Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _3 value "1) C5aR is up-regulated during liver regeneration, 2) the binding of C5a to C5aR promotes a growth response, and 3) C5aR is involved in a cell cycle signaling pathway" provenance.
- _3 value "The only discernable effect of 1,25(OH)(2)D(3) on experimental allergic asthma in WT mice was an increased expression of two Th2-related genes (soluble CD23 and GATA-3) in lungs of BALB/c mice exposed to Ag" provenance.
- _4 value "Figure 2 | Extrinsic and intrinsic apoptotic signalling pathways in neurons. Black lines represent apoptotic pathways, blue lines represent survival pathways. The extrinsic death pathway is initiated by binding of the extracellular ligands, TNFa (tumour necrosis factor-a) or FAS (apoptosis antigen-1) ligand (FASL), to death receptors TNFR1 (TNF-receptor1) and FAS. TNFR1 activation leads to the formation of a TRADD RIP TRAF2 (TNF receptor death domain receptor interacting protein TNF associated factor 2) complex, which signals through the NFkB (nuclear factorkB) survival pathway (blue lines) or the JNK (cJun N teminal kinase)death pathway (black lines). RIP activates procaspase 2 and cleaves BID (BH3 (BCL2 (B-cell leukaemia/lymphoma-2) homology domain 3) interacting agonist). The TRADD FADD FLICE (TNF receptor death domain FAS associated death domain FADD like interleukin 1b) complex activates procaspase 8, triggering apoptosis through caspase 3 or cleavage of BID to tBID (truncated BID). FAS-mediated death occurs through a FADD-mediated activation of procaspase 8 or DAXX (death-associated protein )-mediated activation of JNK. JNK modifies BID to jBID, allowing its translocation to the mitochondrion and release of SMAC/DIABLO (second-mitochondrialderived activator of caspases). The intrinsic apoptotic pathway is initiated at the mitochondrion by diverse stimuli. Membrane permeabilization is mediated by BH3-only proteins, which sequester and inhibit the supression of BAX (B-cell lymphoma 2-associated protein X) by BCL2, allowing mitochondrial BAX translocation and the release of cytochrome c (Cyto c), SMAC/DIABLO, AIF (apoptosis-inducing factor) and HTRA2/OMI (high temperature requirement serine protease 2)." provenance.
- _3 value "Oxidative stress plays a role in the light damage model of retinal degeneration as well as in age-related macular degeneration. The purpose of this study is to identify retinal genes induced by acute photo-oxidative stress, which may function as mediators of apoptosis or as survival factors. To accomplish this, Balb/c mice were exposed to bright cool white fluorescent light for 7 hr. Retinas were then isolated for total RNA preparation followed by Affymetrix DNA microarray analysis to compare gene expression in light damaged mice to unexposed controls. Three independent light damage experiments were carried out and statistical filters were applied to detect genes with expression changes averaging at least two-fold. Quantitative PCR was carried out to confirm altered gene expression. Seventy genes were upregulated at least two-fold immediately following light damage. QPCR confirmed upregulation of all 10 genes tested. The upregulated genes fall into several categories including antioxidants: ceruloplasmin, metallothionein, and heme oxygenase; antiapoptotic gene: bag3, chloride channels: clic1 and clic4; transcription factors: c-fos, fra1, junB, stat1, krox-24 and c/ebp; secreted signaling molecules: chitinase 3-like protein 1 and osteopontin; inflammation related genes: MCP-1 and ICAM1 and others. Upregulation of five interferon-gamma responsive genes suggests elevated interferon levels after light damage. Upregulation of three components of the AP-1 transcription factor is consistent with previous evidence implicating AP-1 in light damage pathogenesis. Four copper or iron binding proteins were upregulated, suggesting that photo-oxidative stress may affect metal homeostasis. The genes found upregulated by light damage may affect the survival of photoreceptors subjected to photo-oxidative stress." provenance.
- _3 value "Oxidative stress plays a role in the light damage model of retinal degeneration as well as in age-related macular degeneration. The purpose of this study is to identify retinal genes induced by acute photo-oxidative stress, which may function as mediators of apoptosis or as survival factors. To accomplish this, Balb/c mice were exposed to bright cool white fluorescent light for 7 hr. Retinas were then isolated for total RNA preparation followed by Affymetrix DNA microarray analysis to compare gene expression in light damaged mice to unexposed controls. Three independent light damage experiments were carried out and statistical filters were applied to detect genes with expression changes averaging at least two-fold. Quantitative PCR was carried out to confirm altered gene expression. Seventy genes were upregulated at least two-fold immediately following light damage. QPCR confirmed upregulation of all 10 genes tested. The upregulated genes fall into several categories including antioxidants: ceruloplasmin, metallothionein, and heme oxygenase; antiapoptotic gene: bag3, chloride channels: clic1 and clic4; transcription factors: c-fos, fra1, junB, stat1, krox-24 and c/ebp; secreted signaling molecules: chitinase 3-like protein 1 and osteopontin; inflammation related genes: MCP-1 and ICAM1 and others. Upregulation of five interferon-gamma responsive genes suggests elevated interferon levels after light damage. Upregulation of three components of the AP-1 transcription factor is consistent with previous evidence implicating AP-1 in light damage pathogenesis. Four copper or iron binding proteins were upregulated, suggesting that photo-oxidative stress may affect metal homeostasis. The genes found upregulated by light damage may affect the survival of photoreceptors subjected to photo-oxidative stress." provenance.
- _3 value "Oxidative stress plays a role in the light damage model of retinal degeneration as well as in age-related macular degeneration. The purpose of this study is to identify retinal genes induced by acute photo-oxidative stress, which may function as mediators of apoptosis or as survival factors. To accomplish this, Balb/c mice were exposed to bright cool white fluorescent light for 7 hr. Retinas were then isolated for total RNA preparation followed by Affymetrix DNA microarray analysis to compare gene expression in light damaged mice to unexposed controls. Three independent light damage experiments were carried out and statistical filters were applied to detect genes with expression changes averaging at least two-fold. Quantitative PCR was carried out to confirm altered gene expression. Seventy genes were upregulated at least two-fold immediately following light damage. QPCR confirmed upregulation of all 10 genes tested. The upregulated genes fall into several categories including antioxidants: ceruloplasmin, metallothionein, and heme oxygenase; antiapoptotic gene: bag3, chloride channels: clic1 and clic4; transcription factors: c-fos, fra1, junB, stat1, krox-24 and c/ebp; secreted signaling molecules: chitinase 3-like protein 1 and osteopontin; inflammation related genes: MCP-1 and ICAM1 and others. Upregulation of five interferon-gamma responsive genes suggests elevated interferon levels after light damage. Upregulation of three components of the AP-1 transcription factor is consistent with previous evidence implicating AP-1 in light damage pathogenesis. Four copper or iron binding proteins were upregulated, suggesting that photo-oxidative stress may affect metal homeostasis. The genes found upregulated by light damage may affect the survival of photoreceptors subjected to photo-oxidative stress." provenance.
- _3 value "Oxidative stress plays a role in the light damage model of retinal degeneration as well as in age-related macular degeneration. The purpose of this study is to identify retinal genes induced by acute photo-oxidative stress, which may function as mediators of apoptosis or as survival factors. To accomplish this, Balb/c mice were exposed to bright cool white fluorescent light for 7 hr. Retinas were then isolated for total RNA preparation followed by Affymetrix DNA microarray analysis to compare gene expression in light damaged mice to unexposed controls. Three independent light damage experiments were carried out and statistical filters were applied to detect genes with expression changes averaging at least two-fold. Quantitative PCR was carried out to confirm altered gene expression. Seventy genes were upregulated at least two-fold immediately following light damage. QPCR confirmed upregulation of all 10 genes tested. The upregulated genes fall into several categories including antioxidants: ceruloplasmin, metallothionein, and heme oxygenase; antiapoptotic gene: bag3, chloride channels: clic1 and clic4; transcription factors: c-fos, fra1, junB, stat1, krox-24 and c/ebp; secreted signaling molecules: chitinase 3-like protein 1 and osteopontin; inflammation related genes: MCP-1 and ICAM1 and others. Upregulation of five interferon-gamma responsive genes suggests elevated interferon levels after light damage. Upregulation of three components of the AP-1 transcription factor is consistent with previous evidence implicating AP-1 in light damage pathogenesis. Four copper or iron binding proteins were upregulated, suggesting that photo-oxidative stress may affect metal homeostasis. The genes found upregulated by light damage may affect the survival of photoreceptors subjected to photo-oxidative stress." provenance.
- _3 value "Oxidative stress plays a role in the light damage model of retinal degeneration as well as in age-related macular degeneration. The purpose of this study is to identify retinal genes induced by acute photo-oxidative stress, which may function as mediators of apoptosis or as survival factors. To accomplish this, Balb/c mice were exposed to bright cool white fluorescent light for 7 hr. Retinas were then isolated for total RNA preparation followed by Affymetrix DNA microarray analysis to compare gene expression in light damaged mice to unexposed controls. Three independent light damage experiments were carried out and statistical filters were applied to detect genes with expression changes averaging at least two-fold. Quantitative PCR was carried out to confirm altered gene expression. Seventy genes were upregulated at least two-fold immediately following light damage. QPCR confirmed upregulation of all 10 genes tested. The upregulated genes fall into several categories including antioxidants: ceruloplasmin, metallothionein, and heme oxygenase; antiapoptotic gene: bag3, chloride channels: clic1 and clic4; transcription factors: c-fos, fra1, junB, stat1, krox-24 and c/ebp; secreted signaling molecules: chitinase 3-like protein 1 and osteopontin; inflammation related genes: MCP-1 and ICAM1 and others. Upregulation of five interferon-gamma responsive genes suggests elevated interferon levels after light damage. Upregulation of three components of the AP-1 transcription factor is consistent with previous evidence implicating AP-1 in light damage pathogenesis. Four copper or iron binding proteins were upregulated, suggesting that photo-oxidative stress may affect metal homeostasis. The genes found upregulated by light damage may affect the survival of photoreceptors subjected to photo-oxidative stress." provenance.
- _5 value "mPus1p pseudouridylates coactivator Steroid Receptor RNA Activator (SRA), and when coexpressed, mPus1p and SRA cooperatively enhance mRARgamma-mediated transcription." provenance.
- _5 value "LPS-binding protein (LBP) and soluble CD14 increased the sensitivity of TLR4-expressing epithelial cells to LPS but were not able to mediate LPS activation of these cells in the absence of soluble MD-2." provenance.
- _4 value "Here we show that hypoxia induces a transient increase in the activity of apoptosis signal-regulating kinase 1 (ASK-1)" provenance.
- _2 value "The recently discovered mitochondrial and nuclear Grx (Grx2) differs from the more abundant cytosolic Grx (Grx1) by its higher affinity toward S-glutathionylated proteins and by being a substrate for thioredoxin reductase. Here, we have successfully established a method to silence the expression of Grx2 in HeLa cells by using short interfering RNA to study its role in the cell. Cells with levels of Grx2 of the control were dramatically sensitized to cell death induced by doxorubicin/adriamycin and phenylarsine oxide but did not show signs of a general increase in oxidative damage with respect to carbonylation and glutathionylation." provenance.
- _5 value "wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed." provenance.
- _5 value "wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed." provenance.
- _5 value "wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed." provenance.
- _5 value "wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed." provenance.
- _5 value "wenty-eight of 150 serum-inducible genes were found to be MKL-dependent. The promoters of the serum-inducible genes were analyzed for SRF binding sites and other common regulatory elements. Putative SRF binding sites were found at a higher rate than in a mouse promoter database but were only identified in 12% of the serum-inducible promoters analyzed." provenance.
- _3 value "Treatment with progesterone (P4) resulted in the induction of CaBP-9k mRNA, and a co-treatment with estrogen (E2) plus P4 evoked a synergic effect on its mRNA level in this tissue. translation of CaBP-9k protein was enhanced by E2, while no difference was observed at the transcriptional level. E2 stimulated the expression levels of ERalpha and PR mRNAs and P4 inhibited the expression of these transcripts at an early time point (12 h) and increased them at 24 and 48 h" provenance.
- _3 value "By contrast, suppressing NF-kappaB inhibition through anti-TNFalpha treatment or induction of IkappaB-super-repressor in later stages of tumour development resulted in apoptosis of transformed hepatocytes and failure to progress to hepatocellular carcinoma. " provenance.
- _4 value "On the normal diet, serum leptin levels of Pik3r1(-/-) mice were significantly higher than in wild-type mice as a result of increased leptin secretion from adipocytes, presumably due to the increased PtdIns(3,4,5)P3 production in adipocytes." provenance.
- _4 value "Binding of AICD to X11alpha was associated with decreased nuclear levels of AICD. (E) Co-expression of Tip60 had no effect on the extranuclear localization of either X11alpha or AICD." provenance.
- _4 value "KGF alone greatly stimulated proliferation and increased cyclin-dependent kinase (cdk) 2 kinase activity and Retinoblastoma susceptibility gene product (Rb) phosphorylation. Cyclin D1, cdk2, and cdc25A protein levels were increased, and p15(Ink4b) and p27(Kip1) protein levels were decreased. (KGF = FGF7)" provenance.
- _4 value "KGF alone greatly stimulated proliferation and increased cyclin-dependent kinase (cdk) 2 kinase activity and Retinoblastoma susceptibility gene product (Rb) phosphorylation. Cyclin D1, cdk2, and cdc25A protein levels were increased, and p15(Ink4b) and p27(Kip1) protein levels were decreased. (KGF = FGF7)" provenance.
- _3 value "In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were investigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. # Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were investigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. # Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were investigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. # Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were investigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. # Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were investigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. # Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were investigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. # Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 1. Temporal- and tissue-specific genes related to glycolysis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 1. Temporal- and tissue-specific genes related to glycolysis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 1. Temporal- and tissue-specific genes related to glycolysis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 1. Temporal- and tissue-specific genes related to glycolysis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 1. Temporal- and tissue-specific genes related to glycolysis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 1. Temporal- and tissue-specific genes related to glycolysis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 1. Temporal- and tissue-specific genes related to glycolysis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 2. Temporal- and tissue-specific genes related to calcium homeostasis up-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "Table 3. Temporal- and tissue-specific genes related to growth down-regulated by hypoxia in the rat fetus " provenance.
- _3 value "In addition, we found that SCN3B levels are upregulated in human cancer cell lines by DNA damaging agents, as well as by overexpression of p53, but not significantly by p63 or p73." provenance.
- _3 value "from full text - Table 4 PGE2- and AE1-329-induced genes not altered upon differentiation treatment" provenance.
- _5 value "The inhibition of PI3K by LY294002 inhibited p70S6K1 and HDM2 activity in the cells." provenance.
- _6 value "The hypertrophic effect of CT-1 was essentially mediated by STAT3, independent of PI3-K, and negatively regulated by ERK1/2 via inhibiting the phosphorylation of STAT3." provenance.
- _3 value "Systemic treatment with pioglitazone increased systemic insulin sensitivity and increased apoE mRNA levels in adipose tissue by 2-3-fold. Treatment of cultured 3T3-L1 adipocytes with ciglitazone increased apoE mRNA levels by 2-4-fold in a dose-dependent manner and increased apoE secretion from cells." provenance.
- _3 value "Systemic treatment with pioglitazone increased systemic insulin sensitivity and increased apoE mRNA levels in adipose tissue by 2-3-fold. Treatment of cultured 3T3-L1 adipocytes with ciglitazone increased apoE mRNA levels by 2-4-fold in a dose-dependent manner and increased apoE secretion from cells." provenance.
- _3 value "Treatment with forskolin, an activator of adenylyl cyclase, restored both CREB-1 and pCREB-1 levels; this resulted in the restoration of CRE-binding, CRE-reporter activity, and CREB-1 and RFC mRNA levels" provenance.
- _3 value "Fig. 3A. Genes identified in differentiation pattern 2" provenance.
- _3 value "Fig. 4. Genes identified in differentiation pattern 3" provenance.
- _3 value "Fig. 5. Genes identified in differentiation pattern 4" provenance.
- _3 value "Furthermore, RNAi-mediated reduction of SKAR decreases cell size." provenance.
- _6 value "RESULTS: Here we identify SKAR as a novel and specific binding partner and substrate of S6K1 but not S6K2. We find that serines 383 and 385 of human SKAR are insulin-stimulated and rapamycin-sensitive S6K1 phosphorylation sites." provenance.
- _7 value "The interaction was confirmed in intact cells by coimmunoprecipitation and colocalization detected using confocal microscopy. We were then able to demonstrate that Sgk1 phosphorylated PMM2 in an in vitro assay. In addition, we found that the enzymatic activity of PMM2 is upregulated by insulin treatment and that Sgk1 completely inhibits PMM2 activity both in the absence and in the presence of insulin stimulation." provenance.
- _3 value "Overexpression of Hath1 in HT29, an aggressive colon cancer cell line, resulted in a significant inhibition on cell proliferation, anchorage-independent growth in soft agar and, more importantly, growth of human colon cancer cell xenografts in athymic nude mice." provenance.
- _6 value "CITED4 blocks the binding of hypoxia-inducible factor 1alpha to p300 in vitro and inhibits hypoxia-inducible factor-1alpha transactivation" provenance.
- _5 value "First, AMPK triggered the acetylation of importin alpha1 on Lys(22), a process dependent on the acetylase activity of p300. Second, AMPK phosphorylated importin alpha1 on Ser(105)" provenance.
- _4 value "Inhibition of COX-2 by acetyl salicylic acid (1 mM), NS-398 (5 microM), or celecoxib (3 microM) abolished the increase in cAMP and markedly reduced alpha(2C)-AR induction in response to serum stimulation." provenance.
- _3 value "The physiological role of alpha(2)-adrenoceptors (alpha(2)-ARs) in cutaneous, arteriolar, vascular smooth muscle cells (VSMs) is to mediate cold-induced constriction." provenance.
- _3 value "TG (50 microM) induced GLUT4 and h-caldesmon expression in 24-h culture of explanted carotid arteries of DOCA salt-hypertensive rats," provenance.
- _3 value "The expression of activated, phosphorylated Akt was increased by PGJ(2) and TG with no significant effect on total Akt levels." provenance.
- _4 value "Although total Rac1 protein was not changed in KO VSMCs, the level of the Rac guanine exchange factor (GEF), Sos1, was decreased." provenance.
- _3 value "Similar to 25 mM glucose, addition of rhCTGF increased MMP-2, TIMP-1, and TIMP-3 mRNA by 2.5-, 2.1-, and 1.6-fold, respectively (P < 0.05) but had no effect on membrane-type (MT)1-MMP or TIMP-2." provenance.
- _3 value "E2 rapidly decreased the expression of Txnip, but increased the levels of cytosolic Txn1 and Txnrd1 as well as mitochondrial Txn2. Using the ER antagonist, ICI 182,780, and mice lacking functional estrogen receptor alpha (ERalpha), we demonstrate that these E2-mediated changes require ERalpha, but not ERbeta" provenance.
- _3 value "we then determined the mRNA levels of Txn1 and the Txnrd3 genes and found that these levels also increased after E2 treatment, with approximately 4-fold induction at the 24-h point for Txn1 and 2.5-fold induction for Txnrd3" provenance.
- _3 value "Consistent with numerous previous reports, we observed that EGF stimulated colony formation in this assay. Fig6A. This effect was completely blocked when LRIG1 was co-expressed, but LRIG1 expression was not able to suppress transformation induced by H-Ras (not shown)." provenance.
- _4 value "We demonstrate that up-regulation of SNARK in response to CD95 ligand and tumor necrosis factor alpha depends on activation of NF-kappaB." provenance.
- _4 value "NF-kB may also up-regulate the expression of pro-apoptotic genes such as Fas ligand, Fas (Cd95), c-myc and p53, thereby sensitizing cells to apoptotic stimuli.[96 ? 98]" provenance.
- _3 value "NO exhibits anti-inflammatory properties which is associated with inhibition of the expression of adhesion molecule (VCAM-1,ICAM-1, E-selectin) and cytokines (IL-8 and IL-6).[100,103,104]" provenance.
- _2 value "ROS are also implicated in the oxidized LDLinduced NF-kB activation, as assessed by the inhibitory effect of antioxidants.[46,59,60]" provenance.
- _5 value "oxidized LDLs inhibit the LPS-induced NF-kB activation and subsequent expression of TNF-a, IL-1b and PAF-receptor in macrophages.[9,64 ? 67]" provenance.
- _4 value "?Oxidized low-density lipoprotein impairs the anticoagulant function of tissue-factor-pathway inhibitor through oxidative modification by its high association and accelerated degradation in cultured human endothelial cells" provenance.
- _4 value "We found that KGF induces a dose- and time-dependent increase in Akt kinase activity and that, as expected, activation of Akt via KGF is PI3K dependent." provenance.
- _5 value "IL-15 promoted specific recruitment of NFAT1 but not NFAT2 to the CX3CR1 promoter, whereas IL-2 had the converse effect." provenance.
- _5 value "The downregulated connexin32 expression was inhibited by treatment with a MAP-kinase inhibitor (PD98059), whereas the upregulated claudin-2 expression was blocked by p38 MAP and PI3-kinase inhibitors (SB203580 and LY294002)" provenance.
- _5 value "Jung et al. [36] recently investigated TNF-a-induced HIF-1a accumulation and demonstrated that an NFkB-mediated event that is normally associated with inflammation and cell survival caused protein accumulation in normoxic cells. Although the report fails to identify the mechanism of HIF-1a accumulation, it is suggested that this might interfere with the pVHL-mediated HIF-1a degradation process. Further studies support the concept of a pVHL-dependent cytotoxicity to TNF-a in RCC cells [37,38]. In particular, it has been reported that RCC cells can be sensitized to TNF-a-induced cytotoxicity by re-introducing wild-type VHL [38]. The authors highlight the fact that TNFreceptor engagement by TNF-a triggers the activation of atypical protein kinase C (aPKC), which, through IKKb phosphorylation, liberates NFkB, thereby initiating the transcription of genes that are involved in apoptosis." provenance.
- _4 value "Several reports have demonstrated that the inactivation of pVHL tumour suppressor function is linked to abnormal extracellular fibronectin arrays in both RCC cells that lack functional pVHL and VHLK-K mouse fibroblasts [44 to 46]. However, the exact nature of such an association and the mechanism by which VHL regulates the assembly of this ECM remain poorly understood. Nevertheless, the restored ability of pVHL-positive transfectants to assemble extracellular fibronectin was mediated by b1 integrins, implying that pVHL controls ECM assembly, at least in part, through integrin signalling [46]." provenance.
- _4 value "Human X box binding protein 1 (XBP-1) is a transcription factor essential for hepatocyte growth, the differentiation of plasma cells, and the unfolded protein response" provenance.
- _6 value "These data identify a novel function of XBP-1 and suggest that regulation of large-scale chromatin unfolding by XBP-1 may be responsible for the enhancement of ERalpha transcriptional activity." provenance.
- _4 value "Using immunoprecipitation assays, we showed that the neuregulin-1beta1 (NRG1beta1) stimulus induced ErbB4 tyrosine phosphorylation and phosphatidylinositol 3-kinase (PI3K) recruitment and activation (as demonstrated by Akt phosphorylation) either directly (ErbB4 cyt1 isoform) or indirectly (ErbB4 cyt2 isoform). " provenance.
- _4 value "Signaling through CD70 on B cells was dependent on the initiation of both PI3K and MEK pathways." provenance.
- _5 value "Inhibition of HDAC3 expression by RNA interference resulted in increased ATF-2 activation in response to LPS stimulation." provenance.
- _4 value "This increase in GMCSF expression was completely inhibited by pretreatment with CSE (Fig. 4A). LPS also induced a 2000-fold increase in IL-8 mRNA expression at 180 min in Beas-2B cells (Fig. 4B). This increase in IL-8 expression was also inhibited by CSE (Fig. 4B)." provenance.
- _3 value "siRNAs that inhibit or enhance DR4- or DR5-mediated cell death" provenance.
- _3 value "siRNAs that inhibit or enhance DR4- or DR5-mediated cell death" provenance.
- _5 value "siRNAs that inhibit or enhance DR4- or DR5-mediated cell death" provenance.
- _3 value "siRNAs that inhibit or enhance DR4- or DR5-mediated cell death" provenance.
- _3 value "siRNAs that inhibit or enhance DR4- or DR5-mediated cell death" provenance.
- _4 value "Overexpression of PTPRO in A549 cells inhibited anchorage-independent growth, delayed reentry of the cells into the cell cycle after release from cell-cycle arrest, and increased susceptibility of the cells to apoptosis." provenance.
- _4 value "evaluating the effect of the FAS inhibitor triclosan on rat mammary carcinogenesis." provenance.
- _4 value "DAX-1 negatively regulates steroid synthesis through the inhibition of StAR expression" provenance.
- _3 value "A key component of the tanning process is the UV-mediated induction of the pro-opiomelanocortin (POMC) and MC1R genes" provenance.
- _5 value "Here we have shown that UV-induced activation of the POMC and MC1R promoters is mediated by p38 stress-activated kinase signaling to the transcription factor, upstream stimulating factor-1 (USF-1)." provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.
- _3 value "TABLE 1 Overlap in alterations of gene expression induced by lovastatin, simvastatin, and pravastatin in the cerebral cortex of C57BL/6 mice" provenance.