Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _3 value "To examine the in vivo role of Raf-1 in the heart, we generated cardiac muscle-specific Raf-1-knockout (Raf CKO) mice with Cre-loxP-mediated recombination. The mice demonstrated left ventricular systolic dysfunction and heart dilatation without cardiac hypertrophy or lethality." provenance.
- _7 value "activation of ERK-MAPK pathway and Sp1 transcription factor play a pivotal role in the induction of TIMP-3 by TGF-beta in chondrocytes" provenance.
- _7 value "activation of ERK-MAPK pathway and Sp1 transcription factor play a pivotal role in the induction of TIMP-3 by TGF-beta in chondrocytes" provenance.
- _5 value "Gal4-SirT1 expression resulted in the deacetylation of H4-K16 and H3-K9, recruitment of H1 within the promoter vicinity, drastically reduced reporter expression, and loss of H3-K79 methylation, a mark restricting silenced chromatin...recruitment and deacetylation of histone H1," provenance.
- _4 value "Ceramide, the hydrolysis product of sphingomyelin, seems to be a key mediator as it mimics mmLDL by inducing activation of the same signaling components" provenance.
- _5 value "Modified assertion" provenance.
- _6 value "hMINK beta moderately activates c-Jun N-terminal kinase (JNK) and associates with Nck" provenance.
- _4 value "This TGF-beta1/Smad3 action involves an inhibitory effect on AP-1 activity and DNA binding that results in an inhibition of the AP-1-driven induction of the PPARbeta/delta promoter" provenance.
- _5 value "Whereas conditions that mimic the initial inflammatory events stimulate PPARbeta/delta expression, TGF-beta1/Smad3 suppresses this inflammation-induced PPARbeta/delta transcription" provenance.
- _6 value "Whereas conditions that mimic the initial inflammatory events stimulate PPARbeta/delta expression, TGF-beta1/Smad3 suppresses this inflammation-induced PPARbeta/delta transcription" provenance.
- _5 value "Modified assertion" provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "See table 6: Genes regulated by gefitinib or cetuximab in A431 cells and with fold change of at least 1.5. " provenance.
- _3 value "PHA-665752 effectively blocked the biological responses to HGF in all assays, with 50% inhibition at 5 to 15 nmol/L concentration and complete inhibition at around 100 nmol/L." provenance.
- _4 value ", Fig. 1C shows that there is no increase in the levels of caspase-3 activity in cells exposed to hyperoxia. In contrast, control cells treated with apoptotic stimuli showed a more than 2.5-fold increase in caspase-3 activity .....Controls show the results from nonapoptotic cells and apoptotic cells that were treated with 1 ?M camptothecin (Sigma, Oakville, ON, Canada) for 24 h." provenance.
- _5 value "Table 1 - Genes regulated by 1 umol/L isoproterenol (activation of beta adrenoceptors) in A7r5 cells. The differential gene expression values between treatment and control were expressed as an expression ratio and tested by Chen test (95% confidence). Among these genes, we pick out ratio values 1.8 or 0.56 as indicating genes with changed expression." provenance.
- _5 value "Table 1 - Genes regulated by 1 umol/L isoproterenol (activation of beta adrenoceptors) in A7r5 cells. The differential gene expression values between treatment and control were expressed as an expression ratio and tested by Chen test (95% confidence). Among these genes, we pick out ratio values 1.8 or 0.56 as indicating genes with changed expression." provenance.
- _5 value "Table 1 - Genes regulated by 1 umol/L isoproterenol (activation of beta adrenoceptors) in A7r5 cells. The differential gene expression values between treatment and control were expressed as an expression ratio and tested by Chen test (95% confidence). Among these genes, we pick out ratio values 1.8 or 0.56 as indicating genes with changed expression." provenance.
- _5 value "Table 1 - Genes regulated by 1 umol/L isoproterenol (activation of beta adrenoceptors) in A7r5 cells. The differential gene expression values between treatment and control were expressed as an expression ratio and tested by Chen test (95% confidence). Among these genes, we pick out ratio values 1.8 or 0.56 as indicating genes with changed expression." provenance.
- _5 value "Table 1 - Genes regulated by 1 umol/L isoproterenol (activation of beta adrenoceptors) in A7r5 cells. The differential gene expression values between treatment and control were expressed as an expression ratio and tested by Chen test (95% confidence). Among these genes, we pick out ratio values 1.8 or 0.56 as indicating genes with changed expression." provenance.
- _3 value "TABLE 2. Statistically significant cytoskeleton-, extracellular matrix-, and adhesion-related genes consistently upmodulated (positive fold change) or downmodulated (negative fold change) across late times of infection [in response to CMV infection]" provenance.
- _3 value "This study investigated the use of the hindlimb suspension (HS) and reloading model of mice for the mapping of ultrastructural and gene expressional alterations underlying load-dependent muscular adaptations. Mice were hindlimb suspended for 7 days or kept as controls (n = 12). Soleus muscles were harvested after HS (HS7, n = 23) or after resuming ambulatory cage activity (reloading) for either 1 day (R1, n = 13) or 7 days (R7, n = 9). Using electron microscopy, a reduction in mean fiber area (-37%) and in capillary-to-fiber ratio (from 1.83 to 1.42) was found for HS7. Subsequent reloading caused an increase in interstitial cells (+96%) and in total capillary length (+57%), whereas mean fiber area and capillary-to-fiber ratio did not significantly change compared with HS. Total RNA in the soleus muscle was altered with both HS (-63%) and reloading (+108% in R7 compared with control). This is seen as an important adaptive mechanism. Gene expression alterations were assessed by a muscle-specific low-density cDNA microarray. The transcriptional adjustments indicate an early increase of myogenic factors during reloading together with an overshoot of contractile (MyHC I and IIa) and metabolic (glycolytic and oxidative) mRNA amounts and suggest mechano-sensitivity of factors keeping the sarcomeres in register (desmin, titin, integrin-beta1). Important differences to published data from former rat studies were found with the mouse HS model for contractile and glycolytic enzyme expression. These species-specific differences need to be considered when transgenic mice are used for the elucidation of monogenetic factors in mechano-dependent muscle plasticity." provenance.
- _7 value "Trx enhances the DNA binding activity of the activator protein 1 (AP1) transcription factor through an activation cascade beginning with Trx, proceeding to another regulatory protein, redox factor-1 (Ref1), and subsequently continuing to AP1 through direct cysteine mediated associations and reduction processes (Xanthoudakis and Curran, 1992; Xanthoudakis et al., 1994; Hirota et al., 1997)." provenance.
- _4 value "Trx facilitates the transcriptional activities of nuclear factor NFkB and the glucocorticoidrecept or via direct associations with their DNA-binding domains (Matthews et al., 1992; Hayashi et al., 1993; Qin et al., 1995; Makino et al., 1999)." provenance.
- _5 value "Trx facilitates the transcriptional activities of nuclear factor NFkB and the glucocorticoidrecept or via direct associations with their DNA-binding domains (Matthews et al., 1992; Hayashi et al., 1993; Qin et al., 1995; Makino et al., 1999)." provenance.
- _4 value "IGF-1-stimulated ATM phosphorylation at both threonine and tyrosine residues, and our results demonstrated that the phosphorylation of tyrosine in the ATM molecule is important for AMPK-alpha subunit phosphorylation during IGF-1 signaling." provenance.
- _5 value "Immunoprecipitates of ATM collected from IGF-1-stimulated cells also caused the phosphorylation of the AMPK-alpha subunit in vitro." provenance.
- _3 value "FLRT3 mRNA and protein characterized by a fibronectin type III domain and a leucine-rich repeat motif was upregulated in damaged sensory neurons." provenance.
- _5 value "The ARF tumor suppressor is widely regarded as an upstream activator of p53-dependent growth arrest and apoptosis" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _3 value "To conduct a genome-wide search for cAMP-responsive genes in KGN cell line, asynchronously growing cells were treated with either vehicle or 25 uM forskolin for 3 h. TABLE 1. List of forskolin-induced genes (2-fold or more)" provenance.
- _6 value "These results are consistent with the hypothesis that CGRP produces hyperalgesia by a direct action on CGRP1 receptors in the spinal cord dorsal horn and suggest that the effects of CGRP are mediated by both PKA and PKC second-messenger pathways." provenance.
- _4 value "Functionally, wild-type KLF6 decreased cellular proliferation of HepG2 cells, while patient-derived mutants did not." provenance.
- _3 value "31 genes were confirmed to be up- or down-regulated during replicative senescence by semi-quantitative RT-PCR. The overexpressions of several genes including CD36, putative lymphocyte G0/G1 switch gene (G0S2), tumor protein D52-like 1 (TPD52L1), chemokine (C-X-C motif) ligand 6, myxovirus resistant gene 1 (MX1), and the down-regulation of the immunoglobulin superfamily containing leucine-rich repeat (ISLR), neurotrimin, insulin-like growth factor 2 associated protein (IGF2A), and apoptosis-related RNA binding protein (NAPOR3) were newly identified." provenance.
- _3 value "31 genes were confirmed to be up- or down-regulated during replicative senescence by semi-quantitative RT-PCR. The overexpressions of several genes including CD36, putative lymphocyte G0/G1 switch gene (G0S2), tumor protein D52-like 1 (TPD52L1), chemokine (C-X-C motif) ligand 6, myxovirus resistant gene 1 (MX1), and the down-regulation of the immunoglobulin superfamily containing leucine-rich repeat (ISLR), neurotrimin, insulin-like growth factor 2 associated protein (IGF2A), and apoptosis-related RNA binding protein (NAPOR3) were newly identified." provenance.
- _5 value "ATM-dependent phosphorylation of numerous effectors in the ATM-signaling pathway, including Nbs1 (Ser(343)), SMC1 (Ser(957)), Chk1 (Ser(317) and Ser(345)), and Chk2 (Ser(33/35) and Thr(68))." provenance.
- _4 value "TNF-alpha induced both phosphorylation and degradation of IKappaB-alpha in A549 cells within several minutes" provenance.
- _5 value "The effects of short interfering RNA (siRNA)-mediated downregulation of Id1 were the same as those following downregulation of c-Myc: decreased expression of cyclins D1 and E, reduced phosphorylation of pRb at Ser780 (a site targeted by cyclin D1-Cdk4) and reduced cyclin E-Cdk2 activity" provenance.
- _4 value "Stimulation of PKCs in U-251 cells for 30 min with 100 nM PMA, showed an increased phosphorylation of mTOR at ser-2448 by 43+/-10-fold compared with untreated cells. Expression of PKC-etaKR, a kinase dead mutant of PKCeta significantly reduced PMA stimulated ser-2448 phosphorylation of mTOR by 54+/-12%. In U-1242 PKCdeltaNPS, a catalytically active PKC expression increased phosphorylation on ser-2448 of mTOR by 322+/-58% as compared to the empty vector, suggesting that PKCeta activates mTOR." provenance.
- _3 value "Most of what is known about the regulation of atrogin-1 is based on studies in skeletal muscle. Atrogin-1, like the RING finger protein MuRF1, is highly inducible at the mRNA level by denervation and disuse" provenance.
- _3 value "Most of what is known about the regulation of atrogin-1 is based on studies in skeletal muscle. Atrogin-1, like the RING finger protein MuRF1, is highly inducible at the mRNA level by denervation and disuse" provenance.
- _3 value "atrogin-1 attenuates the cardiac hypertrophic response with selectivity at the level of calcineurin signaling, insofar as atrogin-1 does not affect the ability of cardiomyocytes to respond to hypertrophic signaling events downstream of calcineurin" provenance.
- _5 value "the calcineurin-inhibitory domain of Cabin/Cain directly inhibits the transcriptional activity of myocyte enhancer factor-2, suggesting an alternative mechanism whereby Cabin/Cain might inhibit cardiac hypertrophy" provenance.
- _5 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _5 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _5 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _5 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _5 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _5 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _5 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _4 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _4 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _4 value "Extensive data indicate that oncoproteins, such as oncogenic H-Ras, initiate signal transduction cascades that ultimately lead to the activation of specific transcription factors. We and others have previously demonstrated that Ras activates the inherent transcriptional activation function of the transcription factor nuclear factor kappaB (NF-kappaB). Supportive of the importance of NF-kappaB in transformation, Ras-induced cellular transformation can be suppressed by expression of IkappaBalpha, an inhibitor of NF-kappaB, or by dominant-negative forms of the upstream activator IkappaB kinase (IKK). However, conclusive evidence for a requirement for NF-kappaB subunits in oncogenic transformation has not been reported. Furthermore, there is little understanding of the gene targets controlled by NF-kappaB that might support oncogenic conversion. The data presented here demonstrate that, although both p65 and c-Rel enhance the frequency of Ras-induced cellular transformation, these NF-kappaB subunits are not essential for Ras to transform spontaneously immortalized murine fibroblasts. Microarray analysis identified a set of genes induced by Ras that is dependent on NF-kappaB for their expression and that likely play contributory roles in promoting Ras-induced oncogenic transformation." provenance.
- _6 value "We speculate that loss of AKR1C1 and AKR1C2 in breast cancer results in decreased progesterone catabolism, which, in combination with increased PR expression, may augment progesterone signaling by its nuclear receptors." provenance.
- _5 value "From mutations file" provenance.
- _5 value "TGF-beta phosphorylation of Smad2/3, an obligatory step of intracellular TGF-beta signaling, was also suppressed by VEGF. VEGF attenuation of TGF-beta action was also demonstrated in two other endothelial cell lines. In conclusion, VEGF attenuates TGF-beta action in the human endothelial cell, specifically at the level of transcription of PAI-1 gene and Smad2/3 phosphorylation" provenance.
- _5 value "Thus, uPA is a potent chemoattractant for basophils that seems to act through exposure of the chemotactic uPAR epitope uPAR84-95, which is an endogenous ligand for FPRL2 and FPRL1." provenance.
- _4 value "Thus, uPA is a potent chemoattractant for basophils that seems to act through exposure of the chemotactic uPAR epitope uPAR84-95, which is an endogenous ligand for FPRL2 and FPRL1." provenance.
- _3 value "Treatment of THP-1 cells with oxidized LDL upregulated the protein levels of 14-3-3 protein eta by 3 fold with a sequence coverage of 4% when compared with LDL and the vehicle." provenance.
- _3 value "Treatment of THP-1 cells with oxidized LDL upregulated the protein levels of heterogenous nuclear ribonucleoprotein A2/B1(p Value = 0.06) with a sequence coverage of 29% when compared with LDL and the vehicle." provenance.
- _3 value "Treatment of THP-1 cells with oxidized LDL upregulated the protein levels of nitric oxide synthase 2A by 3 fold with a sequence coverage of 5% when compared with LDL and the vehicle." provenance.
- _3 value "Treatment of THP-1 cells with oxidized LDL upregulated the protein levels of profilin-1 (p Value = 0.1) with a sequence coverage of 46% when compared with LDL and the vehicle." provenance.
- _2 value "Most prominently, adenoviral gene expression of a dominant-negative PKD isoform, PKD3, primarily inhibits basal glucose uptake and, to a lesser extent, insulin-stimulated glucose uptake, whereas overexpression of wild-type PKD3 significantly enhances basal glucose uptake. Moreover, expression of a PKD3-targeted siRNA significantly inhibits basal glucose uptake. Taken together, our results indicate that PKD, specifically PKD3, directly contributes to insulin-independent basal glucose uptake in L6 skeletal muscle cells." provenance.
- _5 value "Our data show that in a glioma-derived cell line the cytoplasmic tyrosine kinase PYK2 is constitutively associated with HER3 and that stimulation with Heregulin results in PYK2 tyrosine phosphorylation. HER3, but not HER2, mediates the phosphorylation of the C-terminal region of PYK2 to promote a mitogenic response through activation of the MAPK pathway. " provenance.
- _3 value "Results showed that retinoic acid treatment increases the amount of beta-catenin bound to E-cadherin by decreasing its tyrosine-phosphorylation level." provenance.
- _5 value "Results showed that retinoic acid treatment increases the amount of beta-catenin bound to E-cadherin by decreasing its tyrosine-phosphorylation level." provenance.
- _3 value "5-Aza-dCyd was able to re-express VHL in our cell lines both in culture and in xenografted murine tumors." provenance.
- _5 value "The chief phosphorylation sites of Src include tyrosine 416 that results in activation from autophosphorylation and tyrosine 527 that results in inhibition from phosphorylation by C-terminal Src kinase" provenance.
- _4 value "As shown in Fig. 6A, inhibition of PI3K with LY294002 suppressed expression of six cell cycle-related genes (CKS2, HEC, MAD3L, STK15, UBE2C, and ZWINT) in a concentration-dependent manner as" provenance.
- _4 value "As shown in Fig. 6A, inhibition of PI3K with LY294002 suppressed expression of six cell cycle-related genes (CKS2, HEC, MAD3L, STK15, UBE2C, and ZWINT) in a concentration-dependent manner as" provenance.
- _4 value "Five DNA replication and repair-related genes (FEN1, PCNA, RFC4, TOP2A, and TYMS) were suppressed by LY294002 treatment as detected by real time PCR (Fig. 6C)." provenance.
- _4 value "Five DNA replication and repair-related genes (FEN1, PCNA, RFC4, TOP2A, and TYMS) were suppressed by LY294002 treatment as detected by real time PCR (Fig. 6C)." provenance.
- _5 value "The expression of active mAKT1 blocked the down-regulation of CKS2, HEC, UBE2C, and ZWINT genes (cell cycle-related, Fig. 7B); of RFC4 and TYMS genes (DNA replication and repair-related, Fig. 7B); and of HMGB2 and HIST1H4C genes (chromatin-related, Fig. 7, B and C) induced by the anti-HER2 antibody." provenance.
- _5 value "The expression of active mAKT1 blocked the down-regulation of CKS2, HEC, UBE2C, and ZWINT genes (cell cycle-related, Fig. 7B); of RFC4 and TYMS genes (DNA replication and repair-related, Fig. 7B); and of HMGB2 and HIST1H4C genes (chromatin-related, Fig. 7, B and C) induced by the anti-HER2 antibody." provenance.
- _5 value "Whereas Ser43/Ser45 and Thr144 are phosphorylated by PKC (Fig. 1A), it is well documented that PKC can cross-phosphorylate the PKA sites as well (6-8)." provenance.
- _5 value "Whereas Ser43/Ser45 and Thr144 are phosphorylated by PKC (Fig. 1A), it is well documented that PKC can cross-phosphorylate the PKA sites as well (6-8)." provenance.
- _5 value "Within the cardiac isoform's amino-terminal extension, serines are present at residues 23 and 24 (Ser23/Ser24), which serve as substrates for protein kinase A (PKA), which is activated in response to ?-adrenergic stimulation of the heart (3). Several investigations report that PKA-mediated phosphorylation of cTnI results in a reduction in myofilament Ca2+ sensitivity (4), an increase in cross-bridge cycling (5), and increased binding of cTnI to the thin filament. Cardiac TnI is also a substrate for protein kinase C (PKC) phosphorylation at Ser43/Ser45 and Thr144 (position 143 in the human protein) (6). However, the substrate specificity of these sites is not absolute, since PKC can phosphorylate the PKA sites (7-9). " provenance.