Nanopublications LDF server

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• _3 value "During the fasting state, fatty acid oxidation (FAO) in the liver is incomplete; the acetyl-CoA that is generated is not oxidized in the liver, but condenses into ketone bodies (mainly acetoacetate and β-hydroxybutyrate) (Figure 1), which are released into the plasma for subsequent oxidation in extrahepatic tissues." provenance.
• _6 value "LCFAs are activated into LCFA-coenzyme A (acyl- CoA) thioesters by long-chain acyl-CoA synthetases (ACS) located in the outer mitochondrial membrane, microsomes and peroxisomes" provenance.
• _6 value "The long-chain acyl-CoA is converted into an acyl-carnitine by carnitine palmitoyltransferase-I (CPT-I) in the outer mitochondrial membrane." provenance.
• _4 value "Acetyl-CoA moieties can then generate ketone bodies (mainly acetoacetate and β-hydroxybutyrate) via ketogenesis, which is stimulated during fasting." provenance.
• _4 value "After a meal, however, the acetyl-CoA moieties are mainly generated in the liver by the glycolysis of glucose into pyruvate and the oxidative decarboxylation of pyruvate." provenance.
• _3 value "Mitochondrial fatty acid β-oxidation (FAO) and the TCA cycle generate NADH and FADH2, which transfer their electrons (e-) to the mitochondrial respiratory chain (MRC), regenerating NAD+ and FAD used for other β-oxidation (or TCA) cycles" provenance.
• _5 value "Cytochrome c release induces caspase activation and cell death via apoptosis or necrosis." provenance.
• _3 value "Classically, it is considered that the number of normal mtDNA copies must fall below 20–40% of basal levels to induce mitochondrial dysfunction and adverse events [6]. Below this threshold, hepatic mtDNA depletion can impair the MRC. This impairment can hamper the regeneration of NAD+ and FAD, thus leading to a secondary inhibition of the oxidation of fatty acids and pyruvate." provenance.
• _3 value "Classically, it is considered that the number of normal mtDNA copies must fall below 20–40% of basal levels to induce mitochondrial dysfunction and adverse events [6]. Below this threshold, hepatic mtDNA depletion can impair the MRC. This impairment can hamper the regeneration of NAD+ and FAD, thus leading to a secondary inhibition of the oxidation of fatty acids and pyruvate." provenance.
• _3 value "The depletion of mitochondrial glutathione below a critical threshold can impair mitochondrial H2O2 detoxification, which can trigger mitochondrial dysfunction, mitochondrial permeability transition (MPT) and cell death [22]." provenance.
• _3 value "The depletion of mitochondrial glutathione below a critical threshold can impair mitochondrial H2O2 detoxification, which can trigger mitochondrial dysfunction, mitochondrial permeability transition (MPT) and cell death [22]." provenance.
• _8 value "the released cytochrome c binds in the cytosol to Apaf-1 in an ATP-dependent manner to activate caspase-9." provenance.
• _3 value "In contrast, when MPT occurs in most mitochondria in a single cell, ATP generation is compromised because of the collapse of the Δψm, and the resulting ATP depletion triggers cell necrosis [2,24]." provenance.
• _3 value "Mitochondrial permeability transition pore opening, which is calcium-dependent, can be triggered by a variety of endogenous compounds such as iron, ROS, nitric oxide, free fatty acids (and acyl-CoA derivatives), ceramide and bile salts [25,26]." provenance.
• _3 value "Mitochondrial permeability transition pore opening, which is calcium-dependent, can be triggered by a variety of endogenous compounds such as iron, ROS, nitric oxide, free fatty acids (and acyl-CoA derivatives), ceramide and bile salts [25,26]." provenance.
• _7 value "troglitazone and acetaminophen activate c-Jun N-terminal protein kinase (JNK), thus inducing the cleavage of Bid, the translocation of this pro-apoptotic protein to the outer mitochondrial membranes and the release of cytochrome c from mitochondria [32,33]." provenance.
• _3 value "tamoxifen directly inhibits the transfer of electrons within the MRC, and also progressively depletes hepatic mtDNA through a mechanism that may involve the inhibition of mitochondrial topoisomerases and the impairment of mtDNA replication by this DNA-intercalating drug [41,42]." provenance.
• _3 value "some drugs (e.g. amiodarone, amineptine, pirprofen) also inhibit microsomal triglyceride transfer protein (MTP), an enzyme playing a major role in the formation of very-low-density-lipoprotein (VLDL) particles [43]. Such drugs therefore inhibit the two main pathways removing fat from the liver, namely FAO and hepatic VLDL secretion." provenance.
• _3 value "Cationic amphiphilic drugs such as amiodarone, perhexiline, diethylaminoethoxyhexestrol (DEAEH) and tamoxifen can be first protonated in the intermembrane space of mitochondria, and then electrophoretically transported into the mitochondrial matrix thanks to the Δψm [3,4,40,42], as discussed in greater detail below. This transfer across the inner mitochondrial membrane dissipates Δψm (Figure 1) and increases the basal (state 4) mitochondrial respiration. This phenomenon, which is called 'OXPHOS uncoupling', can also be observed in the case of some mitochondrial poisons such as the protonophores 2,4-dinitrophenol (DNP) and carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP)." provenance.
• _3 value "Cationic amphiphilic drugs such as amiodarone, perhexiline, diethylaminoethoxyhexestrol (DEAEH) and tamoxifen can be first protonated in the intermembrane space of mitochondria, and then electrophoretically transported into the mitochondrial matrix thanks to the Δψm [3,4,40,42], as discussed in greater detail below. This transfer across the inner mitochondrial membrane dissipates Δψm (Figure 1) and increases the basal (state 4) mitochondrial respiration. This phenomenon, which is called 'OXPHOS uncoupling', can also be observed in the case of some mitochondrial poisons such as the protonophores 2,4-dinitrophenol (DNP) and carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP)." provenance.
• _3 value "valproic acid inhibits mitochondrial FAO through the sequestration of coenzyme A (a cofactor mandatory for FAO)," provenance.
• _3 value "this antiepileptic drug can induce MPT (Figure 1) [29], which may explain why valproateinduced microvesicular steatosis can be associated with liver cell death [2]." provenance.
• _5 value "In addition, BRG1 and N-CoR, components of nuclear hormone coactivator and corepressor complexes, also interact with PRP4K." provenance.
• _7 value "The differentially migrating forms of PRP4K detected by Western blot analysis (Fig. 2C) suggest that it is posttranslationally modified. Phosphatase treatment of nuclear extracts reduces most PRP4K to the 147-kDa fast-migrating form (Fig. 5D). Thus, the slower-migrating forms of PRP4K are phosphorylated, and it is only the hypophosphorylated (147 kDa) form that is coimmunoprecipitated by BRG1 and PRP6 antibodies (Fig. 5B and C)." provenance.
• _6 value "A strongly labeled doublet (Fig. 6, band B) corresponds to the relative position of PRP4K, a finding consistent with the reported ability of mammalian PRP4K homologues to autophosphorylate (19, 27). Two other prominently labeled proteins correspond in size to BRG1 and PRP6 (Fig. 6, bands A and C, respectively). To confirm that these proteins were indeed BRG1 and PRP6, we carried out kinase assays with BRG1 and PRP6 IP complexes, which also contain coimmunoprecipitated PRP4K (Fig. 5). These immunoprecipitates do exhibit kinase activity, and both phosphorylated PRP6 and BRG1 are much more intense in their respective IP reactions, reflecting the relative increase in each substrate for PRP4K." provenance.
• _5 value "Residual breast carcinomas that had been surgically removed within 48 days after first surgery showed a significant increase in proliferation if they were HER2-positive. Wound drainage fluid and postsurgical serum samples from patients stimulated in-vitro growth of HER2-overexpressing breast carcinoma cells. Removal of HER2 from the cell membrane led to a striking reduction of the induced proliferation." provenance.
• _3 value "In the other five cases, the concentrations of EGF-like factors were below the detection limits in both presurgical and postsurgical serum samples. A highly significant direct correlation (r=0.77, 95% CI 0.49–0.92, p=0.002) was found between EGF in postsurgical serum and cellular damage induced by surgery, measured on the basis of creatine phosphokinase concentration in drainage fluids obtained 1 day after surgery (figure 4). The degree of drainage-fluid-induced MDAMB453 cell proliferation also directly correlated with creatine phosphokinase concentration (r=0.69, 95% CI 0.25–0·91, p=0.009; figure 4)." provenance.
• _5 value "We show that protein kinase C (PKC) alpha is translocated to the plasma membrane and activated by adhesion of MM cells to fibronectin and VEGF. We identify beta(1) integrin modulating VEGF-triggered MM cell migration on fibronectin. We show that transient enhancement of MM cell adhesion to fibronectin triggered by VEGF is dependent on the activity of both PKC and beta(1) integrin. Moreover, we demonstrate that PKC alpha is constitutively associated with beta(1) integrin." provenance.
• _8 value "We show that protein kinase C (PKC) alpha is translocated to the plasma membrane and activated by adhesion of MM cells to fibronectin and VEGF. We identify beta(1) integrin modulating VEGF-triggered MM cell migration on fibronectin. We show that transient enhancement of MM cell adhesion to fibronectin triggered by VEGF is dependent on the activity of both PKC and beta(1) integrin. Moreover, we demonstrate that PKC alpha is constitutively associated with beta(1) integrin." provenance.
• _6 value "We show that protein kinase C (PKC) alpha is translocated to the plasma membrane and activated by adhesion of MM cells to fibronectin and VEGF. We identify beta(1) integrin modulating VEGF-triggered MM cell migration on fibronectin. We show that transient enhancement of MM cell adhesion to fibronectin triggered by VEGF is dependent on the activity of both PKC and beta(1) integrin. Moreover, we demonstrate that PKC alpha is constitutively associated with beta(1) integrin." provenance.
• _10 value "We show that protein kinase C (PKC) alpha is translocated to the plasma membrane and activated by adhesion of MM cells to fibronectin and VEGF. We identify beta(1) integrin modulating VEGF-triggered MM cell migration on fibronectin. We show that transient enhancement of MM cell adhesion to fibronectin triggered by VEGF is dependent on the activity of both PKC and beta(1) integrin. Moreover, we demonstrate that PKC alpha is constitutively associated with beta(1) integrin." provenance.
• _7 value "These data are consistent with PKC alpha-dependent exocytosis of activated beta(1) integrin to the plasma membrane, where its increased surface expression mediates binding to fibronectin; conversely, catalytically active PKC alpha-driven internalization of beta(1) integrin results in MM cell de-adhesion." provenance.
• _7 value "These data are consistent with PKC alpha-dependent exocytosis of activated beta(1) integrin to the plasma membrane, where its increased surface expression mediates binding to fibronectin; conversely, catalytically active PKC alpha-driven internalization of beta(1) integrin results in MM cell de-adhesion." provenance.
• _5 value "These data are consistent with PKC alpha-dependent exocytosis of activated beta(1) integrin to the plasma membrane, where its increased surface expression mediates binding to fibronectin; conversely, catalytically active PKC alpha-driven internalization of beta(1) integrin results in MM cell de-adhesion." provenance.
• _4 value "We show that the regulatory subunit of phosphatidylinositol (PI) 3-kinase (p85) is constitutively associated with FMS-like tyrosine kinase-1 (Flt-1). VEGF stimulates activation of PI 3-kinase, and both MM cell adhesion and migration are PI 3-kinase-dependent. Moreover, both VEGF-induced PI 3-kinase activation and beta(1) integrin-mediated binding to fibronectin are required for the recruitment and activation of PKC alpha." provenance.
• _6 value "We show that the regulatory subunit of phosphatidylinositol (PI) 3-kinase (p85) is constitutively associated with FMS-like tyrosine kinase-1 (Flt-1). VEGF stimulates activation of PI 3-kinase, and both MM cell adhesion and migration are PI 3-kinase-dependent. Moreover, both VEGF-induced PI 3-kinase activation and beta(1) integrin-mediated binding to fibronectin are required for the recruitment and activation of PKC alpha." provenance.
• _5 value "We show that the regulatory subunit of phosphatidylinositol (PI) 3-kinase (p85) is constitutively associated with FMS-like tyrosine kinase-1 (Flt-1). VEGF stimulates activation of PI 3-kinase, and both MM cell adhesion and migration are PI 3-kinase-dependent. Moreover, both VEGF-induced PI 3-kinase activation and beta(1) integrin-mediated binding to fibronectin are required for the recruitment and activation of PKC alpha." provenance.
• _6 value "Figure 4. VEGFR-1/Flt-1 associates with β1-integrin and CADTK and enhances CADTK-phosphorylation, dependent on PKC- and β1-integrin activation." provenance.
• _5 value "(a) Co-immunoprecipitation of CADTK and β1-integrin with PKCα. (b) constitutive association of Flt-1 and CADTK. (c) activation of CADTK upon treatment with PMA (300nM), 20 min. (d) Additional increase of CADTK-phosphorylation in the presence of VEGF (100ng/mL). (e) Dependency of VEGF-induced CADTK activation on PKC and β1-integrin. β1, β1-integrin; pY, phosphotyrosine; C, IP control" provenance.
• _5 value "(a) Co-immunoprecipitation of CADTK and β1-integrin with PKCα. (b) constitutive association of Flt-1 and CADTK. (c) activation of CADTK upon treatment with PMA (300nM), 20 min. (d) Additional increase of CADTK-phosphorylation in the presence of VEGF (100ng/mL). (e) Dependency of VEGF-induced CADTK activation on PKC and β1-integrin. β1, β1-integrin; pY, phosphotyrosine; C, IP control" provenance.
• _5 value "(a) Co-immunoprecipitation of CADTK and β1-integrin with PKCα. (b) constitutive association of Flt-1 and CADTK. (c) activation of CADTK upon treatment with PMA (300nM), 20 min. (d) Additional increase of CADTK-phosphorylation in the presence of VEGF (100ng/mL). (e) Dependency of VEGF-induced CADTK activation on PKC and β1-integrin. β1, β1-integrin; pY, phosphotyrosine; C, IP control" provenance.
• _5 value "When PI 3-kinase activation in MM cells seeded on fibronectin was inhibited by LY294002, PKCα recruitment to the plasma membrane was also abrogated (Fig. 6). These results indicate that VEGF-induced PI 3-kinase activation along with β1 integrin binding to fibronectin activate PKCα." provenance.
• _8 value "When PI 3-kinase activation in MM cells seeded on fibronectin was inhibited by LY294002, PKCα recruitment to the plasma membrane was also abrogated (Fig. 6). These results indicate that VEGF-induced PI 3-kinase activation along with β1 integrin binding to fibronectin activate PKCα." provenance.
• _5 value "Here, we show that repetitive slow fiber type electrical stimulation, but not fast fiber type stimulation, caused HDAC4-GFP, but not HDAC5-GFP, to translocate from the nucleus to the cytoplasm in cultured adult skeletal muscle fibers. HDAC4-GFP translocation was blocked by calmodulin-dependent protein kinase (CaMK) inhibitor KN-62." provenance.
• _3 value "Slow fiber type stimulation increased MEF2 transcriptional activity, nuclear Ca2+ concentration, and nuclear levels of activated CaMKII, but not total nuclear CaMKII or CaM-YFP. Thus, calcium transients for slow, but not fast, fiber stimulation patterns appear to provide sufficient Ca2+-dependent activation of nuclear CaMKII to result in net nuclear efflux of HDAC4." provenance.
• _5 value "Slow fiber type stimulation increased MEF2 transcriptional activity, nuclear Ca2+ concentration, and nuclear levels of activated CaMKII, but not total nuclear CaMKII or CaM-YFP. Thus, calcium transients for slow, but not fast, fiber stimulation patterns appear to provide sufficient Ca2+-dependent activation of nuclear CaMKII to result in net nuclear efflux of HDAC4." provenance.
• _8 value "It is known that CaMK can phosphorylate class II HDACs (Grozinger and Schreiber, 2000; Wang et al., 2000). Phosphorylated intranuclear HDACs bind to 14-3-3 proteins (McKinsey et al., 2001), exposing a nuclear export signal at the HDAC COOH terminus and thus allowing HDAC translocation to the cytoplasm." provenance.
• _5 value "The same stimulation (5 h, followed by 19 h without stimulation) in the presence of the CaMK inhibitor KN-62 gave the same luciferase activity as control. Thus, KN-62 completely blocked the stimulation-dependent increase in MEF2 reporter activity, just as KN-62 completely blocked the stimulation-dependent efflux of HDAC4 from the nucleus (Fig. 2)." provenance.
• _5 value "Leptomycin B binds to the nuclear export mediator protein CRM1, thereby blocking the binding of CRM1 to proteins containing the nuclear export signal (Fukuda et al., 1997) and preventing their nuclear export. During exposure to leptomycin B (40 nM), nuclear HDAC4-GFP continuously increased over a 60-min experimental period, whereas the cytoplasmic fluorescence signal was stable (Fig. 8 A)." provenance.
• _4 value "Over a 60-min period of treatment with 1 μM calyculin A (a PP1 and PP2A phosphatase inhibitor that does not affect PP2B; Ishihara et al., 1989), the nuclear HDAC4-GFP fluorescence decreased linearly with a mean net export rate of -0.71 ± 0.07%/min (Fig. 9 A, 13 nuclei from 5 fibers)." provenance.
• _5 value "Over a 60-min period of treatment with 1 μM calyculin A (a PP1 and PP2A phosphatase inhibitor that does not affect PP2B; Ishihara et al., 1989), the nuclear HDAC4-GFP fluorescence decreased linearly with a mean net export rate of -0.71 ± 0.07%/min (Fig. 9 A, 13 nuclei from 5 fibers)." provenance.
• _5 value "Interestingly, calyculin A also caused a similar rate of efflux of HDAC5-GFP (-0.62 ± 0.05, nine nuclei from six fibers) from nuclei as observed for HDAC4, establishing the ability of HDAC5 to move out of the nucleus even though it did not translocate in response to electrical stimulation." provenance.
• _6 value "LPS + IFNγ caused an increase in monolayer permeability, induction of iNOS and NADPH oxidase type 1 (Nox1) proteins, formation of superoxide, nitric oxide and 3-nitrotyrosine, and increase in PP2A activity in endothelial cells. These effects of LPS + IFNγ were diminished by tripterine (50-200 nM)." provenance.
• _7 value "LPS + IFNγ caused an increase in monolayer permeability, induction of iNOS and NADPH oxidase type 1 (Nox1) proteins, formation of superoxide, nitric oxide and 3-nitrotyrosine, and increase in PP2A activity in endothelial cells. These effects of LPS + IFNγ were diminished by tripterine (50-200 nM)." provenance.
• _7 value "Further, LPS + IFNγ -induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFκB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580. LPS + IFNγ stimulated phosphorylation of ERK, JNK and Jak2, and degradation of IκB, but only Jak2 phosphorylation was sensitive to tripterine (50-200 nM). Further, tripterine diminished the increased vascular permeability in inflamed air pouches." provenance.
• _7 value "Further, LPS + IFNγ -induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFκB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580. LPS + IFNγ stimulated phosphorylation of ERK, JNK and Jak2, and degradation of IκB, but only Jak2 phosphorylation was sensitive to tripterine (50-200 nM). Further, tripterine diminished the increased vascular permeability in inflamed air pouches." provenance.
• _5 value "Further, LPS + IFNγ -induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFκB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580. LPS + IFNγ stimulated phosphorylation of ERK, JNK and Jak2, and degradation of IκB, but only Jak2 phosphorylation was sensitive to tripterine (50-200 nM). Further, tripterine diminished the increased vascular permeability in inflamed air pouches." provenance.
• _6 value "Further, LPS + IFNγ -induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFκB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580. LPS + IFNγ stimulated phosphorylation of ERK, JNK and Jak2, and degradation of IκB, but only Jak2 phosphorylation was sensitive to tripterine (50-200 nM). Further, tripterine diminished the increased vascular permeability in inflamed air pouches." provenance.
• _4 value "The increased endothelial permeability induced by LPS + IFNγ was attenuated by the NADPH oxidase inhibitor apocynin (250 µM; based on Coyle and Kader, 2007), iNOS inhibitor 1400W (50 µM; based on Hortelano et al., 2000), and tripterine (50 nM and 200 nM; based on Allison et al., 2001) (Figure 1B). Neither apocynin, 1400W nor tripterine (50 nM and 200 nM) altered the endothelial permeability in the absence of a pro-inflammatory stimulus (Figure 1B)." provenance.
• _4 value "Nox1 is a catalytic subunit of NADPH oxidase that is expressed in endothelial cells (Sorescu et al., 2004; Wu et al., 2008)." provenance.
• _5 value "Constitutive Akt/protein kinase B (PKB) activity was demonstrated in 16 of 17 cell lines by maintenance of S473 phosphorylation with serum deprivation. Additional analysis of five of 2these NSCLC lines revealed that phosphorylation of S473 and T308 correlated with in vitro kinase activity." provenance.
• _3 value "Fig. 1A shows that the H1155, H157, and H1703 cells exhibit S473 phosphorylation under normal growth conditions and serum deprivation, but A549 and H1355 cells show little S473 phosphorylation in low-serum conditions. Levels of phosphorylated S473 were greatest in the H1155 cells. Regulation of S473 phosphorylation by serum withdrawal was only observed with the A549 cells." provenance.
• _3 value "Phosphorylation patterns for T308, the PDK1 site (Fig. 1B), generally correlated with the S473 pattern; only the H1155, H157, and H1703 cells displayed phosphorylation of Akt/PKB at T308." provenance.
• _4 value "Interestingly, both H1703 and H1155 cells increased T308 phosphorylation when transitioned from normal growth conditions to serum deprivation, indicating that increased T308 phosphorylation might be an adaptive response to the stress of serum deprivation in these cells." provenance.
• _3 value "Fig. 5A shows that in the three cell lines with high Akt/PKB activity, basal levels of apoptosis were potentiated 6–16-fold by LY294002 (Lanes 1)." provenance.
• _6 value "we transiently cotransfected NSCLC cell lines with HA-tagged dominant negative Akt/PKB (K179M Akt/PKB) and GFP and assessed apoptosis in the GFP-positive cells. Fig. 6 shows that in the cell lines with high Akt/PKB activity, transfection of K179M Akt/PKB resulted in a 2–5-fold increase in basal apoptosis." provenance.
• _3 value "platelet adhesion is an essential function in response to vascular injury and is generally viewed as the first step during which single platelets bind through specific membrane receptors to cellular and extracellular matrix constituents of the vessel wall and tissues. This response initiates thrombus formation that arrests hemorrhage and permits wound healing" provenance.
• _7 value "The results demonstrate that the adhesive function of GPIbα is as necessary as that of αIIbβ3 to sustain platelet aggregation at the edge of a growing thrombus" provenance.
• _4 value "Among the substrates required for normal thrombus formation, VWF is unique for its role in initiating platelet adhesion and sustaining platelet aggregation under conditions of elevated shear stress.16,18" provenance.
• _7 value "The integrin αIIbβ3, on the other hand, binds several ligands, in addition to VWF, that are key to the process of platelet adhesion and aggregation, primarily fibrinogen,64 fibronectin, 65 and CD40 ligand.66" provenance.
• _7 value "The integrin αIIbβ3, on the other hand, binds several ligands, in addition to VWF, that are key to the process of platelet adhesion and aggregation, primarily fibrinogen,64 fibronectin, 65 and CD40 ligand.66" provenance.
• _7 value "The integrin αIIbβ3, on the other hand, binds several ligands, in addition to VWF, that are key to the process of platelet adhesion and aggregation, primarily fibrinogen,64 fibronectin, 65 and CD40 ligand.66" provenance.
• _6 value "In the latter study, with blood perfused over fibrillar collagen type I at shear rates between 400 and 1300 sec-1, the isolated deficiency of α2β1 or GPVI-Fc receptor -chain (FcR-g) complex caused an equivalent partial defect of platelet thrombus formation, whereas the combined deficiency caused complete inhibition.97" provenance.
• _5 value "In the latter study, with blood perfused over fibrillar collagen type I at shear rates between 400 and 1300 sec-1, the isolated deficiency of α2β1 or GPVI-Fc receptor -chain (FcR-g) complex caused an equivalent partial defect of platelet thrombus formation, whereas the combined deficiency caused complete inhibition.97" provenance.
• _6 value "These findings delineate a synergistic role for α5β1 and GPVI as laminin receptors, coupled to distinct activation pathways convergent on the function of the Syk tyrosine kinase" provenance.
• _8 value "The platelet membrane is endowed with several collagen receptors, including the integrin α2β1,79–81 GPVI,82,83 GPIV (CD-36),84–86 and the 65-kDa protein (p65) reportedly specific specific for type I collagen.87" provenance.
• _6 value "The platelet membrane is endowed with several collagen receptors, including the integrin α2β1,79–81 GPVI,82,83 GPIV (CD-36),84–86 and the 65-kDa protein (p65) reportedly specific specific for type I collagen.87" provenance.
• _6 value "The platelet membrane is endowed with several collagen receptors, including the integrin α2β1,79–81 GPVI,82,83 GPIV (CD-36),84–86 and the 65-kDa protein (p65) reportedly specific specific for type I collagen.87" provenance.
• _5 value "In human umbilical vein endothelial cells (HUVECs), cigarette smoke extracts (CSE) inhibited VEGF induced tube formation in the matrigel assay. CSE did not affect HUVECs proliferation, but significantly reduced cellular migration in response to VEGF." provenance.
• _4 value "As expected, VEGF treatment significantly induced both migration and proliferation in HUVECs (Figs. 2A–B and Table 1). Interestingly, CSE exposure was associated with a selective inhibition of VEGF-induced HUVEC migration, whereas cellular proliferation was not significantly affected (Figs. 2A– B and Table 1)." provenance.
• _7 value "Surface integrins have been shown to be critical regulators of endothelial cell migration in response to VEGF and NO. Here we found that VEGF-stimulated HUVECs exposed to CSE had a significant reduction in the expression of several surface integrins including αvβ3, αvβ5, α5β1 and α2β1 (Fig. 2C). Moreover, the adhesion of VEGF-stimulated HUVECs was significantly reduced following exposure to 10% CSE, suggesting an impairment of integrin activity/function (Fig. 2D)." provenance.
• _7 value "Surface integrins have been shown to be critical regulators of endothelial cell migration in response to VEGF and NO. Here we found that VEGF-stimulated HUVECs exposed to CSE had a significant reduction in the expression of several surface integrins including αvβ3, αvβ5, α5β1 and α2β1 (Fig. 2C). Moreover, the adhesion of VEGF-stimulated HUVECs was significantly reduced following exposure to 10% CSE, suggesting an impairment of integrin activity/function (Fig. 2D)." provenance.
• _7 value "Surface integrins have been shown to be critical regulators of endothelial cell migration in response to VEGF and NO. Here we found that VEGF-stimulated HUVECs exposed to CSE had a significant reduction in the expression of several surface integrins including αvβ3, αvβ5, α5β1 and α2β1 (Fig. 2C). Moreover, the adhesion of VEGF-stimulated HUVECs was significantly reduced following exposure to 10% CSE, suggesting an impairment of integrin activity/function (Fig. 2D)." provenance.
• _5 value "Similarly, we found that the induction of NO by VEGF in endothelial cell cultures was severely compromised in the presence of CSE, but that NO levels could be normalized with antioxidants (Fig. 4C). Globally, these data suggest that ROS are involved in the impairment of VEGF-induced Akt/eNOS/NO pathway by CSE." provenance.
• _5 value "Similarly, we found that the induction of NO by VEGF in endothelial cell cultures was severely compromised in the presence of CSE, but that NO levels could be normalized with antioxidants (Fig. 4C). Globally, these data suggest that ROS are involved in the impairment of VEGF-induced Akt/eNOS/NO pathway by CSE." provenance.
• _7 value "Because NO is an essential mediator of endothelial cell migration and VEGF-induced angiogenesis, we investigated the effect of CSE exposure on VEGF-dependent Akt/eNOS/NO pathway. VEGF-stimulated HUVECs exposed to CSE show a dose-dependent inhibition of phosphorylated Akt and eNOS (Fig. 4A). Importantly, the activation of Akt and eNOS by VEGF can be rescued following treatment with the antioxidants NAC and vitamin C (Fig. 4B)." provenance.
• _7 value "These data suggest that CSE prevents VEGF-induced endothelial cell migration and tube formation by increasing oxidative stress. The importance of NO in that physiopathology was demonstrated by showing that NO donors (SNAP 75 μM, SNP 0.1 mM) or a cGMP analog (8-Br-cGMP 2 mM) rescued integrin expression (Fig. 5A), cellular migration (Fig. 5B) and tube formation (Fig. 5C) in endothelial cells exposed to CSE." provenance.
• _7 value "These data suggest that CSE prevents VEGF-induced endothelial cell migration and tube formation by increasing oxidative stress. The importance of NO in that physiopathology was demonstrated by showing that NO donors (SNAP 75 μM, SNP 0.1 mM) or a cGMP analog (8-Br-cGMP 2 mM) rescued integrin expression (Fig. 5A), cellular migration (Fig. 5B) and tube formation (Fig. 5C) in endothelial cells exposed to CSE." provenance.
• _7 value "These data suggest that CSE prevents VEGF-induced endothelial cell migration and tube formation by increasing oxidative stress. The importance of NO in that physiopathology was demonstrated by showing that NO donors (SNAP 75 μM, SNP 0.1 mM) or a cGMP analog (8-Br-cGMP 2 mM) rescued integrin expression (Fig. 5A), cellular migration (Fig. 5B) and tube formation (Fig. 5C) in endothelial cells exposed to CSE." provenance.
• _7 value "These data suggest that CSE prevents VEGF-induced endothelial cell migration and tube formation by increasing oxidative stress. The importance of NO in that physiopathology was demonstrated by showing that NO donors (SNAP 75 μM, SNP 0.1 mM) or a cGMP analog (8-Br-cGMP 2 mM) rescued integrin expression (Fig. 5A), cellular migration (Fig. 5B) and tube formation (Fig. 5C) in endothelial cells exposed to CSE." provenance.
• _3 value "These data suggest that CSE prevents VEGF-induced endothelial cell migration and tube formation by increasing oxidative stress. The importance of NO in that physiopathology was demonstrated by showing that NO donors (SNAP 75 μM, SNP 0.1 mM) or a cGMP analog (8-Br-cGMP 2 mM) rescued integrin expression (Fig. 5A), cellular migration (Fig. 5B) and tube formation (Fig. 5C) in endothelial cells exposed to CSE." provenance.
• _6 value "Here we examine the nature of the physical interaction between the αvβ3 integrin and two receptor tyrosine kinases (RTKs), the platelet-derived growth factor receptor β (PDGF-Rβ) and the vascular endothelial growth factor receptor 2 (VEGF-R2, also known as KDR and flk-1). Both of these RTKs associate with the αvβ3 integrin but do not associate with β1 integrins. Furthermore, growth factor stimulation of these RTKs promotes increased cell proliferation and migration when cells are attached to the αvβ3 ligand, vitronectin." provenance.
• _10 value "Here we examine the nature of the physical interaction between the αvβ3 integrin and two receptor tyrosine kinases (RTKs), the platelet-derived growth factor receptor β (PDGF-Rβ) and the vascular endothelial growth factor receptor 2 (VEGF-R2, also known as KDR and flk-1). Both of these RTKs associate with the αvβ3 integrin but do not associate with β1 integrins. Furthermore, growth factor stimulation of these RTKs promotes increased cell proliferation and migration when cells are attached to the αvβ3 ligand, vitronectin." provenance.
• _10 value "Here we examine the nature of the physical interaction between the αvβ3 integrin and two receptor tyrosine kinases (RTKs), the platelet-derived growth factor receptor β (PDGF-Rβ) and the vascular endothelial growth factor receptor 2 (VEGF-R2, also known as KDR and flk-1). Both of these RTKs associate with the αvβ3 integrin but do not associate with β1 integrins. Furthermore, growth factor stimulation of these RTKs promotes increased cell proliferation and migration when cells are attached to the αvβ3 ligand, vitronectin." provenance.
• _6 value "To study the role of αv in the formation of the RTK-integrin complex, we transfected PDGF-Rβ into CHO cells that overexpress the platelet integrin αIIbβ3. As shown in Fig. 5A, equal amounts of PDGF-Rb were coprecipitated with both anti-αIIb and anti-β3 antibodies." provenance.
• _9 value "We have previously shown that the attachment of cells to a substrate through the αvβ3 integrin enhances the ability of insulin and PDGF to stimulate cell proliferation and migration (9,11)." provenance.
• _7 value "Ligation of α6β4 in primary human keratinocytes caused tyrosine phosphorylation of Shc, recruitment of Grb2, activation of Ras and stimulation of the MAP kinases Erk and Jnk." provenance.
• _7 value "Ligation of α6β4 in primary human keratinocytes caused tyrosine phosphorylation of Shc, recruitment of Grb2, activation of Ras and stimulation of the MAP kinases Erk and Jnk." provenance.
• _10 value "Ligation of α6β4 in primary human keratinocytes caused tyrosine phosphorylation of Shc, recruitment of Grb2, activation of Ras and stimulation of the MAP kinases Erk and Jnk. In contrast, ligation of the laminin- and collagen-binding integrins α3β1 and α2β1 did not cause these events." provenance.
• _8 value "Ligation of α6β4 in primary human keratinocytes caused tyrosine phosphorylation of Shc, recruitment of Grb2, activation of Ras and stimulation of the MAP kinases Erk and Jnk. In contrast, ligation of the laminin- and collagen-binding integrins α3β1 and α2β1 did not cause these events." provenance.

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