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• _5 value "Modified assertion" provenance.
• _5 value "We show that EGF stimulation activates the catalytic activity of Brk, which in turn phosphorylates paxillin at Y31 and Y118. These phosphorylation events promote the activation of small GTPase Rac1 via the function of CrkII" provenance.
• _5 value "We show that EGF stimulation activates the catalytic activity of Brk, which in turn phosphorylates paxillin at Y31 and Y118. These phosphorylation events promote the activation of small GTPase Rac1 via the function of CrkII" provenance.
• _5 value "FHL2, CBP/p300, and beta-catenin could synergistically activate androgen receptor-mediated transcription" provenance.
• _4 value "Coordinate regulation of intracellular signaling pathways is central to the ability of mitogens and oncogenes to promote cell cycle progression (24). Two pathways thought to play an important role in committing quiescent cells into S phase are the RAS-activated RAF-MEK-extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3'-kinase (PI3'- kinase)-PDK1-AKT pathways (35, 36). These pathways are reported to influence the expression, activity, or subcellular localization of key components of the cell cycle machinery such as cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CKIs) leading to the appropriate activation of E2F transcription factors (50, 51). In addition to sensing the activation of specific signaling pathways, cells are also able to integrate the extent and timing of signal pathway activation and convert that information into an appropriate biological response (32, 48, 64, 66). For example, depending on the level of expression or activation, activated RAS can promote either cellular immortalization, oncogenic transformation, or cell cycle arrest in the same cell type (20, 48, 64, 66). Under these circumstances, RAS (or RAF)-induced cell cycle arrest is mediated by induced expression of CKIs of the INK4 or CIP/KIP family (29, 37). Interestingly, activation of \"parallel\" signaling pathways can modify the ability of RAS to regulate the G0-G1-Sphase cell cycle transition. For example, RAS-induced cell cycle arrest in Swiss 3T3 cells is prevented by coactivation of Rho signaling pathways (9, 43)." provenance.
• _7 value "Moreover, AKT was able to bypass RAF-induced G1 cell cycle arrest mediated by CKI-dependent inhibition of cyclin E/cdk2 (64)." provenance.
• _5 value "To dissect the biochemical mechanism(s) underlying the ability of these protein kinases to promote the cell division cycle, we used Western blotting to assess the effects of RAF and AKT on the expression of a number of proteins known to be targets of RAF or AKT signaling. Of the various immediate- early targets of RAF signaling that we analyzed (e.g., Fos, Jun, c-Myc, and HB-EGF), none showed evidence of cooperative regulation in response to coactivation of AKT and RAF (data not shown) (11, 33, 34). However, we observed cooperative effects of RAF and AKT on the expression of two key cell cycle regulators, cyclin D1 and p27Kip1. Activation of AKT or RAF alone led to a two- or threefold induction of cyclin D1 expression, respectively (Fig. 2A)." provenance.
• _6 value "ROCK1 and -2, alternatively, activate LIM domain-containing protein kinase 1 (LIMK1) and 2 (LIMK2), which phosphorylate and inhibit the actin depolymerization factor cofilin (cofilin-P). This increases actin polymerization and results in the stabilization of actin stress fibres27. The phosphatase slingshot dephosphorylates cofilin, which blocks actin polymerization." provenance.
• _5 value "Whereas the function of CKIs as tumour suppressors is well characterized in the nucleus, they also seem to function in the cytoplasm,where they regulate cytoskeletal functions. This occurs through the modulation of the Rho signalling pathway. This cytoplasmic function could be oncogenic, as inhibition of the Rho pathway can result in increased migratory capacity. Phosphorylation of p21 on Thr145 by protein kinase B (PKB)/Akt48 or Pim1 inhibits the nuclear localization of p21. In the cytoplasm, p21 can protect the cell from apoptosis, as well as bind and inhibit the Rho kinases ROCK1 and -2 to modulate actin cytoskeleton organization46,47." provenance.
• _4 value "Whereas the function of CKIs as tumour suppressors is well characterized in the nucleus, they also seem to function in the cytoplasm,where they regulate cytoskeletal functions. This occurs through the modulation of the Rho signalling pathway. This cytoplasmic function could be oncogenic, as inhibition of the Rho pathway can result in increased migratory capacity. Phosphorylation of p21 on Thr145 by protein kinase B (PKB)/Akt48 or Pim1 inhibits the nuclear localization of p21. In the cytoplasm, p21 can protect the cell from apoptosis, as well as bind and inhibit the Rho kinases ROCK1 and -2 to modulate actin cytoskeleton organization46,47." provenance.
• _6 value "p27 binds to RhoA and prevents the interaction of RhoA with its activators the guanine-nucleotide exchange factors. Fibroblasts lacking p27 have impaired migration. CIP1 binds to and inhibits Rho kinases (ROCK1 and -2) - downstream effectors of Rho. p57 (KIP2) binds to and targets LIM domain-containing protein kinase (LIMK) to the nucleus, sequestering it in a compartment where it cannot regulate the actin cytoskeleton." provenance.
• _3 value "Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated" provenance.
• _3 value "Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated" provenance.
• _3 value "Table 3 Gene expression in normal old cells relative to normal young cells: selection of genes that are differently expressed and that may specifically contribute to aneuploidy, cell cycle regulation, and proliferation upregulated" provenance.
• _3 value "downregulated" provenance.
• _3 value "downregulated" provenance.
• _7 value "We observed inducible binding of Elk-1 and the SRF after 3 and 24 h of treatment with H. pylori, suggesting that the bacteria alone are sufficient to initiate a cascade of signaling events responsible for villin expression. Thus, H. pylori induction of villin in the stomach correlates with activation and cooperative binding of Elk-1 and the SRF to the proximal promoter of villin." provenance.
• _5 value "Thrombin ligation of protease-activated receptor-1 activated the phosphorylation of syntaxin 4 and Munc18c, which, in turn, disrupted the interaction between syntaxin 4 and Munc18. Protein kinase Calpha activation was required for the phosphorylation of syntaxin 4 and Munc18c as well as the cell surface expression of P-selectin." provenance.
• _3 value "Thus, protease-activated receptor-1-induced protein kinase Calpha activation and phosphorylation of syntaxin 4 and Munc18c are required for the cell surface expression of P-selectin and the consequent binding of neutrophils to endothelial cells." provenance.
• _3 value "We also observed that syntaxin 4 knockdown inhibited the adhesion of neutrophils to thrombin-activated endothelial cells, demonstrating the functional role of syntaxin 4 in promoting endothelial adhesivity." provenance.
• _3 value "In fact, unlike other B-cell molecules (paired box 5 [PAX5], CD19, CD79a, CD20, CD22), which are down-regulated during differentiation from B cells to plasma cells, TPD52 expression reached its maximum levels at the plasma cell stage." provenance.
• _4 value "the functional effects of shRNA-mediated 12/15-LO knockdown were noted by the reduced oxidant stress and chemokine [monocyte chemoattractant protein-1 (MCP-1)] expression in a differentiated mouse monocytic cell line as well as by the reduced cellular adhesion and fibronectin expression in VMSCs. Knocking down 12/15-LO expression also reduced the expression of inflammatory genes, MCP-1, vascular cell adhesion molecule-1, and interleukin-6 in VSMCs" provenance.
• _4 value "the functional effects of shRNA-mediated 12/15-LO knockdown were noted by the reduced oxidant stress and chemokine [monocyte chemoattractant protein-1 (MCP-1)] expression in a differentiated mouse monocytic cell line as well as by the reduced cellular adhesion and fibronectin expression in VMSCs. Knocking down 12/15-LO expression also reduced the expression of inflammatory genes, MCP-1, vascular cell adhesion molecule-1, and interleukin-6 in VSMCs" provenance.
• _4 value "Rosiglitazone has marked anti-inflammatory effects on macrophages [31]. This led us to examine the effect of aspirin, an anti-inflammatory compound that targets IkB kinase and has insulin-sensitizing effects [32]. Remarkably, aspirin dramatically decreased endotoxin-induced resistin expression in a dose-dependent manner (Figure 4C). Both aspirin (via IkB kinase) and rosiglitazone (via PPARg) inhibit NF-kB [31,32], which is activated by LPS. Indeed, treatment of the macrophages with the proteasome inhibitor MG132, which prevents NF-kB activation [33], abrogated endotoxin-induced activation of resistin expression (data not shown). Moreover, treatment of the macrophages with SN50, a cell-permeable peptide that specifically prevents activation of NF-kB by inhibiting its nuclear translocation [34], nearly abolished endotoxin-induced activation of resistin expression (Figure 4D). Thus, activation of NF-kB is required for LPS induction of resistin in human macrophages." provenance.
• _4 value "Rosiglitazone has marked anti-inflammatory effects on macrophages [31]. This led us to examine the effect of aspirin, an anti-inflammatory compound that targets IkB kinase and has insulin-sensitizing effects [32]. Remarkably, aspirin dramatically decreased endotoxin-induced resistin expression in a dose-dependent manner (Figure 4C). Both aspirin (via IkB kinase) and rosiglitazone (via PPARg) inhibit NF-kB [31,32], which is activated by LPS. Indeed, treatment of the macrophages with the proteasome inhibitor MG132, which prevents NF-kB activation [33], abrogated endotoxin-induced activation of resistin expression (data not shown). Moreover, treatment of the macrophages with SN50, a cell-permeable peptide that specifically prevents activation of NF-kB by inhibiting its nuclear translocation [34], nearly abolished endotoxin-induced activation of resistin expression (Figure 4D). Thus, activation of NF-kB is required for LPS induction of resistin in human macrophages." provenance.
• _3 value "The increased level of resistin in humans with obesity is likely an indirect result of elevated levels of inflammatory cytokines characteristic of states of increased adiposity. Hence, obesity and acute inflammation are both hyperresistinemic states associated with insulin resistance. Induction of Resistin Gene and Protein Expression by Endotoxin Treatment of Human Macrophages The regulation of resistin expression was studied in primary cultures of human monocytic cells. Immediately upon plating of elutriated primary human monocytes, resistin gene expression was detectable but highly variable from experiment to experiment (data not shown). One day after plating, resistin gene expression remained detectable at low levels (Figure 1A). Subjection of the cells to a protocol leading to differentiation along the macrophage lineage led to a modest, time-dependent enhancement of resistin gene expression (Figure 1A)." provenance.
• _3 value "In a rat tail-suspension experimental model, we show that after fourteen days of non-weight bearing there is increased expression of MMP-2 in the atrophic soleus and gastrocnemius and decreased expression of TIMP-2." provenance.
• _3 value "It is a member of the serpin family of protease inhibitors and has been shown to reduce angiogenesis." provenance.
• _3 value "Estrogen has been postulated to be involved in inhibition of vascular smooth muscle cell (VSMC) proliferation mainly via estrogen receptor (ER), but the detailed mechanism has remained primarily unknown. Therefore, in this study, microarray analysis was used in two types of cultured human VSMCs: one positive for ER alpha, and the other for ER beta, which were treated by estrogens to detect the estrogen-responsive genes. We also used quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) to evaluate mRNA levels of selective target gene (TG) in these cells. We further studied whether the TG product was involved in inhibition of proliferation using small interfering RNA (siRNA) of the TG transfection. We subsequently used quantitative RT-PCR and in situ hybridization analysis to evaluate the expression of these gene products in human aorta. E4F1, a possible inducer of cell growth arrest, was markedly increased only in ER alpha-positive VSMCs by estrogens in both microarray and RT-PCR analyses. Blocking of E4F1 using siRNA suppressed estrogenic inhibition of ER alpha-positive VSMC proliferation. E4F1 mRNA was abundant in premenopausal female aorta with mild atherosclerotic changes. E4F1 is therefore considered one of the estrogen-responsive genes involving ER alpha-mediated inhibition of VSMC proliferation and may play an important role in estrogen-related atheroprotection of human aorta." provenance.
• _6 value "Akt3 is the major downstream mediator for alsinLF/Rac1-mediated neuroprotection" provenance.
• _4 value "Furthermore, whereas LTB4 production by neutrophils from control subjects was concentration dependently inhibited by the lipophilic antioxidant -tocopherol (Figure 3)," provenance.
• _5 value "erbB2, the ligand-less member of the epidermal growth factor receptor family, was shown to form a complex with the hemidesmosomal integrin alpha6beta4. These results indicate that stimulation of alpha6beta4 increases E-cadherin-mediated cell-cell adhesion and that this mechanism depends on erbB2 activation." provenance.
• _2 value "The transcription factor Miz1 is required for DNA-damage-induced cell-cycle arrest." provenance.
• _5 value "The transcription factor Miz1 is required for DNA-damage-induced cell-cycle arrest." provenance.
• _5 value "A dominant-negative mutant of Ipaf inhibited p53-induced and doxorubicin-induced apoptosis by about 50%." provenance.
• _5 value "In addition, the expression of PO was also diminished in the liver derived from HNF1alpha-null mice." provenance.
• _3 value "The proteasome beta subunit 1 (PSMB1) and 26S ATPase 3 (PSMC3) genes were upregulated in the PFC by 95% and 119% (P<0.001), respectively." provenance.
• _4 value "Herceptin (trastuzumab), an inhibitory antibody to the erbB2 receptor, is a potent chemotherapeutic but causes cardiomyopathies" provenance.
• _3 value "The accurate killing is assured by a vectorial movement of secretory lysosomes along microtubules and focused secretion within the immunological synapse. Here we present an over view of how these key regulators such as AP-3 adaptor protein, RabGGTase enzyme, Rab27a small GTP binding protein, Lyst and Munc13-4 act in a very orchestrated way to deliver the kiss of the death." provenance.
• _3 value "The accurate killing is assured by a vectorial movement of secretory lysosomes along microtubules and focused secretion within the immunological synapse. Here we present an over view of how these key regulators such as AP-3 adaptor protein, RabGGTase enzyme, Rab27a small GTP binding protein, Lyst and Munc13-4 act in a very orchestrated way to deliver the kiss of the death." provenance.
• _3 value "findings suggest that extracellular ATP-induced IL-6 synthesis occurs through P2Y receptors and mobilization of Ca(2+) from internal stores in human osteoblastic cells." provenance.
• _5 value "Alternatively, Kit signaling may also activate JNK kinase, a MAP kinase activated in response to stress [35]. NF1, a GTPase activating protein, is considered to be involved in modulating Ras activation through Kit signaling [36]. NF1 deficiency that occurs in cases of neurofibromatosis may induce an increase in MAP kinase activity. Pathways with JAK/STAT or with Src family members may be involved in Kit signaling [33] (fig. 1). Some studies showed the association of JAK2 with Kit and also its activation by Kit signaling [37]. Other reports also indicated the increased activity of Lyn, a Src family member, by Kit signaling [38]." provenance.
• _6 value "Alternatively, Kit signaling may also activate JNK kinase, a MAP kinase activated in response to stress [35]. NF1, a GTPase activating protein, is considered to be involved in modulating Ras activation through Kit signaling [36]. NF1 deficiency that occurs in cases of neurofibromatosis may induce an increase in MAP kinase activity. Pathways with JAK/STAT or with Src family members may be involved in Kit signaling [33] (fig. 1). Some studies showed the association of JAK2 with Kit and also its activation by Kit signaling [37]. Other reports also indicated the increased activity of Lyn, a Src family member, by Kit signaling [38]." provenance.
• _7 value "Another major signaling pathway is the Ras/MAP kinase cascade [33] (fig. 1). The activated Kit recruits SH-2-containing proteins such as Grb2, Shc and SHP2. Grb2 may bind Kit either directly or indirectly through interaction with Shc or SHP2. Since Grb2 is constitutively associated with Sos, a guanine nucleotide exchange factor, the recruitment of Grb2 to the activated Kit resultes in the colocalization of Sos and Ras and the subsequent activation of Ras. This promotes the interaction of Ras with Raf serinethreonine kinase and then the activation of MEK (a MAP kinase kinase). MEK phosphorylates ERK (a MAP kinase), and ERK phosphorylates a number of substrates, including pp90rsk [33]. Imatinib mesylate also inhibits the phosphorylation of ERK [34]. This process is considered to be due to blocking of the Kit signaling by this drug. Thus, both major signaling pathways of Kit, the PI3K/Akt system and the Ras/MAP kinase cascade, are inhibited by imatinib mesylate." provenance.
• _5 value "Another major signaling pathway is the Ras/MAP kinase cascade [33] (fig. 1). The activated Kit recruits SH-2-containing proteins such as Grb2, Shc and SHP2. Grb2 may bind Kit either directly or indirectly through interaction with Shc or SHP2. Since Grb2 is constitutively associated with Sos, a guanine nucleotide exchange factor, the recruitment of Grb2 to the activated Kit resultes in the colocalization of Sos and Ras and the subsequent activation of Ras. This promotes the interaction of Ras with Raf serinethreonine kinase and then the activation of MEK (a MAP kinase kinase). MEK phosphorylates ERK (a MAP kinase), and ERK phosphorylates a number of substrates, including pp90rsk [33]. Imatinib mesylate also inhibits the phosphorylation of ERK [34]. This process is considered to be due to blocking of the Kit signaling by this drug. Thus, both major signaling pathways of Kit, the PI3K/Akt system and the Ras/MAP kinase cascade, are inhibited by imatinib mesylate." provenance.
• _5 value "Binding to DOK4 and DOK5 is implicated in ERK stimulation, whereas binding to DOK1 is involved in recruiting the NCK adaptor leading to c-Jun N-terminal kinase (JNK) stimulation [10, 40] (fig. 3). Enigma is endowed with LIM and PDZ domains and is involved in shuttling rearranged RET/PTC oncoproteins to the membrane (see below)." provenance.
• _6 value "Shc and FRS2 mediates recruitment of Grb2-SOS complexes leading to Ras/ERK stimulation, and of Grb2-GAB1/2 complexes leading to stimulation of the phosphatidylinositol-3-kinase (PI3K)/AKT pathway. ShcC and IRS are required to trigger PI3K/AKT activation." provenance.
• _4 value "We recently identified three powerful RET inhibitors: two pyrazolo-pyrimidines: 4-amino-5-(4-methylphenyl)- 7-(t-butyl)pyrazolo[3,4-d]-pyrimidine (PP1) and 4-amino- 5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) (PP2), and an anilino- quinazoline: N (4 bromo 2 fluorophenyl) 6 methoxy 7 (1 methylpiperidin 4 yl) methoxy quinazolin 4 amine (ZD6474) [86 88]. These compounds showed half-maximal RET inhibitory concentrations in the nanomolar range (100 nM). When injected into nude mice, fibroblasts transfected with oncogenic RET lost morphological transformation, proliferative autonomy, anchorage-independent growth and tumorigenicity. In addition to inhibition of RET phosphorylation, PP1 induces RET destruction through proteosomal degradation [89]." provenance.
• _5 value "Expression of Spry4 in cultured cells suppressed integrin-mediated cell spreading, and TESK1 reversed the inhibitory effect of Spry4 on cell spreading." provenance.
• _4 value "valproate directly inhibits the glycogen synthase kinases (GSK)-3alpha/beta. The ability of lithium, another inhibitor of GSK3alpha/beta to protect cells from ER stress-induced lipid accumulation suggests that GSK3 plays a central role in signaling downstream effects of ER stress" provenance.
• _5 value "RANKL stimulated the phosphorylation of Ser727 of STAT1, which required p38 activity." provenance.
• _3 value "Exposure of these cells to NmU isopeptides resulted in an increase in intracellular Ca(2+) concentration (EC(50) 4.8 nM for human NmU)." provenance.
• _4 value "NmU also significantly increased the synthesis and release of cytokines including IL-4, IL-5, IL-6, IL-10, and IL-13." provenance.
• _4 value "NmU also significantly increased the synthesis and release of cytokines including IL-4, IL-5, IL-6, IL-10, and IL-13." provenance.
• _5 value "NmU also significantly increased the synthesis and release of cytokines including IL-4, IL-5, IL-6, IL-10, and IL-13." provenance.
• _6 value "maximal NmU-evoked cytokine release required functional phospholipase C, calcineurin, MEK, and PI3K pathways." provenance.
• _7 value "maximal NmU-evoked cytokine release required functional phospholipase C, calcineurin, MEK, and PI3K pathways." provenance.
• _4 value "Seven (7 of 17; CCL2, CCL7, CCL9, CCL11, CXCL1, CXCL5, CXCL10) of the allergen-induced chemokines were induced early after allergen challenge and remained induced throughout the experimental period." provenance.
• _4 value "while seven chemokines (CCL6, CCL8, CCL12, CCL22, CXCL9, CXCL12, and CXCL13) were increased only after a second allergen exposure." provenance.
• _4 value "while seven chemokines (CCL6, CCL8, CCL12, CCL22, CXCL9, CXCL12, and CXCL13) were increased only after a second allergen exposure." provenance.
• _2 value "Interferon gamma receptor 1 (IFNgammaR1) deficiency is a primary immunodeficiency with allelic dominant and recessive mutations characterised clinically by severe infections with mycobacteria. " provenance.
• _5 value "insulin also stimulates the transcriptional activity of nSREB2 and nSREB1A through a mitogen activated protein kinase pathway. The ser117 residue has been identified as the major phosphorylation site for MAPK in SREB1A. Ser432 and Ser455 are described as the MAPK phosphorylation sites in viro and in vivo in SREBP2. These phosphorylations do not modify DNA binding but enhance SREBP2 transactivation capacity. A role for MAPK in the modification of SREB1C transcriptional activity remains controversial. Although the ser117 target of MAPK in SREBP1A is also present in the SREBP1C isoform, the use of inhibitors of teh MAPK pathway in cultured hepatocytes do not antagonize the effect of insulin on SREBP1C target genes, suggesting that SREBP1C is not phosphorylated by MAPK in hepatocytes. We have shown that PKB is able to phosphorylate purified nSREBP1C in vitro. Cotransfection experiments in cultured hepatocytes indicate that phosphorylation by insulin and PKB stimulates the transcriptional activity of nuclear SREBP1C" provenance.
• _3 value "We propose that ANX7 mobilizes Ca(2+) from an endoplasmic reticulum-like pool, which can be recruited to enhance IP3-mediated Ca(2+) release." provenance.
• _3 value "A potent inflammatory mediator, bacterial lipopolysaccharide (LPS), induced Ets-2 at the mRNA and protein level, and this induction preceded the up-regulation of HO-1." provenance.
• _4 value "Blocking Dex-induced MKP-1 induction using small interfering RNA increased ERK1/2 and JNK phosphorylation and decreased cell survival." provenance.
• _5 value "ERK1/2 and JNK inactivation was associated with Ets-like transcription factor-1 (ELK-1) dephosphorylation." provenance.
• _5 value "ERK1/2 and JNK inactivation was associated with Ets-like transcription factor-1 (ELK-1) dephosphorylation." provenance.
• _2 value "Treatment with 10 microM 15d-PGJ2 or ciglitazone for 24 h decreased human umbilical vein endothelial cell (HUVEC) membrane NADPH-dependent O2-. production detected with electron spin resonance spectroscopy." provenance.
• _3 value "Treatment with 15d-PGJ2 or ciglitazone also reduced relative mRNA levels of the NADPH oxidase subunits, nox-1, gp91phox (nox-2), and nox-4, as measured using real-time PCR analysis. " provenance.
• _3 value "Cell adhesion assay showed that CRP enhanced the monocyte adhesion to endothelial cell monolayer by 2-fold, which was partially blocked by an anti-IL-8 antibody." provenance.
• _5 value "During prolonged fasting, plasma glycerol was elevated and the plasma glucose level was maintained in WT mice. In contrast, KO mice showed a disrupted increase of plasma glycerol and rapid reduction of plasma glucose during prolonged fasting." provenance.
• _5 value "We show that Abi promotes Abl-mediated phosphorylation of Cdc2 at tyrosine 15 and inactivation of Cdc2 kinase activity." provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "To investigate this, we used the immunoaffinity profiling approach to identify phosphotyrosine sites in NIH/3T3 cells expressing consitutively active c-Src Y527F tyrosine kinase (Fig 2a). (159 statements)" provenance.
• _5 value "As shown in Figure 4a and b, HIF-1anull cells totally failed to upregulate Ero1-La under hypoxia. Likewise, HIF-1b-null cells were incapable of inducing Ero1-La under hypoxia." provenance.
• _3 value "Expression of Ero1-La mRNA in hepatocellular carcinoma cells was indeed strongly upregulated shortly after exposure to hypoxia, reaching maximal steady-state levels within 12 h (Figure 2b). Elevated levels of Ero1-La protein accompanied increased expression of Ero1-La mRNA (Figure 2c)." provenance.
• _6 value "In HIF-1a-/- cells subjected to hypoxia, VEGF secretion was lower than the normoxic level." provenance.
• _4 value "hydrogen peroxide (H2O2) upregulates the expression of Bfl-1, an antiapoptotic member of the Bcl-2 family, and that this is responsible for the antiapoptotic activity of ROS" provenance.
• _3 value "hydrogen peroxide (H2O2) upregulates the expression of Bfl-1, an antiapoptotic member of the Bcl-2 family, and that this is responsible for the antiapoptotic activity of ROS" provenance.
• _3 value "hydrogen peroxide (H2O2) upregulates the expression of Bfl-1, an antiapoptotic member of the Bcl-2 family, and that this is responsible for the antiapoptotic activity of ROS" provenance.
• _3 value "REDD1 expression is markedly reduced in PC-3 cells treated with LY294002 (LY) or Rapamycin and strongly induced under hypoxic conditions in a hypoxia-inducible factor-1 (HIF-1)-dependent manner." provenance.
• _3 value "LTB(4) appears to be an up-regulating factor on the 5-LOX gene." provenance.
• _3 value "We found that hypotonic solution decreased [Cl(-)](i) and evoked a native I(Cl.vol) in A10 cells. The responses of [Cl(-)](i) and I(Cl.vol) to hypotonic challenge were enhanced by expression of ClC-3, and inhibited by ClC-3 antisense." provenance.
• _3 value "We found that hypotonic solution decreased [Cl(-)](i) and evoked a native I(Cl.vol) in A10 cells. The responses of [Cl(-)](i) and I(Cl.vol) to hypotonic challenge were enhanced by expression of ClC-3, and inhibited by ClC-3 antisense." provenance.
• _6 value "# GeneRif: CD44 and hyaluronic acid regulate in vivo iNOS expression and metalloproteinase activity during inflammation" provenance.

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