Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _5 value "Not Available" provenance.
- _5 value "Not Available" provenance.
- _5 value "Not Available" provenance.
- _5 value "Not Available" provenance.
- _5 value "Entrez Gene summary: Human: The protein encoded by this gene is a member of the thiol-specific antioxidant protein family. This protein is a bifunctional enzyme with two distinct active sites. It is involved in redox regulation of the cell; it can reduce H(2)O(2) and short chain organic, fatty acid, and phospholipid hydroperoxides. It may play a role in the regulation of phospholipid turnover as well as in protection against oxidative injury." provenance.
- _3 value "Not Available" provenance.
- _3 value "Not Available" provenance.
- _6 value "Not Available" provenance.
- _5 value "Entrez Gene summary: Human: The protein encoded by this gene is a proinflammatory cytokine. This cytokine can induce the IFN-gamma production of T cells. The combination of this cytokine and IL12 has been shown to inhibit IL4 dependent IgE and IgG1 production, and enhance IgG2a production of B cells. IL-18 binding protein (IL18BP) can specifically interact with this cytokine, and thus negatively regulate its biological activity." provenance.
- _4 value "AMPK is activated by AMP and inhibited by phosphocreatine (Winder and Hardie, 1996)." provenance.
- _5 value "Activated AMPK is likely to be responsible for increases in NRF-1, cytochrome c and mitochondrial density, suggesting that AMPK activates mitochondrial biogenesis when cellular energy metabolism is stressed (Bergeron et al., 2001)." provenance.
- _4 value "Integrins are receptor proteins that bind and respond to the extracellular matrix and have been identified as possible inducers of hypertrophy signalling in response to mechanical stresses (Carson and Wei, 2000)." provenance.
- _4 value "Satellite cells are usually dormant but they start to proliferate and donate their nuclei to existing muscle fibres in a response to growth factors such as FGF and IGF-1 (Bischoff, 1994)." provenance.
- _3 value "The transcription factor NF kappa B is activated by contraction in rat skeletal muscle (Hollander et al., 2001) and is involved in myogenesis (Lehtinen et al., 1996;Canicio et al., 2001)." provenance.
- _4 value "some induced in all drug-treated male groups (Ppp1r3b), and others repressed in all drug-treated male groups (Cyp26b1, Meox2)." provenance.
- _4 value "some induced in all drug-treated male groups (Ppp1r3b), and others repressed in all drug-treated male groups (Cyp26b1, Meox2)." provenance.
- _7 value "Entrez Gene summary: Rat: SUMMARY: interacts with peroxisome proliferator-activated receptor alpha (PPAR alpha); can form a dimer with other nuclear hormone receptors [RGD] ... Human: The protein encoded by this gene is an unusual orphan receptor that contains a putative ligand-binding domain but lacks a conventional DNA-binding domain. The gene product is a member of the nuclear hormone receptor family, a group of transcription factors regulated by small hydrophobic hormones, a subset of which do not have known ligands and are referred to as orphan nuclear receptors. The protein has been shown to interact with retinoid and thyroid hormone receptors, inhibiting their ligand-dependent transcriptional activation. In addition, interaction with estrogen receptors has been demonstrated, leading to inhibition of function. Studies suggest that the protein represses nuclear hormone receptor-mediated transactivation via two separate steps: competition with coactivators and the direct effects of its transcriptional repressor function. OMIM summary: Human: The nuclear receptor superfamily is a group of transcription factors regulated by small hydrophobic hormones such as retinoic acid, thyroid hormone, and steroids. This superfamily also includes orphan nuclear receptors, such as NR0B2, which are related proteins that do not have known ligands ({7:Seol et al., 1996})." provenance.
- _6 value "from http://harvester.embl.de/harvester/P096/P09619.htm phosphorylates tyr residues at the c-terminus of ptpn11" provenance.
- _6 value "from http://www.ub.rug.nl/eldoc/dis/medicine/n.wilczak/c1.pdf The intrinsic tyrosine kinase activity of the IGF-I receptor is enhanced and phosphorylates multiple substrates, including IRS1 and IRS2 on tyrosine residues" provenance.
- _3 value "Another important mechanism regulating the release of NO is shearing forces acting on the luminal surface of vascular endothelium. By this mechanism, increased flow velocity stimulates calcium release and increased cNOS activity. The inducible form of NOS (iNOS, or Type II NOS) is not calcium-dependent, but instead is stimulated by the actions of cytokines (e.g., tumor necrosis factor, interleukins) and bacterial endotoxins (e.g., lipopolysaccharide). Induction of iNOS occurs over several hours and results in NO production that may be more than a 1,000-fold greater than that produced by cNOS. This is an important mechanism in the pathogenesis of inflammation." provenance.
- _3 value "Inhibition of platelet adhesion to the vascular endothelium (anti-thrombotic) Inhibition of leukocyte adhesion to vascular endothelium (anti-inflammatory) Antiproliferative (e.g., inhibits smooth muscle hyperplasia following vascular injury)" provenance.
- _3 value "Inhibition of vasoconstrictor influences (e.g., inhibits angiotensin II and sympathetic vasoconstriction)" provenance.
- _3 value "Inhibition of vasoconstrictor influences (e.g., inhibits angiotensin II and sympathetic vasoconstriction)" provenance.
- _3 value "Nitric oxide serves many important functions in the cardiovascular system as summarized below: Vasodilation (ligand mediated and flow dependent)" provenance.
- _5 value "The IP3 then stimulates the sarcoplasmic reticulum (SR) to release calcium. The formation of diacylglycerol (DAG) activates protein kinase C (PK-C), which can also contribute to VSM contraction via protein phosphorylation" provenance.
- _5 value "When NO is formed by an endothelial cell, for example, it readily diffuses out of the cell and into adjacent smooth muscle cells where is binds to a heme moiety on guanylyl cyclase and activates this enzyme to produce cGMP from GTP. Increased cGMP activates a kinase that subsequently leads to the inhibition of calcium influx into the smooth muscle cell, and decreased calcium-calmodulin stimulation of myosin light chain kinase (MLCK)." provenance.
- _5 value "When NO is formed by an endothelial cell, for example, it readily diffuses out of the cell and into adjacent smooth muscle cells where is binds to a heme moiety on guanylyl cyclase and activates this enzyme to produce cGMP from GTP. Increased cGMP activates a kinase that subsequently leads to the inhibition of calcium influx into the smooth muscle cell, and decreased calcium-calmodulin stimulation of myosin light chain kinase (MLCK)." provenance.
- _5 value "When NO is formed by an endothelial cell, for example, it readily diffuses out of the cell and into adjacent smooth muscle cells where is binds to a heme moiety on guanylyl cyclase and activates this enzyme to produce cGMP from GTP. Increased cGMP activates a kinase that subsequently leads to the inhibition of calcium influx into the smooth muscle cell, and decreased calcium-calmodulin stimulation of myosin light chain kinase (MLCK)." provenance.
- _4 value "Transfection of NOL7 into CC cells inhibited their growth in mouse xenografts, confirming its in vivo tumor suppressor activity. The induction of tumor dormancy correlated with an angiogenic switch in vitro as well as a decrease in tumor vascularity and an increase in tumor cell apoptosis in vivo." provenance.
- _5 value "In addition to opening the ryanodine receptor, cytoplasmic calcium also stimulates SERCA, which pumps calcium back into the SR. This pump provides another control mechanism to prevent a positive feedback cycle that could irreversibly deplete the SR of calcium. As calcium pumps refill the SR, the rate of Ca2+reuptake slows because of the declining cytoplasmic calcium concentration. ATP also favors SERCA activity; conversely, decreased ATP impairs calcium reuptake. " provenance.
- _4 value "Sodium-pump activity is closely linked to the intracellular calcium concentration via the sodium-calcium exchanger; this antiporter exchanges sodium and calcium in both directions across the sarcolemma. Changes in the concentration of either sodium or calcium ions inside or outside the cell affect the direction and magnitude of sodium-calcium exchange. Under normal conditions, the low intracellular sodium concentration favors sodium influx and clacium efflux. Some drugs take advantage of the functional coupling etween the sodium pump and the sodium-calcium exchanger to exert their effect as positive inotropes. Digoxin is the prototype of an inotropic agent that acts by inhibiting the sodium pump. A sarcolemmal calcium pump also helps to maintain calcium homeostasis by actively extruding calcium from the cytoplasm after cardiac contraction. A high concentration of ATP favors calcium removal (relaxation), both directly via the calcium pump and indirectly via the sodium pump." provenance.
- _5 value "Unlike the other classes, this isoforms lacks a cysteine-rich conserved region, and also lacks the calcium binding domain making it calcium independent. PKC zeta is activated by phosphatidylserine. This PKC isoform appears to be required for the activation of NF kappa B in response to p21 ras, and may be the physiological target for PIP3." provenance.
- _5 value "Entrez Gene summary: Human: Alpha-2-macroglobulin is a protease inhibitor and cytokine transporter. It inhibits many proteases, including trypsin, thrombin and collagenase. A2M is implicated in Alzheimer disease (AD) due to its ability to mediate the clearance and degradation of A-beta, the major component of beta-amyloid deposits." provenance.
- _6 value "GSK PI3K Phase 2, part 1: List of non-position specific phosphorylation effects on parent protein's activity, derived from existing causal assertions of position-specific phosphorylations on the parent protein activity." provenance.
- _7 value "Entrez Gene summary: Human: MaxiK channels are large conductance, voltage and calcium-sensitive potassium channels which are fundamental to the control of smooth muscle tone and neuronal excitability. MaxiK channels can be formed by 2 subunits: the pore-forming alpha subunit and the modulatory beta subunit. The protein encoded by this gene is an auxiliary beta subunit which slows activation kinetics, leads to steeper calcium sensitivity, and shifts the voltage range of current activation to more negative potentials than does the beta 1 subunit." provenance.
- _7 value "Entrez Gene summary: Human: MaxiK channels are large conductance, voltage and calcium-sensitive potassium channels which are fundamental to the control of smooth muscle tone and neuronal excitability. MaxiK channels can be formed by 2 subunits: the pore-forming alpha subunit and the modulatory beta subunit. The protein encoded by this gene is an auxiliary beta subunit which slows activation kinetics, leads to steeper calcium sensitivity, and shifts the voltage range of current activation to more negative potentials than does the beta 1 subunit." provenance.
- _5 value "Entrez Gene summary: Human: MaxiK channels are large conductance, voltage and calcium-sensitive potassium channels which are fundamental to the control of smooth muscle tone and neuronal excitability. MaxiK channels can be formed by 2 subunits: the pore-forming alpha subunit and the modulatory beta subunit. The protein encoded by this gene is an auxiliary beta subunit which slows activation kinetics, leads to steeper calcium sensitivity, and shifts the voltage range of current activation to more negative potentials than does the beta 1 subunit." provenance.
- _5 value "A recent study also demonstrated that activation of PPAR-g by its ligands caused dramatic morphological and nuclear changes that were characteristic of a more differentiated, less malignant state in breast cancer cells. Associated with these changes were the increase of maspin expression and arrest of cell cycle" provenance.
- _5 value "Adipocytes express a combination of five different adrenoreceptor isoforms: alpha1, alpha2, beta1, beta2, and beta3. Lipolysis is signaled by beta adrenergics and anti-lipolytic signal is transduced by the alpha-2 adrenegics and the alpha1 adrenergics are involved in a separate pathway" provenance.
- _5 value "Adipocytes express a combination of five different adrenoreceptor isoforms: alpha1, alpha2, beta1, beta2, and beta3. Lipolysis is signaled by beta adrenergics and anti-lipolytic signal is transduced by the alpha-2 adrenegics and the alpha1 adrenergics are involved in a separate pathway" provenance.
- _7 value "Adipocytes express a combination of five different adrenoreceptor isoforms: alpha1, alpha2, beta1, beta2, and beta3. Lipolysis is signaled by beta adrenergics and anti-lipolytic signal is transduced by the alpha-2 adrenegics and the alpha1 adrenergics are involved in a separate pathway" provenance.
- _4 value "Glucose transport is stimulated bia GLUT4 translocation to the plasma membrane, and lipoprotein lipase secretion (and therefore fatty acid uptake) is enhanced. In addition, insulin reduces dramatically the number of cell surface beta adrenegic receptors, which further desensitizes the adipocyte to lipolytic stimuli" provenance.
- _4 value "TNF alpha, interleukin 1, and some interferons also increase lipolysis. altthough the mechanism is probably post-transcriptional, since Norther blot analysis shows that TNF alpha and the interferons decrease the level of HSL mRNA" provenance.
- _5 value "The insulin receptor is an integral membrane protein that functions as a tetramer composed of two alpha and two beta subunits Insulin-binding to the adipocyte insulin receptor simultaneously stimulates lipogenesis and inhibits lipolysis" provenance.
- _6 value "p274 Phosphorylation of perilipin is correlated with hormone-stimulated lipolysis suggesting that phosphorylated perilipin has reduced affinity for droplets and dissociates from the surface concomitant with HSL association. perilipin null mice are found to have constitutively active HSL" provenance.
- _3 value "p277 Castrated male rats exhibited decreased lipolysis that appeared to be caused both by defective adenylyl cyclase catalysis and a decreased number of beta adrenergic receptors, again implying desensitization to catecholamines. Normal lipolyitic levels could be restored by administration of testosterone." provenance.
- _5 value "p277 Castrated male rats exhibited decreased lipolysis that appeared to be caused both by defective adenylyl cyclase catalysis and a decreased number of beta adrenergic receptors, again implying desensitization to catecholamines. Normal lipolyitic levels could be restored by administration of testosterone." provenance.
- _4 value "p277 Castrated male rats exhibited decreased lipolysis that appeared to be caused both by defective adenylyl cyclase catalysis and a decreased number of beta adrenergic receptors, again implying desensitization to catecholamines. Normal lipolyitic levels could be restored by administration of testosterone." provenance.
- _4 value "p277 Castrated male rats exhibited decreased lipolysis that appeared to be caused both by defective adenylyl cyclase catalysis and a decreased number of beta adrenergic receptors, again implying desensitization to catecholamines. Normal lipolyitic levels could be restored by administration of testosterone." provenance.
- _6 value "page 266 Binding sites for the C/EBP proteins reside within the promoters of the aP2, stearoyl-CoA desaturase and insulin stimulatable glucose transporter genes" provenance.
- _6 value "page 266 Binding sites for the C/EBP proteins reside within the promoters of the aP2, stearoyl-CoA desaturase and insulin stimulatable glucose transporter genes" provenance.
- _6 value "page 266 Binding sites for the C/EBP proteins reside within the promoters of the aP2, stearoyl-CoA desaturase and insulin stimulatable glucose transporter genes" provenance.
- _5 value "page 269 SREBP2 knockout mice are embryonic lethal" provenance.
- _5 value "The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha isoforms and 1 each of beta, gamma, and delta subunits.2 This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. The muscarinic cholinergic receptors belong to a larger family of G protein-coupled receptors. The muscarinic cholinergic receptor 3 controls smooth muscle contraction and its stimulation causes secretion of glandular tissue" provenance.
- _5 value "The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha isoforms and 1 each of beta, gamma, and delta subunits.2 This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. The muscarinic cholinergic receptors belong to a larger family of G protein-coupled receptors. The muscarinic cholinergic receptor 3 controls smooth muscle contraction and its stimulation causes secretion of glandular tissue" provenance.
- _5 value "The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha isoforms and 1 each of beta, gamma, and delta subunits.2 This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. The muscarinic cholinergic receptors belong to a larger family of G protein-coupled receptors. The muscarinic cholinergic receptor 3 controls smooth muscle contraction and its stimulation causes secretion of glandular tissue" provenance.
- _5 value "The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha isoforms and 1 each of beta, gamma, and delta subunits.2 This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. The muscarinic cholinergic receptors belong to a larger family of G protein-coupled receptors. The muscarinic cholinergic receptor 3 controls smooth muscle contraction and its stimulation causes secretion of glandular tissue" provenance.
- _5 value "The muscle acetylcholine receptor consiststs of 5 subunits of 4 different types: 2 alpha isoforms and 1 each of beta, gamma, and delta subunits.2 This gene encodes an alpha subunit that plays a role in acetlycholine binding/channel gating. The muscarinic cholinergic receptors belong to a larger family of G protein-coupled receptors. The muscarinic cholinergic receptor 3 controls smooth muscle contraction and its stimulation causes secretion of glandular tissue" provenance.
- _7 value "Some of the cholesterol-independent beneficial effects of statins, 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, in preventing cardiovascular disease may be due to their antithrombotic properties. Thrombin induces vascular smooth muscle cell (VSMC) proliferation, a primary determinant of atherosclerotic lesion progression. To investigate whether the antithrombotic effects of statins extends to inhibition of cell proliferation, we studied the effect of mevastatin on thrombin-induced rat vascular smooth muscle cell growth. Mevastatin (1 ?M) significantly inhibited thrombin-induced DNA synthesis in rat VSMC and this effect was not due to induction of apoptosis. Thrombin-induced mitogen-activated protein (MAP) kinase activities such as those of extracellular signal-regulated kinase2 (ERK2), Jun N-terminal kinase1 (JNK1) and p38 MAP kinase were significantly inhibited by mevastatin. However, the inhibitory effect was greater on JNK1 and p38 MAP kinase activities than on ERK2 activity. Mevalonate (500 ?M) attenuated the inhibitory effect of mevastatin on thrombin-induced DNA synthesis and MAP kinase activities. Thrombin increased ras and rac1 activities in a time-dependent manner and mevastatin inhibited these activities. Consistent with the inhibition of rac1, mevastatin also inhibited thrombin-induced superoxide production. Exogenous mevalonate reversed the inhibitory effect of mevastatin on thrombin-induced rac1 activation and superoxide production. Mevastatin inhibited thrombin-induced JAK2 and STAT3 tyrosine phosphorylation supporting our earlier results that reactive oxygen species (ROS) mediate the activation of JAK-STAT pathway by thrombin in these cells. Consistent with the role of ROS in thrombin-induced VSMC growth, mevastatin also inhibited ROS mediated transactivation of EGFR receptor induced by thrombin. Together, these results suggest that the antiatherosclerotic effects of statins include inhibition of VSMC proliferation induced by thrombin and this effect is mediated via abrogation of ROS generation." provenance.
- _7 value "Some of the cholesterol-independent beneficial effects of statins, 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, in preventing cardiovascular disease may be due to their antithrombotic properties. Thrombin induces vascular smooth muscle cell (VSMC) proliferation, a primary determinant of atherosclerotic lesion progression. To investigate whether the antithrombotic effects of statins extends to inhibition of cell proliferation, we studied the effect of mevastatin on thrombin-induced rat vascular smooth muscle cell growth. Mevastatin (1 ?M) significantly inhibited thrombin-induced DNA synthesis in rat VSMC and this effect was not due to induction of apoptosis. Thrombin-induced mitogen-activated protein (MAP) kinase activities such as those of extracellular signal-regulated kinase2 (ERK2), Jun N-terminal kinase1 (JNK1) and p38 MAP kinase were significantly inhibited by mevastatin. However, the inhibitory effect was greater on JNK1 and p38 MAP kinase activities than on ERK2 activity. Mevalonate (500 ?M) attenuated the inhibitory effect of mevastatin on thrombin-induced DNA synthesis and MAP kinase activities. Thrombin increased ras and rac1 activities in a time-dependent manner and mevastatin inhibited these activities. Consistent with the inhibition of rac1, mevastatin also inhibited thrombin-induced superoxide production. Exogenous mevalonate reversed the inhibitory effect of mevastatin on thrombin-induced rac1 activation and superoxide production. Mevastatin inhibited thrombin-induced JAK2 and STAT3 tyrosine phosphorylation supporting our earlier results that reactive oxygen species (ROS) mediate the activation of JAK-STAT pathway by thrombin in these cells. Consistent with the role of ROS in thrombin-induced VSMC growth, mevastatin also inhibited ROS mediated transactivation of EGFR receptor induced by thrombin. Together, these results suggest that the antiatherosclerotic effects of statins include inhibition of VSMC proliferation induced by thrombin and this effect is mediated via abrogation of ROS generation." provenance.
- _5 value "Some of the cholesterol-independent beneficial effects of statins, 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, in preventing cardiovascular disease may be due to their antithrombotic properties. Thrombin induces vascular smooth muscle cell (VSMC) proliferation, a primary determinant of atherosclerotic lesion progression. To investigate whether the antithrombotic effects of statins extends to inhibition of cell proliferation, we studied the effect of mevastatin on thrombin-induced rat vascular smooth muscle cell growth. Mevastatin (1 ?M) significantly inhibited thrombin-induced DNA synthesis in rat VSMC and this effect was not due to induction of apoptosis. Thrombin-induced mitogen-activated protein (MAP) kinase activities such as those of extracellular signal-regulated kinase2 (ERK2), Jun N-terminal kinase1 (JNK1) and p38 MAP kinase were significantly inhibited by mevastatin. However, the inhibitory effect was greater on JNK1 and p38 MAP kinase activities than on ERK2 activity. Mevalonate (500 ?M) attenuated the inhibitory effect of mevastatin on thrombin-induced DNA synthesis and MAP kinase activities. Thrombin increased ras and rac1 activities in a time-dependent manner and mevastatin inhibited these activities. Consistent with the inhibition of rac1, mevastatin also inhibited thrombin-induced superoxide production. Exogenous mevalonate reversed the inhibitory effect of mevastatin on thrombin-induced rac1 activation and superoxide production. Mevastatin inhibited thrombin-induced JAK2 and STAT3 tyrosine phosphorylation supporting our earlier results that reactive oxygen species (ROS) mediate the activation of JAK-STAT pathway by thrombin in these cells. Consistent with the role of ROS in thrombin-induced VSMC growth, mevastatin also inhibited ROS mediated transactivation of EGFR receptor induced by thrombin. Together, these results suggest that the antiatherosclerotic effects of statins include inhibition of VSMC proliferation induced by thrombin and this effect is mediated via abrogation of ROS generation." provenance.
- _4 value "Angiotensin II causes hypertension by vasoconstriction and stimulation of aldosterone release and sodium retention." provenance.
- _5 value "% OMIM summary: Human: The process of differentiation from mesodermal precursor cells to myoblasts has led to the discovery of a variety of tissue-specific factors that regulate muscle gene expression. The myogenic basic helix-loop-helix proteins, including myoD ({159970}), myogenin ({159980}), MYF5 ({159990}), and MRF4 ({159991}) are 1 class of identified factors. A second family of DNA binding regulatory proteins is the myocyte-specific enhancer factor-2 (MEF2) family. Each of these proteins binds to the MEF2 target DNA sequence present in the regulatory regions of many, if not all, muscle-specific genes. The MEF2 genes are members of the MADS gene family (named for the yeast mating type-specific transcription factor MCM1, the plant homeotic genes 'agamous ' and 'deficiens ' and the human serum response factor SRF ({600589})), a family that also includes several homeotic genes and other transcription factors, all of which share a conserved DNA-binding domain." provenance.
- _5 value "The tethered ligand that activates PAR1 is SFLLRN and the tethered ligand that activates PAR4 is GYPGQV" provenance.
- _6 value "AMPK is also able to phosphorylate and inactivate HMG CoA reductase and so potentially is in a position to corrdinately regulate both the fatty acid and sterol biosynthetic pathways" provenance.
- _5 value "during fasting, as ATP production falls into deficit and AMP concentrations rise, AMPK could be activated, resulting in phosphorylation and inactivation of ACC AMPK activated directly by AMP, but so is an AMPK kinase that activates AMPK by phosphorylation, whereas a AMPK phosphatase that inactivates AMPK is inhibited by AMP" provenance.
- _3 value "the activity of the ACCbeta form and the concentration of malonyl-CoA in skeletal muscle decreases within seconds of the initiation of exercise the mechanism by which activity of the beta form is regulated in muscle appears to involve both allosteric regulation by citrate and reversible phosphorylation, since activity of AMPK is elevated during muscle contraction" provenance.
- _5 value "the activity of the ACCbeta form and the concentration of malonyl-CoA in skeletal muscle decreases within seconds of the initiation of exercise the mechanism by which activity of the beta form is regulated in muscle appears to involve both allosteric regulation by citrate and reversible phosphorylation, since activity of AMPK is elevated during muscle contraction" provenance.
- _4 value "the activity of the ACCbeta form and the concentration of malonyl-CoA in skeletal muscle decreases within seconds of the initiation of exercise the mechanism by which activity of the beta form is regulated in muscle appears to involve both allosteric regulation by citrate and reversible phosphorylation, since activity of AMPK is elevated during muscle contraction" provenance.
- _4 value "Entrez Gene GeneRifs summary: Human: DEC1 encodes a basic helix-loop-helix protein expressed in various tissues. Expression in the chondrocytes is responsive to the addition of Bt2cAMP. Differentiated embryo chondrocyte expressed gene 1 is believed to be involved in the control of cell differentiation." provenance.
- _5 value "Cotransfection with Ptx1 in CV-1 cells resulted in a strong stimulation of alpha-subunit promoter activity, that was significantly diminished with mutation of the - 398/ - 385 region that disrupts the Ptx1 binding site, suggesting that this factor may play a role in thyrotrope-specific activation." provenance.
- _10 value "Alternatively, this integrin complex can interact with tenascin-C, thus favoring the clustering of EGF receptors and EGF-dependent growth (Jones et al., 1997)." provenance.
- _4 value "Cell adhesion is critical for receptor activation based on two experimental observations: (i) VEGF-A165-dependent VEGFR-2 phosphorylation was strongly activated in adherent cell, but showed a substantially reduced response in suspended cells; and" provenance.
- _6 value "During vasculogenesis, angioblasts and early endothelial cells secrete into extracellular matrix Del1, which is a recently discovered ligand for avb3 involved in vascular remodeling (Hidai et al., 1998). In addition, ligation of this integrin complex also promotes a calcium influx required for endothelial motility (Leavesley et al., 1993). The expression of avb3 integrin is induced in microvascular endothelial cells by vascular endothelial growth factor-A (VEGF-A) (Senger et al., 1997), a highly specific activator of in vitro endothelial cell migration and proliferation and in vivo angiogenesis (Thomas, 1996; Ferrara and Davis-Smyth, 1997)." provenance.
- _6 value "Therefore, avb3 associates with the tyrosine-phosphorylated PDGF and insulin receptor (Vuori and Ruoslahti, 1994; Rousseau et al., 1997) and its natural ligand vitronectin enhances the biological activity of PDGF-b (Schneller et al., 1997;Woodard et al., 1998)." provenance.
- _6 value "Through its phosphorylated tyrosine residues, the activated VEGFR-2 associates with the adapter molecules Shc, Grb2 and Nck, to Ras GTPase activating protein, p59fyn, pp62yes and phospholipase Cg, and to the tyrosine phosphatases SHP-1 and SHP-2" provenance.
- _4 value "VEGFR-2 phosphorylation and mitogenicity induced by VEGF-A165 were enhanced in cells plated on the alphavbeta3 ligand, vitronectin" provenance.
- _6 value "VEGFR-2 phosphorylation and mitogenicity induced by VEGF-A165 were enhanced in cells plated on the alphavbeta3 ligand, vitronectin" provenance.
- _6 value "VEGFR-2 phosphorylation and mitogenicity induced by VEGF-A165 were enhanced in cells plated on the alphavbeta3 ligand, vitronectin" provenance.
- _7 value "tyrosine-phosphorylated VEGFR-2 co-immunoprecipitated with beta3 integrin subunit" provenance.
- _3 value "Socs1 suppresses the mitogenic potential of Kit while maintaining Steel factor-dependent cell survival signals." provenance.
- _4 value "Modified assertion" provenance.
- _3 value "using antisera specific for JNK-1 and -2 dually phosphorylated on Thr-183 and Tyr-185. t-RA inhibited JNK phosphorylation by serum in a biphasic pattern (Fig. 1A)." provenance.
- _4 value "Inhibition of CKII mediated phosphorylation of APE/Ref-1 blocked mutagen-stimulated increase in AP-1 binding. It also abrogated the induction of c-Jun protein and rendered cells more sensitive to induced DNA damage" provenance.
- _5 value "Inhibition of CKII mediated phosphorylation of APE/Ref-1 blocked mutagen-stimulated increase in AP-1 binding. It also abrogated the induction of c-Jun protein and rendered cells more sensitive to induced DNA damage" provenance.
- _3 value "We show here that the topoisomerase poison etoposide, like ultra violet irradiation, inhibits Mdm2 synthesis." provenance.
- _5 value "We also found that c-Myc antagonized C/EBP alpha-mediated transactivation of gadd45. Analysis of systematically altered forms of C/EBP alpha revealed that c-Myc antagonism targeted the antimitotic, transcriptional activation domain of C/EBP alpha." provenance.
- _5 value "GM-CSF treatment of human neutrophils activates the Janus kinase/signal transducers and activators of transcription (Jak/STAT) pathway and, more specifically, Jak2, STAT3, and STAT5B in neutrophils." provenance.
- _6 value "CTGF expression induced by high glucose was partially suppressed by anti-TGF-beta1 antibody and by the protein kinase C inhibitor GF 109203X. Together, these data suggest that 1) high glucose stimulates mesangial CTGF expression by TGFbeta1-dependent and protein kinase C dependent pathways, and 2) CTGF may be a mediator of TGFbeta1-driven matrix production within a diabetic milieu." provenance.
- _3 value "Here, suppression subtractive hybridization identified 15 genes differentially induced when primary human mesangial cells are exposed to high glucose (30 mM versus 5 mM) in vitro. These genes included (a) known regulators of mesangial cell activation in diabetic nephropathy (fibronectin, caldesmon, thrombospondin, and plasminogen activator inhibitor-1), (b) novel genes, and (c) known genes whose induction by high glucose has not been reported. Prominent among the latter were genes encoding cytoskeleton-associated proteins and connective tissue growth factor (CTGF), a modulator of fibroblast matrix production." provenance.
- _5 value "The addition of recombinant CTGF to cultured mesangial cells enhanced expression of extracellular matrix proteins. High glucose stimulated expression of transforming growth factor beta1 (TGF-beta1), and addition of TGF-beta1 to mesangial cells triggered CTGF expression. CTGF expression induced by high glucose was partially suppressed by anti-TGF-beta1 antibody and by the protein kinase C inhibitor GF 109203X." provenance.
- _3 value "Loss of this enzyme activity after oxidative stress and upregulation of the enzyme chain hydrolyzing extracellular ATP after transient forebrain ischemia have also been reported." provenance.
- _5 value "Treatment of GCPs with Shh prevents differentiation and induces a potent, long-lasting proliferative response. This response can be inhibited by basic fibroblast growth factor or by activation of protein kinase A. Blocking Shh function in vivo dramatically reduces GCP proliferation. " provenance.
- _6 value "Treatment of GCPs with Shh prevents differentiation and induces a potent, long-lasting proliferative response. This response can be inhibited by basic fibroblast growth factor or by activation of protein kinase A. Blocking Shh function in vivo dramatically reduces GCP proliferation. " provenance.
- _4 value "The reduction in neovascularization in the NOD mice was the result of a lower level of vascular endothelial growth factor (VEGF) in the ischemic tissues, as assessed by Northern blot, Western blot and immunohistochemistry." provenance.
- _4 value "The reduction in neovascularization in the NOD mice was the result of a lower level of vascular endothelial growth factor (VEGF) in the ischemic tissues, as assessed by Northern blot, Western blot and immunohistochemistry." provenance.
- _5 value "we analyzed CD44 expression in the intestinal mucosa of mice and humans with genetic defects in either APC or Tcf-4, leading to constitutive activation or blockade of the beta-catenin/Tcf-4 pathway... the intestinal epithelium of Tcf-4-/- mice did not show any CD44 staining (Figure 5D) (via immunohistochemistry from full text)" provenance.
- _4 value "The addition of IGF-1 was characterized by a 33% (P < 0.01), 27% (P < 0.05), and 25% (P < 0.05) decrease in AT1 receptor at 5, 10, and 20 hours, respectively." provenance.
- _4 value "Modified assertion" provenance.
- _3 value "IL-1beta increased the production of PGE2 by rat lung myofibroblasts" provenance.