" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _7 value "ANGPTL3 bound to alpha(v)beta(3) and induced integrin alpha(v)beta(3)-dependent haptotactic endothelial cell adhesion and migration and stimulated signal transduction pathways characteristic for integrin activation, including phosphorylation of Akt, mitogen-activated protein kinase, and focal adhesion kinase" provenance.
- _7 value "ANGPTL3 bound to alpha(v)beta(3) and induced integrin alpha(v)beta(3)-dependent haptotactic endothelial cell adhesion and migration and stimulated signal transduction pathways characteristic for integrin activation, including phosphorylation of Akt, mitogen-activated protein kinase, and focal adhesion kinase" provenance.
- _5 value "Modified assertion" provenance.
- _4 value "Elastase-mediated phosphatidylserine receptor cleavage impairs apoptotic cell clearance in cystic fibrosis and bronchiectasis. " provenance.
- _4 value "These studies demonstrate that increased sEH expression in the Ang II hypertensive kidney leads to increased EET hydration. Moreover, sEH plays a role in the regulation of blood pressure, and inhibition of sEH during Ang II hypertension is antihypertensive." provenance.
- _6 value "Detailed analyses revealed that overexpression of CBP or p300 with PPARgamma enhanced the expression of PPARgamma target genes in NIH3T3 cells" provenance.
- _4 value "We conclude that oxLDL not only elicits an oxidative burst upon first contact, but also promotes desensitization of macrophages via activation of PPARgamma. Desensitization of macrophages may have important consequences for the behavior of macrophages/foam cells in atherosclerotic lesions." provenance.
- _5 value "We show that stimulation of murine and human macrophages with the heat shock proteins gp96 and hsp70 results in induction of inducible NO synthase and the production of NO." provenance.
- _5 value "The bFGF released by elastase and added to lung fibroblasts or vascular wall smooth muscle cells is capable of repressing elastin gene transcription (21) or inducing cell proliferation (15), respectively." provenance.
- _3 value "the concentrations of proinflammatory cytokines, such as interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma were highly increased during sepsis" provenance.
- _3 value "Table 3. Genes whose expression is affected by cold stress. [table excludes genes whose change in expression has only been observed by genomic or proteomic technologies (i.e., not yet confirmed by other techniques)]" provenance.
- _5 value "Modified assertion" provenance.
- _2 value "% However, estrogen also triggers rapid activation of classical second messengers (cAMP, calcium, and inositol triphosphate) and stimulation of intracellular signaling cascades mitogen-activated protein kinase (MAP K), PI3K and eNOS." provenance.
- _5 value "Ariadne: Moreover, PSF recruits the corepressor mSin3A to the hCYP17 promoter, resulting in repression, which is then alleviated upon cAMP stimulation and subsequent activation of SF-1" provenance.
- _2 value "Stimulation of dendritic cells with histamine resulted in F-actin polymerization and cyclic adenosine monophosphate production through H2R" provenance.
- _7 value "The primary substrates of CDK4/6 and CDK2 in G1 progression are the members of the retinoblastoma protein family RB,p107 and p130 The activity of the RB proteins is modulated by sequential phosphorylation by CDK4/6cyclinD and CDK2cyclinE complexes" provenance.
- _3 value "angiogenesis: adrenomedullin, angiopoietin-2, cyclooxygenase-2, endothelin-1 and -2, fibroblast growth factor-3, hepatocyte growth factor, histone deacetylase, monocyte chemotactic protein-1, nitric oxide synthase, osteopontin, placental growth factor, Tie-2, transforming growth factor alpha, beta1 and beta3" provenance.
- _3 value "angiogenesis: adrenomedullin, angiopoietin-2, cyclooxygenase-2, endothelin-1 and -2, fibroblast growth factor-3, hepatocyte growth factor, histone deacetylase, monocyte chemotactic protein-1, nitric oxide synthase, osteopontin, placental growth factor, Tie-2, transforming growth factor alpha, beta1 and beta3" provenance.
- _3 value "glycolysis and glucose uptake: aldolase-A, enolase-1, glucose transporter-1, -3, glyceraldehyde-3-phosphate dehydrogenase, hexokinase-1, hexokinase-2, lactate dehydrogenase-A, phosfructokinase-C, phosfructokinase-L, phosphoglycerate kinase-1, pyruvate kinase-M" provenance.
- _3 value "hypoxia also induces EPO production in renal cells (to increase hemoglobin production) and tyrosine hydroxylase synthesis in neural cells (involved in catecholamine production)" provenance.
- _3 value "clusterin does have a slight protective effect against apoptosis under some conditions." provenance.
- _5 value "Basal and LIT induced IL-1beta and TNF-alpha production were inhibited by Bay-x-1005 in a dose dependent manner, while the addition of NS-398 caused a potent stimulatory effect. lit from nci meta A potent skin irritating sesquiterpene lactone isolated from the roots of Thapsia garganica L. (Apiaceae). It also acts as a non-phorbol-ester-type tumor promoter which discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca(2+)-ATPase. (Biochem Pharmacol 1987;36(5):621-6; Proc Natl Acad Sci USA 1991;88(16):7096-100)" provenance.
- _6 value "Anti-phosphotyrosine immunoblotting of JAK1 immunoprecipitates revealed that the loss of TCPTP resulted in a significant increase in the tyrosine phosphorylation of JAK1 compared to wild-type control BMDM" provenance.
- _3 value "Oleate and palmitate also induced expression of chemokines (MCP-1 and GRO1 oncogene) and genes of the acute phase response (serum amyloid A3). Increases in transcriptional modulators such as ATF3, CCAAT/enhancer binding protein-beta (C/EBPbeta), C/EBPdelta, and c-fos were also seen" provenance.
- _4 value "Here, we show that heat-shock proteins (HSPs), such as HSP90, HSP70, and HSP32, induce the production of interleukin 6 and tumor necrosis factor alpha and increase the phagocytosis and clearance of Abeta peptides." provenance.
- _5 value "Experiments using adenoviral delivery of Ets1 in human fibroblasts have established that Ets1 strongly suppresses TGF-beta induction of collagen type I and other matrix-related genes and reverses TGF-beta-dependent inhibition of MMP-1." provenance.
- _3 value "We have previously shown that hypoxia (2% O2), when compared to standard oxygen tension (20% O2), upregulates the mRNA levels of the human alpha1(I) (COL1A1) procollagen gene and transforming growth factor-beta1 (TGF-beta1) in human dermal fibroblasts." provenance.
- _5 value "FGF-1 treatment significantly increased the activation of extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2)" provenance.
- _5 value "Both Akt expression and serum treatment induced phosphorylation of Mdm2 at Ser186." provenance.
- _4 value "Three functional domains appear to be potentially important for the regulation of human NET (hNET) gene transcription: an upstream enhancer region at -4.0 to -3.1 kb, a proximal domain at -133 to -75 bp, and a middle silencer region between these two domains. DNase I footprinting analysis of the proximal promoter region shows that a subdomain at -128 to -80 bp is protected in a cell-specific manner. We provide evidence that multiple protein factors interact with the proximal promoter domain to critically regulate the transcriptional activity of the hNET gene. In the middle of this proximal subdomain resides a homeodomain (HD)-binding core motif, which interacts with HD factors, including Phox2a and HoxA5, in an NA-specific manner. Cotransfection analyses suggest that HoxA5 and Phox2a may transactivate the hNET gene promoter. " provenance.
- _2 value "BMP7 inhibits 1,25(OH)2-vitamin D3-induced differentiation of human osteoblasts, whereas TGFbeta1 stimulates it" provenance.
- _5 value "Modified assertion" provenance.
- _3 value "Alterations in Ca(2+) homeostasis and accumulation of unfolded proteins in the endoplasmic reticulum (ER) lead to an ER stress response. Prolonged ER stress may lead to cell death. Glucose-regulated protein (GRP) 78 (Bip) is an ER lumen protein whose expression is induced during ER stress. GRP78 is involved in polypeptide translocation across the ER membrane, and also acts as an apoptotic regulator by protecting the host cell against ER stress-induced cell death, although the mechanism by which GRP78 exerts its cytoprotective effect is not understood. The present study was carried out to determine whether one of the mechanisms of cell death inhibition by GRP78 involves inhibition of caspase activation. Our studies indicate that treatment of cells with ER stress inducers causes GRP78 to redistribute from the ER lumen with subpopulations existing in the cytosol and as an ER transmembrane protein. GRP78 inhibits cytochrome c-mediated caspase activation in a cell-free system, and expression of GRP78 blocks both caspase activation and caspase-mediated cell death. GRP78 forms a complex with caspase-7 and -12 and prevents release of caspase-12 from the ER. Addition of (d)ATP dissociates this complex and may facilitate movement of caspase-12 into the cytoplasm to set in motion the cytosolic component of the ER stress-induced apoptotic cascade. These results define a novel protective role for GRP78 in preventing ER stress-induced cell death." provenance.
- _3 value "Of the LPS-regulated proteins identified by peptide mass fingerprinting for which probes were present on the oligonucleotide microarray... Similarly, CAP1, Rho-GAP1, and ficolin 1 were down-regulated at both the mRNA transcript and protein levels" provenance.
- _3 value "Of the LPS-regulated proteins identified by peptide mass fingerprinting for which probes were present on the oligonucleotide microarray... Similarly, CAP1, Rho-GAP1, and ficolin 1 were down-regulated at both the mRNA transcript and protein levels" provenance.
- _5 value "Of the LPS-regulated proteins identified by peptide mass fingerprinting for which probes were present on the oligonucleotide microarray... Similarly, CAP1, Rho-GAP1, and ficolin 1 were down-regulated at both the mRNA transcript and protein levels" provenance.
- _5 value "Both putative promoter sequences were TATA-less, CAAT-less, contained highly GC-rich sites, and had multiple putative regulatory cis-elements (e.g., AP1, AP2, C/EBP, SP1, NF1, and GATA). The activities of the putative promoters were confirmed" provenance.
- _7 value "Activation of IL-4Ralpha by IL-13 or IL-4 induced signal transducer and activation of transcription-6 (STAT6), p42/ p44 ERK, p38, and to a lesser extent, SAPK/JNK mitogen-activated protein kinase phosphorylation." provenance.
- _5 value "Co-transfection of the MAO B promoter with dominant negative forms of Ras, Raf-1, MEKK1, MEK1, MEK3, MEK7, ERK2, JNK1, and p38/RK inhibit the PMA-dependent activation of the MAO B promoter" provenance.
- _5 value "Recombinant active PKB/Akt phosphorylated recombinant 14-3-3zeta in an in vitro kinase assay. Transfection of active PKB/Akt into HEK293 cells resulted in phosphorylation of 14-3-3zeta. Based on a motif search of 14-3-3zeta, a potential PKB/Akt phosphorylation site, Ser-58, was mutated to alanine. PKB/Akt was unable to phosphorylate this mutant protein." provenance.