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• _3 value "TABLE 2 Genes that change in transition from non-tumor tissue in non-smokers (Nns) to tumor tissue in non-smokers (Tns). All fold changes are greater than or equal to 1.3. NOTE: THIS TABLE WAS PUT IN AS CAUSAL FOR THE PURPOSES OF THE INDICATED PROJECT ONLY. IT IS CLEARLY NOT CAUSAL BUT CORRELATIVE [BCD]." provenance.
• _4 value "Supershift analyses revealed that oxLDL stimulates binding of the transcription factors Nrf1, Nrf2, and c-jun to the AREs" provenance.
• _3 value "PURPOSE: To understand the genetic regulatory pathways underlying the retinoic acid (RA) induction of cone arrestin, gene array technology and other molecular tools were used to profile global gene expression changes in human retinoblastoma cells. METHODS: Weri-Rb-1 retinoblastoma cells were cultured in the absence or presence of RA for various periods. DNA microarray analysis profiled gene expression followed by real-time PCR and Northern and immunoblot analyses to confirm the change in expression of selected retinal genes and their gene products. Additional methodology included flow cytometry analysis, immunocytochemistry, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. RESULTS: DNA microarray analysis of approximately 6800 genes revealed RA-induced upregulation of cone-specific genes and downregulation of rod-specific genes in Weri-Rb-1 cells. Other significantly upregulated mRNAs included chicken ovalbumin upstream promoter-transcription factor (COUP-TF1), retinoid X receptor (RXR)-gamma, thyroid hormone receptor (TR)-beta2, and guanylyl cyclase-activating protein (GCAP)-1. Real-time PCR and/or Northern blot analysis confirmed the expression changes of a subset of genes including the upregulation of a pineal- and retina-specific transcription factor, CRX. RA treatment also led to G(0)/G(1) cell cycle arrest and increased both the intensity of human cone arrestin (hCAR)-immunoreactivity and the number of apoptotic cells. The cell-cycle-arrest stage correlated with the observed microarray results in which the RA treatment downregulated critical genes such as cyclins (cyclin E, cyclin D3) and cyclin-dependent kinases (CDK5, CDK10). CONCLUSIONS: These data suggest that RA induces a subpopulation of retinoblastoma cells to differentiate toward a cone cell lineage while selectively leading other cells into apoptosis." provenance.
• _3 value "PURPOSE: To understand the genetic regulatory pathways underlying the retinoic acid (RA) induction of cone arrestin, gene array technology and other molecular tools were used to profile global gene expression changes in human retinoblastoma cells. METHODS: Weri-Rb-1 retinoblastoma cells were cultured in the absence or presence of RA for various periods. DNA microarray analysis profiled gene expression followed by real-time PCR and Northern and immunoblot analyses to confirm the change in expression of selected retinal genes and their gene products. Additional methodology included flow cytometry analysis, immunocytochemistry, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. RESULTS: DNA microarray analysis of approximately 6800 genes revealed RA-induced upregulation of cone-specific genes and downregulation of rod-specific genes in Weri-Rb-1 cells. Other significantly upregulated mRNAs included chicken ovalbumin upstream promoter-transcription factor (COUP-TF1), retinoid X receptor (RXR)-gamma, thyroid hormone receptor (TR)-beta2, and guanylyl cyclase-activating protein (GCAP)-1. Real-time PCR and/or Northern blot analysis confirmed the expression changes of a subset of genes including the upregulation of a pineal- and retina-specific transcription factor, CRX. RA treatment also led to G(0)/G(1) cell cycle arrest and increased both the intensity of human cone arrestin (hCAR)-immunoreactivity and the number of apoptotic cells. The cell-cycle-arrest stage correlated with the observed microarray results in which the RA treatment downregulated critical genes such as cyclins (cyclin E, cyclin D3) and cyclin-dependent kinases (CDK5, CDK10). CONCLUSIONS: These data suggest that RA induces a subpopulation of retinoblastoma cells to differentiate toward a cone cell lineage while selectively leading other cells into apoptosis." provenance.
• _3 value "PURPOSE: To understand the genetic regulatory pathways underlying the retinoic acid (RA) induction of cone arrestin, gene array technology and other molecular tools were used to profile global gene expression changes in human retinoblastoma cells. METHODS: Weri-Rb-1 retinoblastoma cells were cultured in the absence or presence of RA for various periods. DNA microarray analysis profiled gene expression followed by real-time PCR and Northern and immunoblot analyses to confirm the change in expression of selected retinal genes and their gene products. Additional methodology included flow cytometry analysis, immunocytochemistry, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. RESULTS: DNA microarray analysis of approximately 6800 genes revealed RA-induced upregulation of cone-specific genes and downregulation of rod-specific genes in Weri-Rb-1 cells. Other significantly upregulated mRNAs included chicken ovalbumin upstream promoter-transcription factor (COUP-TF1), retinoid X receptor (RXR)-gamma, thyroid hormone receptor (TR)-beta2, and guanylyl cyclase-activating protein (GCAP)-1. Real-time PCR and/or Northern blot analysis confirmed the expression changes of a subset of genes including the upregulation of a pineal- and retina-specific transcription factor, CRX. RA treatment also led to G(0)/G(1) cell cycle arrest and increased both the intensity of human cone arrestin (hCAR)-immunoreactivity and the number of apoptotic cells. The cell-cycle-arrest stage correlated with the observed microarray results in which the RA treatment downregulated critical genes such as cyclins (cyclin E, cyclin D3) and cyclin-dependent kinases (CDK5, CDK10). CONCLUSIONS: These data suggest that RA induces a subpopulation of retinoblastoma cells to differentiate toward a cone cell lineage while selectively leading other cells into apoptosis." provenance.
• _5 value "PhosphoElm data from PMID 15212693" provenance.
• _4 value "The enzyme is inhibited by several compounds including quercitin, ethacrynic acid, indomethacin and sodium valproate." provenance.
• _3 value "cAMP synthesis by the enzyme adenylyl cyclase" provenance.
• _5 value "Table I. FKHR activation augments the expresson of genes involved in myotube fusion" provenance.
• _4 value "CT105 (beta-secretase product of APP) in presence of IFN-gamma induced CREB phosphorylation on ser-133." provenance.
• _5 value "apigenin, a selective casein kinase 2 (CK2) inhibitor, was found to inhibit response% IFN-gamma stimulated CK2 activity and the level of phosphorylated cAMP response element-binding protein, which is known to induce ICER gene transcription, and this response was inhibited in the presence of apigenin." provenance.
• _4 value "The splicing of the c-src exon N1 is controlled by an intricate combination of positive and negative RNA elements. Most previous work on these sequences focused on intronic elements found upstream and downstream of exon N1. However, it was demonstrated that the 5' half of the N1 exon itself acts as a splicing enhancer in vivo. Here we examine the function of this regulatory element in vitro. We show that a mutation in this sequence decreases splicing of the N1 exon in vitro. Proteins binding to this element were identified as hnRNP A1, hnRNP H, hnRNP F, and SF2/ASF by site-specific cross-linking and immunoprecipitation. The binding of these proteins to the RNA was eliminated by a mutation in the exonic element. The activities of hnRNP A1 and SF2/ASF on N1 splicing were examined by adding purified protein to in vitro splicing reactions. SF2/ASF and another SR protein, SC35, are both able to stimulate splicing of c-src pre-mRNA. However, splicing activation by SF2/ASF is dependent on the N1 exon enhancer element whereas activation by SC35 is not. In contrast to SF2/ASF and in agreement with other systems, hnRNP A1 repressed c-src splicing in vitro. The negative activity of hnRNP A1 on splicing was compared with that of PTB, a protein previously demonstrated to repress splicing in this system. Both proteins repress exon N1 splicing, and both counteract the enhancing activity of the SR proteins. Removal of the PTB binding sites upstream of N1 prevents PTB-mediated repression but does not affect A1-mediated repression. Thus, hnRNP A1 and PTB use different mechanisms to repress c-src splicing. Our results link the activity of these well-known exonic splicing regulators, SF2/ASF and hnRNP A1, to the splicing of an exon primarily controlled by intronic factors. In contrast to SF2/ASF and in agreement with other systems, hnRNP A1 repressed c-src splicing in vitro." provenance.
• _2 value "TPA, okadaic acid, and orthovanadate enhanced cell proliferation as measured by a 5-bromo-2'-deoxyuridine incorporation assay." provenance.
• _4 value "In the IFN-alpha signal transduction pathway, Jak1 phosphorylation induced by IFN-alpha is dramatically suppressed in MeV-infected cells; however, phosphorylation induced by IFN-gamma is not. [From Materials and Methods] Rabbit antibodies against Tyr1022/1023-phosphorylated Jak1 and Tyr1007/1008-phosphorylated Jak2 were acquired from BioSource International (Camarillo, CA)." provenance.
• _3 value "The following table is supplemental material from highwire." provenance.
• _5 value "We have found that activation of the MEK5-ERK5 pathway causes the phosphorylation and stabilization of c-Fos and Fra-1.Phosphorylation of c-Fos appears to be mediated by ERK5 and a kinase(s) lying downstream of ERK5, and the MEK5-ERK5 pathway-dependent phosphorylation sites on c-Fos are different from the ERK1/2 pathway-dependent ones. Interestingly, activation of the MEK5-ERK5 pathway, but not that of the ERK1/2 pathway, is found to markedly increase the transactivation activity of c-Fos. Furthermore, our results show that the C-terminal half of ERK5 is necessary for the maximal activation of the transactivation activity of c-Fos and Fra-1." provenance.
• _5 value "These findings provide direct evidence that DEC1 negatively regulates the expression of DEC2, which is largely achieved through direct DNA binding to the E-box in the proximal promoter of DEC2." provenance.
• _3 value "Low-density lipoprotein (LDL) stimulated MCP-1 in a concentration-dependent manner" provenance.
• _3 value "Supporting Table 5/6. Genes having expression that was specifically up/down regulated during senescence in human fibroblasts. By using cDNA microarrays to concurrently compare the expression of 31,000 genes in senescent, quiescent, and early passage proliferating cells, we identified distinct transcriptional perturbations that characterize telomere-dependent irreversible proliferative arrest in human fibroblasts and HMECs. ##Statistics: Pearson correlation coefficients were calculated between pairs of microarrays using all spots that satisfied filter parameters. A modified t-score (32) was used to determine the significance of transcriptional alterations. We permuted data from all spots randomly 5,000 times to determine the rate at which random data exceeded modified t-score thresholds and defined this value as the false positive rate (FPR). To estimate the false negative rate (FNR), we randomly selected 30 genes whose expression exceeded the modified t-score thresholds and added log2(R/G) ratios randomly selected from spots that passed data filters (i.e., ?noise?); FNR was defined by how frequently the average expression level of these proband genes became negative after noise was added. Calculated FPR and FNR values assume that none of the changes in randomly selected data have biological significance. Additionally, as the selection of t-score thresholds that produced nonoverlapping gene groupings constrained the independence of FPRs and FNRs, the calculated FPR and FNR values for some gene groupings are overestimates. ##" provenance.
• _5 value "TBL1 and TBLR1 are functionally redundant but essential for repression by unliganded thyroid hormone receptor." provenance.
• _4 value "NGF has previously been shown to increase Tau protein expression in PC12 cells (Sado et al., 1995 )." provenance.
• _5 value "ciliary neurotrophic factor, CNTF, activation of gp130 in NSCs rapidly increased Notch1 expression" provenance.
• _5 value "Here we report that Itgb6-null mice develop age-related emphysema that is completely abrogated either by transgenic expression of versions of the beta6 integrin subunit that support TGF-beta activation, or by the loss of Mmp12. Furthermore, we show that the effects of Itgb6 deletion are overcome by simultaneous transgenic expression of active TGF-beta1." provenance.
• _3 value "Vascular endothelial growth factors (VEGFs), acting through a family of tyrosine kinase receptors,VEGFRs, are the key stimulators of endothelial-cell growth10,11.Other factors, such as angiopoietins and platelet-derived growth factors (PDGFs), recruit supporting cells." provenance.
• _3 value "In post-menopausal women, local oestrogen synthesis relies on aromatase." provenance.
• _4 value "PGE2 can activate prostaglandin E receptors on breast cancer cells, which increase cAMP levels and activate aromatase expression." provenance.
• _2 value "overexpression of NCOA1 increases tamoxifen's agonist activity in experimental cell systems105,106 treatment of breast cancer cell lines with the HDAC inhibitor Trichostatin A (TSA) inhibited their proliferation." provenance.
• _2 value "overexpression of NCOA1 increases tamoxifen's agonist activity in experimental cell systems105,106 treatment of breast cancer cell lines with the HDAC inhibitor Trichostatin A (TSA) inhibited their proliferation." provenance.
• _5 value "TPA-induced genes, such as Sprr1A, Saa3, JunB, Il4ralpha, Gp38, RalGDS and Slpi" provenance.
• _5 value "TPA-induced genes, such as Sprr1A, Saa3, JunB, Il4ralpha, Gp38, RalGDS and Slpi" provenance.
• _4 value "both EP1 and EP3 are required for adrenocorticotropic hormone release in response to LPS." provenance.
• _2 value "Uteroplacental insufficiency and subsequent intrauterine growth retardation (IUGR) increase the risk of insulin resistance in humans and rats." provenance.
• _3 value "Using differential display analysis, we identified eight down-modulated clones in exposed cells: 26S proteasome non-ATPase subunit Pad1, ubiquitin-conjugating enzyme Ube2i, extracellular proteinase inhibitor Expi or Wdnm1, cytochrome-c oxidase Cox7c, microtubule-associated protein-1 light chain-3 (Map1lc3), nascent-associated complex alpha Naca, transforming acidic coiled-coil Tacc3, stearoyl-CoA desaturase (Scd), keratin 6 alpha," provenance.
• _4 value "A catalytically active SGK is produced after cellular exposure to a variety of extracellular signals, such as serum growth factors [3, 22], insulin or IGF-1 [22, 49, 50], oxidative stress [22, 49], hyperosmotic conditions [31] and glucocorticoids (P. Buse et al. , manuscript submitted)." provenance.
• _4 value "The functionally defined DNA elements in the SGK promoter have been established for the glucocorticoid receptor (GR), p53 tumor suppressor protein (p53), and a Sp1 site that is a downstream target of hyperosmotic stress and follicle stimulating hormone." provenance.
• _4 value "heat shock stimulates SGK expression (M. L. L. Leong, et al., J. Biol. Chem., in press), and the SGK promoter contains consensus binding sites for HSF and ATF6 (hatched boxes labeled HSF and ATF6 in figure 2), which are activated by heat shock and the unfolded protein response in cells." provenance.
• _4 value "heat shock stimulates SGK expression (M. L. L. Leong, et al., J. Biol. Chem., in press), and the SGK promoter contains consensus binding sites for HSF and ATF6 (hatched boxes labeled HSF and ATF6 in figure 2), which are activated by heat shock and the unfolded protein response in cells." provenance.
• _5 value "the SGK promoter contains consensus DNA elements for Smad and Fast-1 binding (hatched boxes labeled SMAD 3/4 and Fast-1 in figure 2) that are activated by TGF-beta receptor signaling, This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4. The association with SMAD4 is important for the translocation of this protein into the nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors. This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants encoding the same protein have been observed." provenance.
• _5 value "the SGK promoter contains consensus DNA elements for Smad and Fast-1 binding (hatched boxes labeled SMAD 3/4 and Fast-1 in figure 2) that are activated by TGF-beta receptor signaling, This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4. The association with SMAD4 is important for the translocation of this protein into the nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors. This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants encoding the same protein have been observed." provenance.
• _6 value "TIMP3 blocks the binding of VEGF to VEGF receptor-2 and inhibits downstream signaling and angiogenesis" provenance.
• _5 value "PTH- and 1,25-(OH)2 Vitamin D3-induced bone resorption could also be inhibited by catalase" provenance.
• _4 value "The angiogenic switch can be induced at a predictable time and usually more rapidly, by introduction of oncogenes into the tumors. When the human non-angiogenic osteosarcoma was transfected with the ras oncogene, neovascularized tumors appeared within 2 weeks [7]." provenance.
• _3 value "The profound effects of 17beta-estradiol on cell growth, differentiation, and general homeostasis of the reproductive and other systems, are mediated mostly by regulation of temporal and cell type-specific expression of different genes. In order to understand better the molecular events associated with the activation of the estrogen receptor (ER), we have used microarray technology to determine the transcriptional program and dose-response characteristics of exposure to a potent synthetic estrogen, 17 alpha-ethynyl estradiol (EE), during prepubertal development. Changes in patterns of gene expression were determined in the immature uterus and ovaries of Sprague-Dawley rats on postnatal day (PND) 24, 24 h after exposure to EE, at 0.001, 0.01, 0.1, 1 and 10 micro g EE/kg/day (sc), for four days (dosing from PND 20 to 23). The transcript profiles were compared between treatment groups and controls using oligonucleotide arrays to determine the expression level of approximately 7000 annotated rat genes and over 1740 expressed sequence tags (ESTs). Quantification of the number of genes whose expression was modified by the treatment, for each of the various doses of EE tested, showed clear evidence of a dose-dependent treatment effect that follows a monotonic response, concordant with the dose-response pattern of uterine wet-weight gain and luminal epithelial cell height. The number of genes whose expression is affected by EE exposure increases according to dose. At the highest dose tested of EE, we determined that the expression level of over 300 genes was modified significantly (p dose-dependent analysis of the transcript profile revealed a set of 88 genes whose expression is significantly and reproducibly modified (increased or decreased) by EE exposure (p demonstrate that, exposure to a potent estrogenic chemical during prepubertal maturation changes the gene expression profile of estrogen-sensitive tissues. Furthermore, the products of the EE-regulated genes identified in these tissues have a physiological role in different intracellular pathways, information that will be valuable to determine the mechanism of action of estrogens. Moreover, those genes could be used as biomarkers to identify chemicals with estrogenic activity." provenance.
• _3 value "The profound effects of 17beta-estradiol on cell growth, differentiation, and general homeostasis of the reproductive and other systems, are mediated mostly by regulation of temporal and cell type-specific expression of different genes. In order to understand better the molecular events associated with the activation of the estrogen receptor (ER), we have used microarray technology to determine the transcriptional program and dose-response characteristics of exposure to a potent synthetic estrogen, 17 alpha-ethynyl estradiol (EE), during prepubertal development. Changes in patterns of gene expression were determined in the immature uterus and ovaries of Sprague-Dawley rats on postnatal day (PND) 24, 24 h after exposure to EE, at 0.001, 0.01, 0.1, 1 and 10 micro g EE/kg/day (sc), for four days (dosing from PND 20 to 23). The transcript profiles were compared between treatment groups and controls using oligonucleotide arrays to determine the expression level of approximately 7000 annotated rat genes and over 1740 expressed sequence tags (ESTs). Quantification of the number of genes whose expression was modified by the treatment, for each of the various doses of EE tested, showed clear evidence of a dose-dependent treatment effect that follows a monotonic response, concordant with the dose-response pattern of uterine wet-weight gain and luminal epithelial cell height. The number of genes whose expression is affected by EE exposure increases according to dose. At the highest dose tested of EE, we determined that the expression level of over 300 genes was modified significantly (p dose-dependent analysis of the transcript profile revealed a set of 88 genes whose expression is significantly and reproducibly modified (increased or decreased) by EE exposure (p demonstrate that, exposure to a potent estrogenic chemical during prepubertal maturation changes the gene expression profile of estrogen-sensitive tissues. Furthermore, the products of the EE-regulated genes identified in these tissues have a physiological role in different intracellular pathways, information that will be valuable to determine the mechanism of action of estrogens. Moreover, those genes could be used as biomarkers to identify chemicals with estrogenic activity." provenance.
• _4 value "exposure of cholangiocytes to dibutyryl-cAMP (100 microm) resulted in co-redistribution of all three proteins to the apical cholangiocyte plasma membrane. After administration of secretin to rats in vivo, bile flow increased, and AQP1, CFTR, and AE2 co-redistributed to the apical cholangiocyte membrane" provenance.
• _4 value "exposure of cholangiocytes to dibutyryl-cAMP (100 microm) resulted in co-redistribution of all three proteins to the apical cholangiocyte plasma membrane. After administration of secretin to rats in vivo, bile flow increased, and AQP1, CFTR, and AE2 co-redistributed to the apical cholangiocyte membrane" provenance.
• _5 value "c-Src regulates NAD(P)H oxidase-derived *O2- generation acutely by stimulating p47phox phosphorylation and translocation and chronically by increasing protein content of gp91phox, p22phox, and p47phox in Ang II-stimulated cells" provenance.
• _5 value "Protein interaction studies demonstrated physical association of HDAC4 with SRF in living cells. The SRF/HDAC4 co-association was disrupted by treatment of cells with hypertrophic agonists such as angiotensin-II and a Ca2+ ionophore, ionomycin. Furthermore, activation of Ca2+/calmodulin-dependent protein kinase (CaMK)-IV prevented SRF/HDAC4 interaction and derepressed SRF-dependent transcription activity." provenance.
• _5 value "This study was aimed to determine whether beta-adrenergic receptor (beta-AR) stimulated by isoproterenol (ISO) activates signal transducers and activators of transcription (STAT) in mouse heart and, if so, to examine the underlying mechanism. We found that treatment of adult male mice by ISO (15 mg/kg body weight, intraperitoneal) caused a delayed STAT3 activation (at 60-120 min), which was fully abolished by beta-AR antagonist, propranolol. ISO-induced phosphorylation of STAT3 was markedly enhanced by phosphodiesterase inhibitor amrinone, indicating that cAMP is critically involved in beta-AR-mediated STAT3 activation. In addition, beta-AR stimulation significantly increased gene expression of interleukin-6 (IL-6) family of cytokines (IL-6, leukemia inhibitory factor, ciliary neurotrophic factor, and cardiotrophin-1). IL-6 protein levels in serum and mouse myocardium were also significantly increased in response to ISO treatment. In cultured cardiac fibroblasts, IL-6 level was enhanced significantly after ISO (10-6 mol/liter) stimulation for 2 h and then peaked at 12 h, whereas the response of IL-6 in cultured cardiomyocytes to ISO stimulation was not significant, suggesting that ISO-induced increase in IL-6 is primarily from cardiac fibroblasts rather than cardiomyocytes. Most importantly, IL-6 could activate STAT3 in a time-dependent manner in cultured cardiomyocytes, and inhibition of IL-6 level by anti-IL-6-neutralizing antibody clearly attenuated ISO-induced phosphorylation of STAT3 in myocardium. Taken together, these results indicate that beta-AR stimulation leads to a delayed STAT3 activation via an IL-6 family of cytokine-mediated pathway and that cardiac fibroblasts, but not cardiomyocytes, is probably the predominant source of IL-6 in response to ISO stimulation in mouse myocardium." provenance.
• _4 value "# Ariadne: Studies of WT cells indicated that TNF caused increased expression of c-Jun, JunB, JunD, c-Fos, Fra1, and Fra2 (Fig. 3 ). [Expression]" provenance.
• _4 value "The JNK-deficient cells exhibited decreased expression of c-Jun, JunD, c-Fos, Fra1, and Fra2; decreased phosphorylation of c-Jun and JunD; and decreased AP-1 DNA binding activity." provenance.
• _5 value "Modified assertion" provenance.
• _6 value "Human PGC1beta-1a and -2a isoforms localized to the cell nucleus and, specifically, the isoform PGC1beta-1a co-activated peroxisome-proliferator-activated receptor-gamma, -alpha and the thyroid hormone receptor beta1." provenance.
• _4 value "Glucose (11.1 and 22.2 mm) induced a parallel decrease in PMCA transcription, expression, and activity. In contrast the sugar induced a parallel increase in NCX transcription, expression, and activity." provenance.
• _4 value "an important example of DNA-independent actions of steroids is transrepression of the proinflammatory transcription factors AP1 and NFKB. GR weakly interacts with and inhibits its AP1-dependent transcription without altering its DNA binding" provenance.
• _4 value "Oxidative stress induces in endothelial cells a quick and transient coactivation of both stress-activated protein kinase-2/p38 and extracellular signal-regulated kinase (ERK) mitogen-activated protein kinases. We found that inhibiting the ERK pathway resulted, within 5 min of oxidative stress, in a misassembly of focal adhesions characterized by mislocalization of key proteins such as paxillin." provenance.
• _6 value "Increased PTEN expression was required for the RRM1-induced suppression of cell motility and FAK phosphorylation." provenance.
• _5 value "Modified assertion" provenance.
• _2 value "Recently, a tocopherol-dependent transcription factor (tocopherol-associated protein) has been discovered. In cultured cells it has been demonstrated that vitamin E inhibits inflammation, cell adhesion, platelet aggregation and smooth muscle cell proliferation." provenance.
• _5 value "Modified assertion" provenance.
• _5 value "the procollagen lysyl hydroxylase (PLOD1) promoter is regulated by Nkx2.5. Mechanistically, PITX2C and Nkx2.5 synergistically regulate ANF and PLOD1 expression through binding to their respective DNA elements. Surprisingly, PITX2A activation of the ANF and PLOD1 promoters is repressed by co-transfection of Nkx2.5 in the C3H10T1/2 embryonic fibroblast cell line" provenance.
• _5 value "Modified assertion" provenance.
• _5 value "It has long been known that TN stimulates the activating cleavage of Plg by tPA, though, no details about the process have been known [2]. The present study verifies the activating ability of TN and shows that the presence of TN increases the association between tPA and Plg by 10-fold." provenance.
• _4 value "Regulation studies in mouse Y1 cells showed that cAMP down-regulates 17 beta HSDXI enzymatic activity (40% vs. 32%, P < 0.05) and reduces gene expression to undetectable levels. All-trans-retinoic acid did not affect 17 beta HSDXI expression or activity, but addition of the retinoid together with cAMP significantly decreased activity over cAMP alone." provenance.
• _5 value "# Ariadne: In some chromaffin cells, both AT1 and AT2 receptor stimulation could increase phosphorylation of Fra-2, leading to stimulation of TH mRNA production. [Regulation]" provenance.
• _5 value "PhosphoElm data from PMID 15212693" provenance.
• _4 value "downregulation of the expression of inhibitors of apoptosis proteins (IAPs) Bcl-2, Bcl-X(L), and survivin and upregulation of pro-apoptotic p53 and Bax" provenance.
• _5 value "Table 2. Genes with similar changes in expression in NOS3-/- and NOS1-/- relative to WT" provenance.
• _4 value "FTIs did not modulate bcl2, bclxL, and bclxS expression, whereas they increased inducible nitric oxide (iNOS) mRNA and protein levels, resulting in higher NO production." provenance.
• _3 value "PURPOSE: Oxidative stress (OS) is believed to be a major contributor to age-related cataract and other age-related diseases. METHODS: cDNA microarrays were used to identify the spectrum and range of genes with transcript levels that are altered in response to acute H(2)O(2)-induced OS in human lens epithelial (HLE) cells. HLE cells were treated with 50 microM H(2)O(2) for 1 hour in the absence of serum, followed by a return to complete medium. RNAs were prepared from treated and untreated cells at 0, 1, 2, and 8 hours after H(2)O(2) treatment. RESULTS: The data showed 1171 genes that were significantly up- and downregulated in response to H(2)O(2) treatment. Several functional subcategories of genes were identified, including those encoding DNA repair proteins, antioxidant defense enzymes, molecular chaperones, protein biosynthesis enzymes, and trafficking and degradation proteins. Differential expression of selected genes was confirmed at the level of RNA and/or protein. Many of the identified genes (e.g., glutathione S-transferase [MGST2], thioredoxin reductase beta, and peroxiredoxin 2) have been identified as participants in OS responses in the lens and other systems. Some genes induced by OS in the current study (e.g., oxygen regulated protein [ORP150] and heat shock protein [HSP40]) are better known to respond to other forms of stress. Two genes (receptor tyrosine kinase [AXL/ARK] and protein phosphatase 2A) are known to be differentially expressed in cataract. Most of the genes point to a novel pathways associated with OS. CONCLUSIONS: The present data provide a global perspective on those genes that respond to acute OS, point to novel genes and pathways associated with OS, and set the groundwork for understanding the functions of OS-related genes in lens protection and disease." provenance.
• _4 value "Poly(ADP-ribose) polymerase activation in turn depletes the intracellular concentration of its substrate NAD(+), slowing the rate of glycolysis, electron transport, and ATP formation, and produces an ADP-ribosylation of the GAPDH." provenance.
• _4 value "Superoxide overproduction is accompanied by increased nitric oxide generation, due to an endothelial NOS and inducible NOS uncoupled state, a phenomenon favoring the formation of the strong oxidant peroxynitrite, which in turn damages DNA." provenance.
• _4 value "These processes result in acute endothelial dysfunction in diabetic blood vessels that, convincingly, also contributes to the development of diabetic complications. These new findings may explain why classic antioxidants, such as vitamin E, which work by scavenging already-formed toxic oxidation products, have failed to show beneficial effects on diabetic complications and may suggest new and attractive \"causal\" antioxidant therapy. New low-molecular mass compounds that act as SOD or catalase mimetics or L-propionyl-carnitine and lipoic acid, which work as intracellular superoxide scavengers, improving mitochondrial function and reducing DNA damage, may be good candidates for such a strategy, and preliminary studies support this hypothesis. This \"causal\" therapy would also be associated with other promising tools such as LY 333531, PJ34, and FP15, which block the protein kinase beta isoform, poly(ADP-ribose) polymerase, and peroxynitrite, respectively. While waiting for these focused tools, we may have other options: thiazolinediones, statins, ACE inhibitors, and angiotensin 1 inhibitors can reduce intracellular oxidative stress generation," provenance.
• _3 value "elevated levels of serum leptin were observed in SPARC-null mice" provenance.
• _5 value "Further studies evaluating the calcium response that is triggered upon MCP-1 interaction with its receptor, CCR2, indicate that this response is not altered by antisense or sense ODN treatment, thus supporting our hypothesis that PKCbeta is critical for post-receptor signal transduction downstream of the immediate calcium signal." provenance.
• _5 value "BAG-1 may function to suppress the GADD34-mediated cellular stress response and support a role for BAG-1 in the survival of cells undergoing stress" provenance.
• _5 value "squamous cell carcinoma lines engineered to express constitutively active Akt underwent EMT, characterized by down-regulation of the epithelial markers desmoplakin, E-cadherin, and beta-catenin and up-regulation of the mesenchymal marker vimentin." provenance.
• _5 value "Insulin receptor-phosphorylated IRS5/DOK4 associates with RasGAP, Crk, Src, and Fyn, but not phosphatidylinositol 3-kinase p85, Grb2, SHP-2, Nck, or phospholipase Cgamma Src homology 2 domains, and activates MAPK in cells." provenance.
• _8 value "deletion and mutation studies demonstrated that the 2 LXR response elements [LXREs] in the Srebp1c promoter region are responsible for this inhibitory effect of Ppars Ppars reduce binding of LXR/RXR to LXRE" provenance.
• _4 value "ESULTS: TUDC induced a rapid activation of focal adhesion kinase (FAK) and Src, as shown by an increase in Y418 phosphorylation and a decrease in Y529 phosphorylation of Src." provenance.
• _4 value "These data further suggest that SP and NK-1R, which promote IFN-gamma synthesis, are part of the Th1 pathway of immunity." provenance.
• _6 value "Interestingly, the effect of the lipoxygenase products 13(S)-HODE and 15(S)-HETE as well as of the drug rosiglitazone were preferentially enhanced by the coactivator CREB-binding protein, whereas the effect of the cyclooxygenase product 15-deoxy-Delta(12,14)-prostaglandin J(2) was preferentially enhanced by steroid receptor coactivator-1. A way to word this?" provenance.
• _4 value "We also showed that thrombin induced dephosphorylation of beta-catenin and phosphorylation of p120. Thrombin-induced interendothelial gap formation and increased endothelial permeability were blocked by protein kinase C inhibition using chelerythrine [PKC-dependent, though obviously not directly]." provenance.
• _4 value "PhosphoElm data from PMID 15212693" provenance.
• _3 value "Another carboxyl-terminal binding partner of Cas, AND-34/BCAR3 (AND-34), functions synergistically with Cas to enhance Src activation and cell migration" provenance.
• _4 value "Interestingly, we have found that forced expression of Nkx3.2 in somitic tissue will block the induction of GATA-4, -5, and -6 by BMP signals and that repression of GATA-6 expression by Nkx3.2 requires an NBE-like sequence in the GATA-6 promoter. 3 Thus, members of the GATA gene family are potential direct targets of Nkx3.2 in vivo and therefore could potentially play a role in modulating chondrogenesis." provenance.
• _5 value "Sgt1 binds not only to S100A6 but also to S100B and S100P, other members of the S100 family." provenance.
• _5 value "p38, but not ERK or JNK, was found in a complex with Gadd45 proteins. The region of interaction was mapped to amino acids 71 to 96, and the central portion (amino acids 71 to 124) of Gadd45a was required for p38 MAPK activation in the presence of H-ras." provenance.
• _5 value "Tumor histologies appear to correlate with the specific DBDs rather than the particular TET component in these fusions." provenance.
• _5 value "Tumor histologies appear to correlate with the specific DBDs rather than the particular TET component in these fusions." provenance.
• _5 value "Tumor histologies appear to correlate with the specific DBDs rather than the particular TET component in these fusions." provenance.
• _5 value "Tumor histologies appear to correlate with the specific DBDs rather than the particular TET component in these fusions." provenance.
• _5 value "Additionally, treatment of mice with multiple Src inhibitors resulted in inhibition of phosphorylation of FAK (Y861) and of a putative Src autophosphorylation epitope (Y419) in HT-29 human colon tumor xenografts. " provenance.
• _3 value "# Ariadne: The runti homology domain transcription factors mediate repression of the bone sialoprotein promoter: evidence for a context dependent activity of Cbfa proteins. [Expression] # Ariadne: Bone sialoprotein mediates human endothelial cell attachment and migration and promotes angiogenesis. [Regulation] # Ariadne: In addition it has been demonstrated that BSP mediates human umbilical vein endothelial cell attachment and migration, thereby demonstrating an angiogenic capacity (11) . [Regulation]" provenance.
• _5 value "This study establishes that HER2/HRG signaling selectively upregulates Tyr phosphorylation of c-Src at Tyr-215 located within the SH2 domain, increases c-Src kinase activity and selectively upregulates Tyr phosphorylation of FAK at Tyr-861. HER2-overexpressing tumors showed increased levels of c-Src phosphorylation at Tyr-215. These findings suggest that HER2/HRG influence metastasis of breast cancer cells through a novel signaling pathway involving phosphorylation of FAK tyrosine 861 via activation of c-Src tyrosine 215." provenance.
• _3 value "A 2-fold increase of Cap G protein and a 5-fold increase of Cap G mRNA were observed in cells exposed to a plaque-free flow as compared with static cultures." provenance.
• _5 value "PhosphoElm data from PMID 15212693" provenance.
• _5 value "Modified assertion" provenance.
• _7 value "PPARgamma/RXR binds to a response element between -459 and -472 bp in the human SR-BI promoter." provenance.
• _6 value "Although CREB thus seems to be an important factor in the induction of PGC-1-alpha , the increased effect of CaMKIV in combination with CnA suggests that factors in addition to CREB are likely to be involved in the transcription of the PGC-1-alpha gene in muscle. Because MEF2 and NFAT transcription factors are known targets of CaMKIV and CnA in muscle fiber-type determination, we tested the role of these factors in the control of the PGC-1-alpha promoter. MEF2C, MEF2D, or NFATc3 alone did not have a significant effect on the function of the 2-kb PGC-1-alpha promoter (Fig. 2A). However, because MEF2 proteins are known to be coactivated by PGC-1-alpha (7), we also tested these factors in cotransfection experiments. As shown in Fig. 2A, a coactivation by PGC-1-alpha of both MEF2C and MEF2D, but not NFAT, was observed on the PGC-1-alpha promoter. These data suggest that PGC-1-alpha might participate in the activation of its own promoter and that the MEF2 proteins may function both in the regulation of PGC-1-alpha expression and as downstream targets of PGC-1-alpha coactivation of other muscle-selective genes." provenance.

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