Nanopublications

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quote value "Paroxetine tablets are indicated for the treatment of Posttraumatic Stress Disorder (PTSD). The efficacy of paroxetine tablets in the treatment of PTSD was established in two 12-week placebo-controlled trials in adults with PTSD" assertion.
quote value "Escitalopram oral solution, USP is indicated for the acute treatment of Generalized Anxiety Disorder (GAD) in adults" assertion.
quote value "In the context of Digital Humanities research, usage of the Linked Data Scopes ontology contributes to transparency of the research." provenance.
quote value "Pseudo-repeats in doublecortin make distinct mechanistic contributions to microtubule regulation." provenance.
quote value "the FAIR Principles put specific emphasis on enhancing the ability of machines to automatically find and use the data" provenance.
quote value "OpenBiodiv encompasses data extracted from more than 5000 scholarly articles published by Pensoft and many more taxonomic treatments extracted by Plazi from journals of other publishers. The data from both sources are converted to Resource Description Framework (RDF) and integrated in a graph database using the OpenBiodiv-O ontology and an RDF version of the Global Biodiversity Information Facility (GBIF) taxonomic backbone." provenance.
quote value "Unfortunately, in science and education, knowledge and data are often intermingled with copyrighted expressions of the same. Many publishers establish barriers to knowledge sharing by asserting copyright on non-copyrightable plain or formal expressions of that knowledge. In the area of biodiversity, often dealing with textually expressed data or data expressed in images, this is a major obstacle." provenance.
quote value "Obesity showed closest association with knee osteoarthritis when accompanied by metabolic abnormality." provenance.
_3 value "Oxidation and nitration of macromolecules, such as proteins, DNA and lipids, are prominent in atherosclerotic arteries." provenance.
_3 value "Arterial cells are highly susceptible to oxidative stress, which can induce both necrosis and apoptosis (programmed cell death) [1,2]" provenance.
_3 value "One such risk factor is oxLDL, which exert pro-apoptotic effects on a variety of cell lineages, including endothelial cells and VSMCs, both in cultured cells and in arteries [19?26]. Increased formation of oxygen radicals (and other radical species) facilitates LDL oxidation and influences oxidation-sensitive mechanisms [15]." provenance.
_3 value "The peptide hormone angiotensin II and pro-inflammatory cytokines also trigger the apoptotic program in endothelial cells [33,34]." provenance.
_3 value "Aging, one of the major predictors for atherosclerotic lesion formation, increases the sensitivity of endothelial cells to apoptosis induced by in vitro and in vivo stimuli [35?37]." provenance.
_3 value "Aging, one of the major predictors for atherosclerotic lesion formation, increases the sensitivity of endothelial cells to apoptosis induced by in vitro and in vivo stimuli [35?37]." provenance.
_4 value "Shear stress enhances expression of the gene encoding the endothelial nitric oxide synthase (eNOS) and further stimulates its enzymatic activity, leading to physiologic low concentrations of nitric oxide (NO) within endothelial cells [44?46]. This continuous generation of NO prevents the apoptosis of endothelial cells, thereby protecting the endothelial monolayer from injury [47,48]." provenance.
_5 value "Shear stress enhances expression of the gene encoding the endothelial nitric oxide synthase (eNOS) and further stimulates its enzymatic activity, leading to physiologic low concentrations of nitric oxide (NO) within endothelial cells [44?46]. This continuous generation of NO prevents the apoptosis of endothelial cells, thereby protecting the endothelial monolayer from injury [47,48]." provenance.
_3 value "More importantly, intervention with L-arginine has induced beneficial effects on atherosclerosis in experimental and human studies [46,49]." provenance.
_3 value "In addition, another oxygen-radical scavenger enzyme, catalase, can prevent VSMC apoptosis triggered by hydrogen peroxide [27,65]." provenance.
_4 value "The proto-oncogene c-myc can promote cell death (probably mediated through p53) or cell proliferation, depending on its expression level. It functions as a nuclear phosphoprotein with particular properties of a transcription factor [68,69]. In serum deprived cultures, cells overexpressing c-myc readily undergo apoptosis. In addition, deregulation of c-myc causes apoptosis of VSMCs deprived of growth factors or treated with cytokines such as interferon-g [70]." provenance.
_9 value "Tissue factor (TF) is a 47 kDa transmembrane glycoprotein that initiates blood coagulation by binding coagulation factor VII and its activated form (factor VIIa), to produce a high-affinity complex [72] that proteolytically activates factors IX and X, leading to thrombin generation." provenance.
_7 value "Tissue factor (TF) is a 47 kDa transmembrane glycoprotein that initiates blood coagulation by binding coagulation factor VII and its activated form (factor VIIa), to produce a high-affinity complex [72] that proteolytically activates factors IX and X, leading to thrombin generation." provenance.
_3 value "TF works at the surface of cell membranes, and its activity is highly dependent on the presence of phosphatidylserine (PS), an anionic phospholipid that is redistributed on the cell surface during apoptotic death and confers a potent pro-coagulant activity to the apoptotic cell [74]." provenance.
_6 value "TIMP-3 can be anti-angiogenic by direct binding to vascular endothelial growth factor (VEGF) receptor 2 in a matrix-metalloproteinase- independent manner [94]." provenance.
_6 value "Phosphorylation at Ser473, along with Thr308 of its activation loop, is deemed necessary for Akt function, although the regulatory mechanisms and physiological importance of each phosphorylation site remain to be fully understood." provenance.
_5 value "We next examined the Akt T-loop Thr308 phosphorylation in wild-type and SIN1?/? cells. We found that although Ser473 phosphorylation was completely abolished in the SIN1?/? cells, Thr308 phosphorylation of Akt was not blocked (Figure 3A)." provenance.
_5 value "To identify a function that could be linked specifically to Akt-Ser473 phosphorylation, we further examined known Akt substrates that may have defective phosphorylation in SIN1?/? cells. We found that phosphorylation of FoxO1/3a (also called FKHR/FKHRL1) (Greer and Brunet, 2005), was affected in SIN1?/? cells. In particular, phosphorylation of FoxO1/3a at Thr24/Thr32 was significantly decreased in the absence of SIN1 under normal growing and restimulated conditions (Figure 4A)." provenance.
_5 value "To identify a function that could be linked specifically to Akt-Ser473 phosphorylation, we further examined known Akt substrates that may have defective phosphorylation in SIN1?/? cells. We found that phosphorylation of FoxO1/3a (also called FKHR/FKHRL1) (Greer and Brunet, 2005), was affected in SIN1?/? cells. In particular, phosphorylation of FoxO1/3a at Thr24/Thr32 was significantly decreased in the absence of SIN1 under normal growing and restimulated conditions (Figure 4A)." provenance.
_6 value "To identify a function that could be linked specifically to Akt-Ser473 phosphorylation, we further examined known Akt substrates that may have defective phosphorylation in SIN1?/? cells. We found that phosphorylation of FoxO1/3a (also called FKHR/FKHRL1) (Greer and Brunet, 2005), was affected in SIN1?/? cells. In particular, phosphorylation of FoxO1/3a at Thr24/Thr32 was significantly decreased in the absence of SIN1 under normal growing and restimulated conditions (Figure 4A)." provenance.
_5 value "We also found that the recombinant FoxO1 could not be phosphorylated at Thr24/32 in vitro by an Akt mutant harboring an alanine mutation in either Thr308 or Ser473, whereas a Ser473 to Ala mutated Akt could still phosphorylate recombinant GSK3 (Figure S2). These results indicate that Akt-Ser473 phosphorylation is required for FoxO1/3a phosphorylation at Thr24/32." provenance.
_5 value "We also found that the recombinant FoxO1 could not be phosphorylated at Thr24/32 in vitro by an Akt mutant harboring an alanine mutation in either Thr308 or Ser473, whereas a Ser473 to Ala mutated Akt could still phosphorylate recombinant GSK3 (Figure S2). These results indicate that Akt-Ser473 phosphorylation is required for FoxO1/3a phosphorylation at Thr24/32." provenance.
_6 value "Likewise, phosphorylation of another translational regulator, 4E-BP1, at the mTOR target site Thr37/46 (Gingras et al., 1999), was also not impaired in SIN1?/? cells (Figure 5A)." provenance.
_5 value "Akt Ser473 was strongly induced in wild-type cells by different growth factors such as the platelet-derived growth factor, epidermal growth factor, and insulin, even in the absence of amino acids and glucose (Figure 5B). In SIN1?/? cells, Akt-Ser473 phosphorylation was not induced by any type of stimulus." provenance.
_4 value "The VHL-mediated proteolytic degradation of HIF suppresses a transcription programme that is normally engaged by HIF as part of the adaptive response of the cell to hypoxia, such as the activation of vascular endothelial growth factor (VEGF), which is a potent angiogenic factor that is involved in the formation and differentiation of blood vessels." provenance.
_6 value "Transcriptional control is also maintained by a specific acetylation (Ac) event at lysine 532 and an additional asparagine hydroxylation (OH) event at position 863, both of which act as negative regulators of the transcriptional activity of HIF." provenance.
_5 value "These hydroxylases are all Fe(II)- and 2-oxoglutarate-dependent dioxygenases that require molecular oxygen. Therefore, HIFa becomes stabilized under hypoxic conditions in which oxygen availability is low." provenance.
_5 value "These hydroxylases are all Fe(II)- and 2-oxoglutarate-dependent dioxygenases that require molecular oxygen. Therefore, HIFa becomes stabilized under hypoxic conditions in which oxygen availability is low." provenance.
_5 value "These hydroxylases are all Fe(II)- and 2-oxoglutarate-dependent dioxygenases that require molecular oxygen. Therefore, HIFa becomes stabilized under hypoxic conditions in which oxygen availability is low." provenance.
_5 value "These hydroxylases are all Fe(II)- and 2-oxoglutarate-dependent dioxygenases that require molecular oxygen. Therefore, HIFa becomes stabilized under hypoxic conditions in which oxygen availability is low." provenance.
_5 value "These hydroxylases are all Fe(II)- and 2-oxoglutarate-dependent dioxygenases that require molecular oxygen. Therefore, HIFa becomes stabilized under hypoxic conditions in which oxygen availability is low." provenance.
_6 value "RCC cells lacking functional pVHL overexpress various growth factors, including platelet-derived growth factor b (PDGFb), VEGF and transforming growth factor (TGF)-a [25]. The latter is a bona fide renal-cell mitogen that activates the Ras?Raf?MAP kinase signalling cascade through its cognate epidermal growth factor (EGF) cell-surface receptor [26]." provenance.
_6 value "The overproduction of TGF-a in RCC cells is, at least in part, HIF-dependent and a major contributory event that confers a growth advantage to these cells [25,27]." provenance.
_6 value "In particular, it has been reported that RCC cells can be sensitized to TNF-a-induced cytotoxicity by re-introducing wild-type VHL [38]. The authors highlight the fact that TNFreceptor engagement by TNF-a triggers the activation of atypical protein kinase C (aPKC), which, through IKKb phosphorylation, liberates NFkB, thereby initiating the transcription of genes that are involved in apoptosis" provenance.
_5 value "In particular, it has been reported that RCC cells can be sensitized to TNF-a-induced cytotoxicity by re-introducing wild-type VHL [38]. The authors highlight the fact that TNFreceptor engagement by TNF-a triggers the activation of atypical protein kinase C (aPKC), which, through IKKb phosphorylation, liberates NFkB, thereby initiating the transcription of genes that are involved in apoptosis" provenance.
_4 value "pVHL has also been implicated in tumour invasion and metastasis, which represent complex multi-step processes that require the proteolytic degradation of the basement membrane and tissue matrix, changes in cell polarity and motility, and the attachment and detachment of cells to and from the extracellular matrix (ECM) [41]." provenance.
_4 value "Nevertheless, the restored ability of pVHL-positive transfectants to assemble extracellular fibronectin was mediated by b1 integrins, implying that pVHL controls ECM assembly, at least in part, through integrin signalling [46]. A recent development has demonstrated that an ubiquitin-like molecule, NEDD8, covalently modifies pVHL and that a neddylation- defective pVHL mutant, despite retaining its ability to degrade HIF, fails to promote the assembly of a fibronectin matrix [47]." provenance.
_5 value "Nevertheless, the restored ability of pVHL-positive transfectants to assemble extracellular fibronectin was mediated by b1 integrins, implying that pVHL controls ECM assembly, at least in part, through integrin signalling [46]. A recent development has demonstrated that an ubiquitin-like molecule, NEDD8, covalently modifies pVHL and that a neddylation- defective pVHL mutant, despite retaining its ability to degrade HIF, fails to promote the assembly of a fibronectin matrix [47]." provenance.
_5 value "In contrast to protein-binding inhibition, evidence has shown that pVHL binds to both atypical PKC isoforms (l and z) through its b-domain, and in the case of activated aPKCl, mediates its turnover as part of the E3-ligase function of pVHL [39,40]. Although the functional significance of this inhibition remains elusive, given the central role for atypical PKCs (especially aPKCz) in establishing cell polarity in conjunction with PAR6 and the GTPase CDC42 [49], one could envisage a scenario whereby the loss of pVHL leads to altered cell polarity and, by extension, aberrant cell migration." provenance.
_5 value "In contrast to protein-binding inhibition, evidence has shown that pVHL binds to both atypical PKC isoforms (l and z) through its b-domain, and in the case of activated aPKCl, mediates its turnover as part of the E3-ligase function of pVHL [39,40]. Although the functional significance of this inhibition remains elusive, given the central role for atypical PKCs (especially aPKCz) in establishing cell polarity in conjunction with PAR6 and the GTPase CDC42 [49], one could envisage a scenario whereby the loss of pVHL leads to altered cell polarity and, by extension, aberrant cell migration." provenance.
_6 value "This same study demonstrated that the loss of VHL function negatively regulates tissue inhibitor of metalloproteinase 2 (TIMP-2), resulting in the upregulation of matrix metalloproteinase 2 (MMP2) and MMP9, thereby implicating pVHL in the control of these molecules." provenance.
_5 value "The gene encoding the chemokine receptor CXCR4 has been discovered as a novel HIF target based on a microarray comparison of genetic profiles derived from VHL-null RCC cells and their isogenic wild-type VHLexpressing counterparts [52]." provenance.
_4 value "The fact that CXCR4 is a hypoxia-inducible gene provided a potential mechanistic explanation for CXCR4 upregulation during tumour cell evolution. CXCR4- induced cell-surface expression due to the loss of VHL function confers enhanced migratory potential to RCC cells in response to its cognate ligand stromal-derived factor 1 (SDF1)." provenance.
_6 value "The fact that CXCR4 is a hypoxia-inducible gene provided a potential mechanistic explanation for CXCR4 upregulation during tumour cell evolution. CXCR4- induced cell-surface expression due to the loss of VHL function confers enhanced migratory potential to RCC cells in response to its cognate ligand stromal-derived factor 1 (SDF1)." provenance.
_7 value "Localization of GTP-bound Ras to the inner surface of the cell membrane activates several downstream effectors, most notably the serine/threonine kinase Raf, which is the first signaling element in the MAPK pathway. 2,67,68 As shown in Figure 1, other downstream effectors of Ras include the PI3K cell survival pathway, the small GTP-binding proteins Rac and Rho, and the stress-activated protein kinase pathway (also referred to as the c-jun N-terminal kinase [JNK] pathway). 69-71 In addition, in response to cellular stress and cytokine stimulation mediated through Ras, the dual-specificity p38MAPK kinases (MKK3 and MKK6) and the JNK kinases (MKK4 and MKK7) phosphorylate p38MAPK and JNK, respectively. 72-76" provenance.
_7 value "GTP-bound Ras interacts directly with Raf and mobilizes the inactive protein from the cytoplasm (Figs 1 and 2). Once the Ras-Raf complex is translocated to the cell membrane, Ras activates the serine/threonine kinase function of Raf through an association between its Ras-binding domain (RBD) in the amino-terminal regulatory region and Ras-GTP." provenance.
_7 value "Raf is also activated by Ras-independent activators, including the soluble non-RTK Src and Janus kinase 1, which are involved in cytokine signaling.86 Other Ras-independent activators of Raf include interferon beta, protein kinase C (PKC) alpha, antiapoptotic proteins (eg, Bcl-2), scaffolding proteins (eg, ceramide-activated protein kinase), ultraviolet light, ionizing radiation, retinoids, erythropoietin, and dimerization between Raf isoforms 86-94 (Fig 3)." provenance.
_7 value "Furthermore, the kinase activity of Raf is inhibited by its interactions with cholesterol-rich lipid rafts in the cell membrane and phosphorylation by protein kinases A (PKA) and B (PKB/Akt), as shown in Figure 2.95-98" provenance.
_5 value "Additional support for the diverse functionality of Raf family members is provided by the disparate responses of B-Raf and C-Raf to identical stimuli, as well as the distinct messages that each isoform relays downstream to Rap1, which is a small GTPase that functions as both an activator and repressor of Raf.115 Rap1-mediated stimulation of B-Raf by cyclic adenosine monophosphate (cAMP) phosphorylates ERK, whereas stimulation of C-Raf inhibits ERK phosphorylation.115" provenance.
_7 value "The Rho family of small GTPases, consisting of Rho, Rac, and cyclin-dependent kinase (Cdc) 42, regulate cytoskeletal organization during the cell cycle and also mediate Ras-induced activation of Raf, especially C-Raf.134-136 These GTPases do not directly bind to Raf but, instead, signal by activating downstream kinases. Rho signals by activating the serine/threonine protein kinases N1 and N2 and Rho-associated kinase 1, whereas Rac and Cdc42 signal through p21-activated kinase (PAK).134-136" provenance.
_6 value "Phosphorylation. Raf is principally activated by phosphorylation of specific amino acid residues as shown for each isoform in Figure 4. From an evolutionary standpoint, the Raf activation sites are highly conserved from yeast to humans. Several amino acids in Raf, particularly serine (S) 259 and S621, which bind 14-3-3 and maintain C-Raf in a closed auto-inhibited conformation, are phosphorylated in the basal state.137 On stimulation, Ras-GTP displaces 14-3-3 from S259, and C-Raf is translocated to the cell membrane, where it can be dephosphorylated at S259 by protein phosphatase 2A or other phosphatases.126 S259 also represents the site of inhibitory phosphorylation by PKB/Akt, PKA, and serum glucocorticoid-inducible kinase.121,138,139 Phosphorylation at S621 seems to have greater significance because mutations at this site inactivate Raf's kinase activity. Hence, a balance of phosphorylation and dephosphorylation is required to prime Raf in the basal state before stimulation by Ras or mitogens.137" provenance.
_6 value "GeneRif: Glucose-regulated protein 78 is induced by chronic hypoxia in human gastric tumor cells through a protein kinase C-epsilon/ERK/AP-1 signaling cascade." provenance.
_5 value "Modified assertion" provenance.
_4 value "TGF-beta2 markedly downregulated Cdk4 synthesis and slightly upregulated p27 synthesis" provenance.
_7 value "Using the chimeric-receptor EGLT in which the extracellular domain of epidermal growth factor receptor was fused to the transmembrane and intracellular domains of Flt-1, we also demonstrate that CDC42 and Rac1 are activated by EGLT. Previously, we showed that phosphatidylinositol 3-kinase is required for Flt-1-mediated antiproliferative activity, but phospholipase C is not required." provenance.
_5 value "Modified assertion" provenance.
_6 value "Nuclear Receptor: CAR Ligand: Xenobiotic, Phenobarbitol CYP Enzyme: ^CYP2B, ^CYP2C Cytosolic binding protein: ? ABC transporter: ^ABCC3" provenance.
_4 value "we cloned a gene that encodes another arachidonic acid-using enzyme, fatty acid CoA ligase 4 (FACL4), and showed that overexpression of this enzyme prevents apoptosis" provenance.
_3 value "Unlike IGF-I, IGF-II treatment had no effect on T3-induced or hydrocortisone-induced GHRH receptor expression in either neonates or adults." provenance.
_4 value "PGE2-induced IL6 synthesis was dose-dependently inhibited by the p38 MAPK inhibitor, SB202190. This indicates that p38 MAPK activates the release of IL6." provenance.
_3 value "Ca2+ induced the HAT activities of both CBP and P/CAF in HaCaT cells." provenance.
_5 value "Modified assertion" provenance.
_4 value "AGC kinases that are downstream of PI(3)K include serum- and glucocorticoid- regulated kinase and the atypical PKCs, PKC-z and -l. Akt and/or the atypical PKCs seem to be required for insulin stimulated glucose transport.." provenance.
_3 value "Activated ERK can translocate into the nucleus, where it catalyses the phosphorylation of transcription factors such as p62TCF, initiating a transcriptional programme that leads to cellular proliferation or differentiation." provenance.
_4 value "Akt has been suggested to be important in transmission of the insulin signal, by phosphorylation of the enzyme GSK-3 (see below), the forkhead transcription factors and cAMP response element-binding protein38,39 Other AGC kinases that are downstream of PI(3)K include serum- and glucocorticoid- regulated kinase and the atypical PKCs, PKC-z and -l42. Akt and/or the atypical PKCs seem to be required for insulinstimulated glucose transport." provenance.
_5 value "At least nine intracellular substrates of the insulin/IGF-I receptor kinases have been identified (Fig. 2). Four of these belong to the family of insulin-receptor substrate (IRS) proteins9. Other substrates include Gab-1, p60dok, Cbl, APS and isoforms of Shc10." provenance.
_6 value "Expression of dominant-interfering CAP mutants that cannot bind to Cbl or flotillin inhibit Cbl translocation and insulin-stimulated glucose uptake." provenance.
_4 value "Insulin also profoundly inhibits lipolysis in adipocytes, primarily through inhibition of the enzyme hormone sensitive lipase71. This enzyme is acutely regulated by control of its phosphorylation state, which is activated by PKA-dependent phosphorylation, and inhibited as a result of a combination of kinase inhibition and phosphatase activation. Insulin inhibits the activity of the lipase primarily through reductions in cAMP levels, owing to the activation of a cAMP-specific phosphodiesterase in fat cells72." provenance.
_5 value "Insulin also profoundly inhibits lipolysis in adipocytes, primarily through inhibition of the enzyme hormone sensitive lipase71. This enzyme is acutely regulated by control of its phosphorylation state, which is activated by PKA-dependent phosphorylation, and inhibited as a result of a combination of kinase inhibition and phosphatase activation. Insulin inhibits the activity of the lipase primarily through reductions in cAMP levels, owing to the activation of a cAMP-specific phosphodiesterase in fat cells72." provenance.
_4 value "Insulin also profoundly inhibits lipolysis in adipocytes, primarily through inhibition of the enzyme hormone sensitive lipase71. This enzyme is acutely regulated by control of its phosphorylation state, which is activated by PKA-dependent phosphorylation, and inhibited as a result of a combination of kinase inhibition and phosphatase activation. Insulin inhibits the activity of the lipase primarily through reductions in cAMP levels, owing to the activation of a cAMP-specific phosphodiesterase in fat cells72." provenance.
_3 value "Osmolality of the mammalian renal medulla is high because of the operation of the urinary concentrating mechanism. To understand molecular events during the early phase of cellular adaptation to hypertonicity, we performed comprehensive searches for genes induced in response to hypertonicity using a cell line (mIMCD3) derived from the inner medullary collecting duct of mouse kidney. PCR-based subtractive hybridization of cDNA pools and cDNA microarray analysis were used. We report 12 genes whose mRNA expression is significantly increased within 4 h after exposure to hypertonicity. The increase in mRNA expression was the result of increased transcription. Many are either stress response genes or growth regulatory genes, supporting the notion that hypertonicity evokes the stress response and growth regulation in cells. Experiments using inhibitors revealed that mitogen-activated protein kinases were commonly involved in signaling for the induction of genes by hypertonicity. Tyrosine kinases and phosphatidylinositol 3-kinase also play a significant role. Signaling pathways for stimulation of transcription appeared quite diverse in that each gene was sensitive to different combinations of inhibitors." provenance.
_4 value "Upon addition of TNF-alpha there was a concomitant increase in the monocyte activation marker, CD14." provenance.
_7 value "Our results show that VEGF induces the association of CADTK with the b1 integrin/PKCa protein complex...VEGFR immunoprecipitation and immunoblotting studies using anti-Flt-1 and anti-CADTK Abs showed specific constitutive association...VEGF increased (2-fold) fibronectin-induced CADTK tyrosine phosphorylation in MM.1S cells; equivalent loading of proteins was confirmed by stripping and reprobing the membrane with anti-CADTK Ab. The PKC activator PMA enhanced constitutive phosphorylation of CADTK (Fig. 4c). Finally, VEGF-triggered CADTK activation was blocked by both the PKC inhibitor BIM I and a b1 integrin neutralizing mAb...These results indicate that the activation of CADTK in adherent MM cells is influenced by both PKC- and b1 integrin-mediated signaling pathways." provenance.
_8 value "these data show that activation of PI 3-kinase is an early event in the VEGF-triggered Flt-1 signaling cascade...These results indicate that VEGF-induced PI 3-kinase activation along with b1 integrin binding to fibronectin activate PKCa." provenance.
_5 value "Treatment of cells with beta-catenin antisense oligodeoxynucleotides resulted in a decrease in the levels of axin2 and human naked cuticle (hnkd) mRNAs. Interestingly, the proteins encoded by both of these mRNAs are known inhibitors of the beta-catenin pathway." provenance.
_3 value "Rapamycin... targets a form of PP2A that regulates protein synthesis" provenance.
_5 value "Treatment of MIF (10 microg/ml) led to phosphorylation of multiple cellular proteins of 60, 34 and 30 kDa in comparison with the control and the phosphorylated 60 kDa protein was considered to be an autophosphorylated member of the Src tyrosine kinases and autophosphorylation was enhanced at 3 minutes after stimulation but the protein level was sustained up to 1 hour. Further, treatment of PP2, a selective inhibitor of Src kinases markedly suppressed the upregulation of MMP13 induced by MIF. Thus, MIF enhanced the kinase activity but protein level was not increased." provenance.
_3 value "Since Grp94 is known to inhibit apoptosis by maintaining intracellular Ca(2+) homeostasis" provenance.
_4 value "Aldose reductase inhibition increased glycolysis and glucose oxidation" provenance.
_5 value "AKT activation resulted in the repression of c-myc, early growth response 1 (EGR1), transforming growth factor beta receptor III (TGF-betar III), and thrombospondin-1 (THBS1)." provenance.
_5 value "An analysis of endogenous BCL-X(L) levels in AFX-expressing cells revealed enhanced down-regulation of the transcript ( approximately 1.3-1.7-fold) and protein, and BCL-6 directly binds to and suppresses the BCL-X(L) promoter." provenance.
_4 value "Cells induced to synthesize an active form of AFX die by activating the apoptotic death pathway" provenance.
_4 value "Although the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors cerivastatin, fluvastatin, and pitavastatin were not ligands for these three nuclear receptors in the CARLA, they induced transcriptional activation of PPARalpha/RXRalpha, PPARdelta/RXRalpha, and PPARgamma2/RXRalpha." provenance.
_5 value "Fz1 similarly activates RhoA (Figure 1A) and beta-catenin signaling (Yang-Snyder et al., 1996)" provenance.
_6 value "Since Daam1 binds to Dvl and RhoA, we tested whether Daam1 forms a ternary complex with Dvl and RhoA. We immunoprecipitated the endogenous RhoA from 293T cells treated with or without Wnt-1 CM. Strikingly, we found that the endogenous Dvl protein is associated with RhoA only upon Wnt stimulation (Figure 2G)." provenance.
_7 value "We also employed double-strand (ds) RNA mediated interference (RNAi) (Elbashir et al., 2001) to deplete endogenous Daam1 protein. The ds RNAi oligo for Daam1 reduces the protein level of Daam1, but not of RhoA, ?-catenin (Figure 3C) or Dvl2 (not shown). Importantly, the RNAi oligo inhibits RhoA activation by Wnt-1, Fz, or Dvl, but not by Ephexin (Figure 3C). A control ds RNAi oligo has no effect on Daam1 or RhoA protein level or RhoA activation (Figure 3C). Thus, Daam1 is essential for Wnt/Fz/Dvl activation of RhoA. AN ACTIVATED DAAM1 INDUCES RHO ACTIVATION IN A RHO-GEF-DEPENDENT MANNER Previous studies suggest that deletion of the amino terminal domain results in constitutive activation of FH proteins by releasing an intramolecular inhibition (Watanabe et al. 1999; Tominaga et al. 2000 and Westendorf 2001). C-Daam1 thus may represent an activated form of Daam1. Indeed, while the full length Daam1 is inactive, C-Daam1 overexpression causes activation of RhoA, but not of Rac or Cdc42 (Figure 3D). C-Daam1 activation of RhoA is not affected by ?PDZ-Dvl (Figure 3A), which inhibits RhoA activation by Fz or Dvl (Figure 1F), further demonstrating that Daam1 functions downstream of Dvl in Rho activation." provenance.
_5 value "In various cell types, AKT phosphorylates and inhibits glycogen synthase kinase-3 (GSK-3). Upon serum stimulation of EC, GSK-3beta was phosphorylated at Ser-9." provenance.
_5 value "Modified assertion" provenance.
_5 value "CDO and BOC form complexes in a cis fashion via association of both their ectodomains and their intracellular domains. A soluble fusion protein that contains the entire BOC ectodomain functions similarly to full-length BOC to promote myogenic differentiation, indicating that the intracellular region is dispensable for its activity in this system. Furthermore, a dominant-negative form of CDO inhibits the pro-myogenic effects of soluble BOC, suggesting that BOC is dependent on CDO for its activity." provenance.
_4 value "Proteomic methods have been used to monitor changes in protein synthesis in the first 4 h following stimulation of human lung fibroblasts with endothelin-1. Using pulsed [(35)S]methionine labeling, about 70 proteins with altered protein synthesis could be detected, and the 35 proteins showing the largest changes were identified by mass spectrometry." provenance.
_5 value "Proteomic methods have been used to monitor changes in protein synthesis in the first 4 h following stimulation of human lung fibroblasts with endothelin-1. Using pulsed [(35)S]methionine labeling, about 70 proteins with altered protein synthesis could be detected, and the 35 proteins showing the largest changes were identified by mass spectrometry." provenance.
_5 value "administration of a diet supplemented with high levels of cholesterol increases the expression of Cyp7a1, bile acid synthesis and excretion in wild-type mice, but not in Lxra null or Lxrb null mice" provenance.