Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _4 value "We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC." provenance.
- _4 value "We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC." provenance.
- _4 value "We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC." provenance.
- _4 value "We reported previously that transcription factor nuclear factor (NF)-kappaB is constitutively activated in human and murine squamous cell carcinomas (SCCs). The role of NF-kappaB in the cumulative changes in gene expression with transformation and progression of the murine SCC Pam 212 and after switching off NF-kappaB by a dominant negative inhibitor kappaB mutant (IkappaBalphaM) was explored by profiling with a 15,000-element cDNA micoarrray. Remarkably, NF-kappaB modulated the expression of 60% of the 308 genes differentially expressed between normal keratinocytes and metastatic SCCs. NF-kappaB directly or indirectly modulated expression of programs of genes functionally linked to proliferation, apoptosis, adhesion, and angiogenesis. Among these, changes in expression of cyclin D1, inhibitor of apoptosis-1, mutant Trp53, and beta-catenin detected with modulation of NF-kappaB by microarray were confirmed by Western and Northern blot. NF-kappaB DNA binding motifs were detected in the promoter of approximately 63% of genes showing increased expression and 33% of the genes showing decreased expression. The ACTACAG motif implicated in the NF-kappaB-dependent down-regulation of mRNA expression of MyoD and Sox9 was detected in the coding portion of about 15% of genes showing increased or decreased expression. Inactivation of NF-kappaB inhibited malignant phenotypic features including proliferation, cell survival, migration, angiogenesis, and tumorigenesis. These results provide evidence that NF-kappaB is an important modulator of gene expression programs that contribute to the malignant phenotype of SCC." provenance.
- _5 value "Silencing of p150(Glued) expression by small interference RNA reduced the stimulus-induced phosphorylation of MKK3/6 and p38 MAPKs. The similar adverse effect was also seen when the cytoplasmic dynein motor was disrupted by other means." provenance.
- _4 value "Similarly, the p150Glued siRNA could also specifically reduce the tumor necrosis factor -induced phosphorylation of MKK3/6 and p38 MAPK." provenance.
- _4 value "#------------------------------------------------------------------------------- Eleven genes were found to be upregulated by ANG II. These encode the proteins for ferredoxin, Nor1, Nurr1, c6orf37, CAT-1, A20, MBLL, M-Ras, RhoB, GADD45alpha, and a novel protein designated FLJ45273." provenance.
- _4 value "#------------------------------------------------------------------------------- Eleven genes were found to be upregulated by ANG II. These encode the proteins for ferredoxin, Nor1, Nurr1, c6orf37, CAT-1, A20, MBLL, M-Ras, RhoB, GADD45alpha, and a novel protein designated FLJ45273." provenance.
- _3 value "In the study reported here, we isolated a p53-regulated gene named NDRG1 (N-Myc down-regulated gene 1). Its expression is induced by DNA damage in a p53-dependent fashion. The promoter region of the NDRG1 gene contains a p53 binding site that confers p53-dependent transcriptional activation via a heterologous reporter" provenance.
- _8 value "RNA interference and inducible gene expression approaches suggest that NDRG1 is necessary but not sufficient for p53-mediated caspase activation and apoptosis." provenance.
- _5 value "VRK1 phosphorylates c-Jun in Ser63 and Ser73 in vitro, the same residues targeted by the N-terminal kinase of c-Jun (JNK). This phosphorylation induces the stabilization and accumulation of the c-Jun protein. VRK1 phosphorylates the endogenous c-Jun in Ser63. VRK1 activates c-Jun dependent transcription, which is dependent on phosphorylation of Ser63 and Ser73. The c-Jun with Ser63Ala and Ser73Ala substitutions is not transcriptionally active when cotransfected with VRK1. VRK1 interacts with c-Jun but not with JNK. The cotransfection of VRK1 and JNK has an additive effect on the transcriptional activation of c-Jun" provenance.
- _4 value "We also show that all KLF6 effects on c-Jun were largely dependent on phorbol ester (TPA/ionomycin) extracellular stimulation, which enhanced KLF6 nuclear translocation and transcriptional activity and modified its phosphorylation status." provenance.
- _8 value "It is a glycosylphosphatidylinositol(GPI)-linked cell surface receptor for both GDNF and NTN, and mediates activation of the RET tyrosine kinase receptor." provenance.
- _4 value "An early confluent culture of C2C12 cells pretreated with 10 microg/ml of cycloheximide (CHX) for 30 minutes and then treated with 300ng/ml of BMP-2 (bone morphogenetic protein2) for 1 day induced the expression of Dlx5. Moreover when Dlx5 was over-expressed by transfecting C2C12 cells with the Dlx5 expression vector, Alp expression was stimulated even in the absence of BMP-2 treatment and that Dlx5 and the product of its target gene, Runx2, stimulated ALP promoter activity in an additive manner. However, because Dlx5 continued to stimulate ALP expression in Runx2(-/-) cells, the ALP stimulatory activity of Dlx5 is independent of Runx2. Thus it suggests that Alp is a downstream target of Dlx5 and that Dlx5 and Runx5 can both regulate its expression." provenance.
- _4 value "Estradiol induced ERK activation was partially blocked (10-20%) by the EGFR antibody." provenance.
- _4 value "TGF-alpha directly binds to the EGF receptor and activates it by tyrosine phosphorylation." provenance.
- _5 value "By contrast, serum- and glucocorticoid-inducible kinase 1 (SGK1) was significantly induced in a p53-dependent manner after DNA damage, and this induction was through extracellular signal-regulated kinase 1/2-mediated posttranslational regulation." provenance.
- _2 value "Acute and 24-h hypoxia decreased JO2 of A549 cell mitochondrial complexes I, II, and III by 30-40%. Reoxygenation restored complex I activity after acute hypoxia but not after 24-h hypoxia. ATP was decreased 30% after 24-h hypoxia, but lactate production rate was not affected." provenance.
- _3 value "Furthermore, OS increased gp91phox (nox2) and nox1 mRNA levels while decreasing nox4. In contrast, BMP4 induced nox1 mRNA expression, whereas nox2 and nox4 were decreased or not affected, respectively" provenance.
- _3 value "Similar to OS, BMP4 stimulated H2O2 and O2- production in ECs." provenance.
- _3 value "These studies have shown that MCT4 and 4 proteins are transiently up-regulated by a single bout of exercise, involving post-transcriptional and transcriptional mechanisms" provenance.
- _4 value "These results suggest that PI3K mediates T3-dependent activation of Akt/PKB, mTOR, and p70S6K. More importantly it indicates that T3-dependent PI3K activation is an initial event leading to the activation of Akt/PKB, mTOR, and p70S6K." provenance.
- _4 value "Expression of MyoD and myogenin, but not of Myf5, was abrogated in FGF6 engineered mpc." provenance.
- _5 value "On the other hand, the E2-ER beta complex induced the rapid and persistent phosphorylation of p38/MAPK which, in turn, was involved in caspase-3 activation and cleavage of poly(ADP-ribose)polymerase, driving cells into the apoptotic cycle." provenance.
- _4 value "These findings suggest that clusterin may contribute to conferring resistance to oxidative stress-mediated cellular injury on prostate cancer cells, especially in the presence of androgen." provenance.
- _3 value "G(0) growth arrest conditions (i.e., serum and growth factor withdrawal or Oncostatin M (OSM) treatment) result in the activation of JAK1, JAK2, and Tyk 2, members of the Janus kinase family of non-receptor tyrosine kinases, in MCF-10A and MCF-12A cells." provenance.
- _5 value "IL-6 family cytokines (Interleukin-6 and Oncostatin M (OSM))-increase STAT3 phosphorylation (pSTAT3), increase CCAAT enhancer binding protein delta (C/EBPdelta) gene expression" provenance.
- _4 value "alpha chimaerin which has 91% homology to human alpha2 chimaerin, was also up-regulated following exposure to BDNF figure shows NGF also induces" provenance.
- _5 value "Constitutive expression of Sharp-1 in C2C12 myoblasts promotes cell cycle exit causing a decrease in cyclin D1 expression but blocks terminal differentiation. Although MyoD expression is not inhibited, the induction of differentiation-specific genes such as myogenin, MEF2C, and myosin heavy chain is impaired by Sharp-1 overexpression. We demonstrate that the interaction of Sharp-1 with MyoD and E-proteins results in reduced DNA binding and transactivation from MyoD-dependent E-box sites." provenance.
- _3 value "Nmu(-/-) mice showed increased body weight and adiposity, hyperphagia, and decreased locomotor activity and energy expenditure." provenance.
- _3 value "Nmu(-/-) mice showed increased body weight and adiposity, hyperphagia, and decreased locomotor activity and energy expenditure." provenance.
- _5 value "These data indicate that in BMMC, Lyn contributes to SCF-induced phosphorylation of Kit, as well as phosphorylation of Jnks and Stat3." provenance.
- _6 value "These data indicate that in BMMC, Lyn contributes to SCF-induced phosphorylation of Kit, as well as phosphorylation of Jnks and Stat3." provenance.
- _5 value "Endothelial cells expressing human HO-1 via retroviral transfer exhibit approximately 7-fold higher levels of PGT RNA and equivalently elevated uptake of [(3)H]PGE(2)." provenance.
- _4 value "We conclude that macrophage 12/15-LO plays a dominant role in the development of atherosclerosis by promoting endothelial inflammation and foam cell formation" provenance.
- _3 value "TABLE 1. Anti-apoptotic, Pro-apoptotic, and Stress-Related Genes Quantified by Microarray Analysis after Nonlethal Oxidative Injury in RPE Cells up" provenance.
- _3 value "up" provenance.
- _5 value "B: genes upregulated in foxa2 deletion" provenance.
- _5 value "B: genes upregulated in foxa2 deletion" provenance.
- _5 value "B: genes upregulated in foxa2 deletion" provenance.
- _5 value "table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion" provenance.
- _5 value "table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion" provenance.
- _5 value "table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion" provenance.
- _5 value "table 4: gene expressions altered in foxa2 deletion A: genes downregulated in foxa2 deletion" provenance.
- _2 value "In this study, we examined cell viability and gene expression profile in hepatoma cell lines treated with TSA The MTT assay demonstrated that TSA showed cell growth inhibition not only in a concentration-dependent but also a time-dependent manner on all cell lines studied. The TUNEL assay also revealed the potential of TSA to induce apoptosis." provenance.
- _3 value "The microarray analysis revealed that 8 genes including collagen type 1, alpha2 (COL1A2), insulin-like growth factor binding protein 2 (IGFBP2), integrin, alpha7 (ITGA7), basigin (BSG), quiescin Q6 (QSCN6), superoxide dismutase 3, extracellular (SOD3), nerve growth factor receptor (NGFR), and p53-induced protein (PIG11) exhibited substantial induction (ratio >2.0) after TSA treatment in multiple cell lines." provenance.
- _5 value "Ryk is required for neurite outgrowth induced by Wnt-3a and in the activation of T cell factor (TCF) induced by Wnt-1." provenance.
- _4 value "Severely hypomethylated Dnmt[3a-/-,3b-/-] ES cells have increased histone acetylation levels," provenance.
- _3 value "We found that both LH and ER induced the expression of rCOX-2, rHAS-2, and rTSG-6 mRNA." provenance.
- _4 value "Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated" provenance.
- _4 value "Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated" provenance.
- _4 value "Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated" provenance.
- _4 value "Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated" provenance.
- _4 value "Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated" provenance.
- _4 value "Table 1. Genes regulated >2-fold in the Cln5-/- mice (3- and 4.5-month-old) upregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _4 value "downregulated" provenance.
- _5 value "Ninjurin1-overexpressing clones exhibited strong growth inhibition due to G1 cell cycle arrest, which is associated with a posttranscriptional increase in p21WAF1/Cip1, a decrease of cyclin-dependent kinase 2 activity and the hypophosphorylation of Rb." provenance.
- _5 value "These data suggest that Spred-1 negatively regulates hematopoiesis by suppressing not only SCF-induced but also IL-3-induced ERK activation." provenance.
- _7 value "These data suggest that Spred-1 negatively regulates hematopoiesis by suppressing not only SCF-induced but also IL-3-induced ERK activation." provenance.
- _5 value "IRAK1 can directly use Stat3 as a substrate and cause Stat3 serine 727 phosphorylation. Splenocytes from IRAK1-deficient mice fail to exhibit LPS-induced Stat3 serine phosphorylation and IL-10 gene expression" provenance.
- _4 value "In rat brain cortical slices, histamine synthesis can be stimulated by depolarization and inhibited by H(3) agonists." provenance.
- _4 value "Inhibition of depolarization-stimulated histamine synthesis by the histamine H(3) receptor agonist imetit was impaired by preincubation with pertussis toxin and by the presence of a myristoylated peptide (myristoyl-N-QEHAQEPERQYMHIGTMVE-FAYALVGK) blocking the actions of G-protein betagamma subunits. The stimulation of another G(i/o)-coupled receptor, adenosine A(1), also decreased depolarization-stimulated histamine synthesis." provenance.
- _4 value "We show that histamine synthesis stimulation by depolarization with 30 mM K(+) requires extracellular calcium entry, mostly through N-type channels, and subsequent activation of calcium/calmodulin-dependent protein kinase type II. In vitro, this kinase phosphorylated and activated histidine decarboxylase, the histamine-synthesizing enzyme." provenance.
- _3 value "acceleration in terminal differentiation (ie, increased keratin 10 and filaggrin expression)." provenance.
- _5 value "This partially phenocopies the defect in mice deficient for Rnx, a metaHox homeodomain transcription factor, that we demonstrate here is capable of forming a DNA-binding complex with Pbx3. Rnx expression is unperturbed in Pbx3-deficient mice, but its ability to enhance transcription in vitro as a complex with TALE proteins is compromised in the absence of Pbx3. Thus, Pbx3 is essential for respiration and, like its DNA-binding partner Rnx, is critical for proper development of medullary respiratory control mechanisms" provenance.
- _6 value "Upstream activators of p38 MAP kinases, MKK3 and MKK6, increased PITX2a and Pitx2c activity" provenance.
- _6 value "the activity of lecithin-cholesterol acyltransferase was severely impaired in CBS(-/-) mice." provenance.
- _6 value "Nur77 can inhibit transactivation mediated by the NF-kappaB components p65 and c-Rel" provenance.
- _3 value "104303_i_at 1500004O14Rik NM_025901 67005 EST" provenance.
- _3 value "161872_f_at 1110049G11Rik NM_025410 66192 RIKEN cDNA 1110049G11 gene" provenance.
- _3 value "95611_at Lpl NM_008509 16956 lipoprotein lipase" provenance.
- _3 value "Table 1. Group 1: Genes upregulated by RA at 6 h" provenance.
- _3 value "Table 1. Group 1: Genes upregulated by RA at 6 h" provenance.
- _3 value "Table 2. Group 1: Genes downregulated by RA at 6 h" provenance.
- _3 value "Table 2. Group 1: Genes downregulated by RA at 6 h" provenance.
- _3 value "Table 2. Group 1: Genes downregulated by RA at 6 h" provenance.
- _3 value "Table 2. Group 1: Genes downregulated by RA at 6 h" provenance.
- _3 value "Table 3. Group 2: Genes induced by RA at all times" provenance.
- _3 value "Table 3. Group 2: Genes induced by RA at all times" provenance.
- _3 value "Table 4. Group 3: Genes suppressed by RA" provenance.
- _3 value "Table 4. Group 3: Genes suppressed by RA" provenance.
- _3 value "Table 4. Group 3: Genes suppressed by RA" provenance.
- _3 value "Table 4. Group 3: Genes suppressed by RA" provenance.
- _3 value "Altogether, these results demonstrate that pfkfb3 is a hypoxia-inducible gene that is stimulated through HIF interaction with the consensus HRE site in its promoter region." provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _5 value "PhosphoElm data from PMID 15212693" provenance.
- _5 value "In this study, we provide evidence that the VEGF-dependent tyrosine phosphorylation of caveolin-1 induces interaction of the protein with the membrane-type 1 matrix metalloproteinase (MT1-MMP). This interaction requires the phosphorylation of caveolin-1 on tyrosine 14 by members of the Src family of protein kinases, such as Src and Fyn, because it is completely abolished by expression of a catalytically inactive Src mutant or by site-directed mutagenesis of tyrosine 14 of caveolin-1. " provenance.
- _5 value "We have recently shown that stimulation of endothelial cells with vascular endothelial growth factor (VEGF) induces dissociation of caveolin-1 from the VEGFR-2 receptor, followed by Src family kinase-dependent tyrosine phosphorylation of the protein (Labrecque, L., Royal, I., Surprenant, D. S., Patterson, C., Gingras, D., and Beliveau, R. (2003) Mol. Biol. Cell 14, 334-347). " provenance.
- _4 value "CXCL12 increased MMP-2 expression by LNCaP and PC3; however, MMP-9 expression was elevated only in PC3 cells after CXCL12-CXCR4 ligation." provenance.
- _4 value "Expression of HES-1 in T47D cells inhibited G1/S-phase transition and activation of Cdk2 elicited by estrogen." provenance.
- _4 value "HES-1 inhibits both estrogen- and heregulin-beta1-stimulated growth of breast cancer cells" provenance.
- _3 value "proliferation caused by heregulin-beta1 treatment of T47D cells was inhibited by all-trans retinoic acid and this effect was mediated by HES-1." provenance.
- _3 value "proliferation caused by heregulin-beta1 treatment of T47D cells was inhibited by all-trans retinoic acid and this effect was mediated by HES-1." provenance.
- _4 value "proliferation caused by heregulin-beta1 treatment of T47D cells was inhibited by all-trans retinoic acid and this effect was mediated by HES-1." provenance.
- _6 value "proliferation caused by heregulin-beta1 treatment of T47D cells was inhibited by all-trans retinoic acid and this effect was mediated by HES-1." provenance.
- _3 value "two important downstream target genes of estrogen and heregulin-beta1 that are regulated through E2F-1, cyclin E and NPAT, were both regulated in a similar fashion by all-trans retinoic acid, and these effects were antagonized by dominant-negative HES-1." provenance.
- _6 value "Modified assertion" provenance.
- _3 value "Treatment of a cancer cell line with a demethylating agent, 5-aza-2'-deoxycytidine, restored the expression of 13 genes, RASGRF2, ADAM23, NEF3, NKX2-8, HAND1, EGR4, PRG2, FBN2, CDH2, TLL1, NPTX1, NTSR1 and THBD, showing their silencing by methylation of their 5' CGIs." provenance.