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PMID |
Sentence |
1 |
14520699
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Human T-cell leukemia virus type 1 Tax activates cyclin-dependent kinase inhibitor p21/Waf1/Cip1 expression through a p53-independent mechanism: Inhibition of cdk2.
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2 |
14520699
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Tax transfection resulted in enhanced expression of p21 protein in T and fibroblastoid cells.
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3 |
14520699
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Similarly, Tax-expressing cells have higher amounts of endogenous p21 protein and RNA.
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4 |
14520699
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However, neither Tax-negative, HTLV-1 transformed cells or HTLV-1-negative T cell lines had detectable levels of p21 protein and RNA.
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5 |
14520699
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CREB/ATF defective Tax mutant (M47) activated the p21 promoter significantly less efficiently.
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6 |
14520699
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Tax activated wild type (wt) p21 promoter in p53-negative Jurkat and p53-positive A301cells, irrespective of endogenous p53 status, and activated a mutant p21 promoter containing a p53 responsive element (p53RE) deletion as strongly as wt promoter.
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7 |
14520699
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Of importance, cdk2 activity was almost completely abolished in Tax-induced p21-expressing MT-2 cells, suggesting that Tax-induced p21 predominantly affects the activity of cdk2, a late G1 and S phase kinase.
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8 |
14520699
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Taken together, these findings suggest that HTLV-1 Tax activates p21/Waf1/Cip1, a cell growth inhibitor, in a p53-independent mechanism through CREB/ATF-related transcription factors, and inhibits cdk2.
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9 |
14520699
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Human T-cell leukemia virus type 1 Tax activates cyclin-dependent kinase inhibitor p21/Waf1/Cip1 expression through a p53-independent mechanism: Inhibition of cdk2.
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10 |
14520699
|
Tax transfection resulted in enhanced expression of p21 protein in T and fibroblastoid cells.
|
11 |
14520699
|
Similarly, Tax-expressing cells have higher amounts of endogenous p21 protein and RNA.
|
12 |
14520699
|
However, neither Tax-negative, HTLV-1 transformed cells or HTLV-1-negative T cell lines had detectable levels of p21 protein and RNA.
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13 |
14520699
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CREB/ATF defective Tax mutant (M47) activated the p21 promoter significantly less efficiently.
|
14 |
14520699
|
Tax activated wild type (wt) p21 promoter in p53-negative Jurkat and p53-positive A301cells, irrespective of endogenous p53 status, and activated a mutant p21 promoter containing a p53 responsive element (p53RE) deletion as strongly as wt promoter.
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15 |
14520699
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Of importance, cdk2 activity was almost completely abolished in Tax-induced p21-expressing MT-2 cells, suggesting that Tax-induced p21 predominantly affects the activity of cdk2, a late G1 and S phase kinase.
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16 |
14520699
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Taken together, these findings suggest that HTLV-1 Tax activates p21/Waf1/Cip1, a cell growth inhibitor, in a p53-independent mechanism through CREB/ATF-related transcription factors, and inhibits cdk2.
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17 |
16972797
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HABP cleaves kininogen in vitro, releasing the vasoactive peptide bradykinin, and activates plasminogen activators, suggesting a vascular cell-directed physiological function of this novel plasma protease.
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18 |
16972797
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On the one hand, HABP releases bradykinin from cell surface-bound or soluble kininogen and triggers a bradykinin B2-receptor-dependent mobilisation of intracellular Ca2+.
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19 |
16972797
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On the other hand, HABP activates the p44/42-dependent MAPK (ERK1/2) signalling cascade independent of the B2-receptor, but involving the fibroblast growth factor receptor-1 and basic fibroblast growth factor.
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20 |
16972797
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This signalling pathway leads to phosphorylation of the kinases Raf, MEK1/2 and ERK1/2.
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21 |
16972797
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The extracellular activity of HABP also affects the gene expression level through phosphorylation of two transcription factors, the cAMP-responsive element binding protein CREB and the proto-oncogene c-Myc.
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22 |
19540594
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Requirement of TLR4 and CD14 in dendritic cell activation by Hemagglutinin B from Porphyromonas gingivalis.
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23 |
19540594
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Using an endotoxin free rHagB preparation, our results show that stimulation of murine bone marrow-derived DC with rHagB leads to upregulation of the costimulatory molecules CD86 and CD40, activation of p38 and ERK MAP kinases, transcription factors NF-kappaB, CREB and IRF-3 and the production of IL-6, TNF-alpha, IL-12p40 and to a lesser extent IL-10 and IFN-beta.
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24 |
19540594
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This activation process was absolutely dependent on TLR4 and CD14.
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25 |
19540594
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While upregulation of CD86 was independent of the adaptor molecule MyD88, CD40 upregulation and optimal cytokine (IL-6, TNF-alpha, IL-12p40, IL-10 and IFN-beta) production required both MyD88 and TRIF molecules.
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26 |
20006311
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ESAT-6 also inhibited T-cell production of IL-17 and TNF-a, but not IL-2.
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27 |
20006311
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ESAT-6 reduced IFN-gamma mRNA levels by inhibiting the expression of the transcription factors, ATF-2, c-Jun and CREB, which upregulate IFN-gamma gene expression in T cells through binding to the IFN-gamma proximal promoter.
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28 |
20685939
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This study focused on the capacity of CREB proteins to regulate IFN-gamma transcription in CD3(+) T cells obtained from tuberculosis (TB) patients and persons with latent tuberculosis infection (LTBI) in China.
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29 |
20685939
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EMSA (in vitro) and ChIP (in vivo) experiments suggested CREB could bind to the IFN-gamma proximal promoter in persons with LTBI, whereas no binding was detected in TB patients.
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30 |
20685939
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These results suggested that CREB could promote the transcription and production of IFN-gamma through binding with the IFN-gamma proximal promoter, but the regulatory role of CREB was decreased in tuberculosis patients owing to diminished expression of CREB proteins, which in turn reduced the IFN-gamma production.
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31 |
20685939
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This study focused on the capacity of CREB proteins to regulate IFN-gamma transcription in CD3(+) T cells obtained from tuberculosis (TB) patients and persons with latent tuberculosis infection (LTBI) in China.
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32 |
20685939
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EMSA (in vitro) and ChIP (in vivo) experiments suggested CREB could bind to the IFN-gamma proximal promoter in persons with LTBI, whereas no binding was detected in TB patients.
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33 |
20685939
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These results suggested that CREB could promote the transcription and production of IFN-gamma through binding with the IFN-gamma proximal promoter, but the regulatory role of CREB was decreased in tuberculosis patients owing to diminished expression of CREB proteins, which in turn reduced the IFN-gamma production.
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34 |
20685939
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This study focused on the capacity of CREB proteins to regulate IFN-gamma transcription in CD3(+) T cells obtained from tuberculosis (TB) patients and persons with latent tuberculosis infection (LTBI) in China.
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35 |
20685939
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EMSA (in vitro) and ChIP (in vivo) experiments suggested CREB could bind to the IFN-gamma proximal promoter in persons with LTBI, whereas no binding was detected in TB patients.
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36 |
20685939
|
These results suggested that CREB could promote the transcription and production of IFN-gamma through binding with the IFN-gamma proximal promoter, but the regulatory role of CREB was decreased in tuberculosis patients owing to diminished expression of CREB proteins, which in turn reduced the IFN-gamma production.
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37 |
21031251
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The innate immune response mainly represented by Toll-like receptors and Nod-like receptors that recognize their specific ligands, activate transcription factors as NF-kB, AP-1, CREB-1, inducing production of inflammatory cytokines such as IL -8, IL-12, IL-6, IL-1β, IL-18, TNF-α and IL-10.
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38 |
22473996
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We here demonstrate that M. bovis BCG triggers Toll-like receptor 2 (TLR2)-dependent microRNA-155 (miR-155) expression, which involves signaling cross talk among phosphatidylinositol 3-kinase (PI3K), protein kinase Cδ (PKCδ), and mitogen-activated protein kinases (MAPKs) and recruitment of NF-κB and c-ETS to miR-155 promoter.
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39 |
22473996
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Genetic and signaling perturbations presented the evidence that miR-155 regulates PKA signaling by directly targeting a negative regulator of PKA, protein kinase inhibitor alpha (PKI-α).
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40 |
22473996
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The miR-155-triggered activation of caspase-3, BAK1, and cytochrome c translocation involved signaling integration of MAPKs and epigenetic or posttranslational modification of histones or CREB.
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41 |
22593239
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Several genes, including CREB1, EP300, MYB, PAX5, and SPI1/PU.1, were sequenced from FPS-affected and unaffected foals.
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42 |
22606348
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The genes validated as critical for influenza virus replication were ADAMTS7, CPE, DPP3, MST1, and PRSS12, and pathway analysis showed these genes were in global host cell pathways governing inflammation (NF-κB), cAMP/calcium signaling (CRE/CREB), and apoptosis.
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43 |
24394593
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A TDG/CBP/RARα ternary complex mediates the retinoic acid-dependent expression of DNA methylation-sensitive genes.
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44 |
24394593
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TDG interacts with the histone acetylase CREB-binding protein (CBP) to activate CBP-dependent transcription.
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45 |
24394593
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In addition, TDG also interacts with the retinoic acid receptor α (RARα), resulting in the activation of RARα target genes.
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46 |
24394593
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Here we provide evidence for the existence of a functional ternary complex containing TDG, CBP and activated RARα.
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47 |
24586148
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Using a series of ChIP assays, we show that Tax recruits CREB and CREB Binding Protein (CBP) onto a c-AMP Responsive Element (CRE) present in the gem promoter.
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48 |
24586148
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We show that Gem co-localizes with F-actin and is involved both in T-cell spontaneous cell migration as well as chemotaxis in the presence of SDF-1/CXCL12.
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