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PMID |
Sentence |
1 |
1335239
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We demonstrate interaction between the AP-1 constituents c-fos and c-jun and thyroid hormone receptor in this region by transient transfection experiments using a -125 to +37 bp hTSH beta fragment.
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2 |
8473495
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Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter.
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3 |
8473495
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These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT.
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4 |
8243829
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Exposure of all three beta-cell lines to nerve growth factor increased NGFI-A and c-fos mRNA steady-state levels, showing that these receptors are functional.
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5 |
8275944
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Insulin treatment of control rats demonstrated a marked 8-fold transient increase (15 min) in c-fos mRNA in white adipose tissue, which returns to basal levels by 5 h.
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6 |
8275944
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However, insulin treatment of insulin-deficient diabetic rats resulted in a prolonged increase in c-fos message levels in adipose tissue without any significant change in the time course of c-fos mRNA induction/repression in cardiac muscle.
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7 |
8275944
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These data demonstrate that in contrast to c-jun, c-fos is transiently increased in both cardiac muscle and adipose tissue by insulin treatment.
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8 |
8275944
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Furthermore, transrepression of the c-fos gene is specifically attenuated in adipose tissue of insulin-deficient diabetic rats, but not in cardiac muscle.
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9 |
7512956
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Insulin also stimulated phosphorylation of c-Fos and several Fos-related proteins (pp72, pp45, and pp39) as indicated by precipitation with anti-c-Fos antibody following exposure to denaturating conditions.
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10 |
7512956
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This is associated with changes in AP-1-mediated gene expression in vivo, suggesting that AP-1 phosphorylation by insulin plays a role in insulin-regulated gene expression.
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11 |
8049217
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However, they fail to undergo insulin-stimulated internalization, do not regulate the phosphorylation of insulin receptor substrate 1, and are unable to mediate an insulin-stimulated increase in DNA synthesis and c-jun and c-fos expression.
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12 |
7656336
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The low c-Fos expression in the female NOD thymocytes was most prominent in CD3low thymocytes. c-Jun expression of the CD3low thymocytes was also lower in the female NOD mice.
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13 |
7656336
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Administrations of h-LT, h-TNF, and h-IL-2, which has been reported to prevent IDDM in NOD mice by systemic administration, significantly up-regulated c-Fos expression in CD3low thymocytes.
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14 |
7656336
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From these results, it is assumed that a relationship may exist between the high diabetes incidence and the defective c-Fos expression in female NOD mice and between the prevention of IDDM and the amelioration of the defective c-Fos expression with h-LT in female NOD mice.
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15 |
9519750
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Treatment of these cells with c-fos antisense DNA or protein kinase C inhibitor inhibited the stimulatory effect of glucose on LPL mRNA expression.
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16 |
10799542
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Tyr(985) and ERK activation similarly mediate c-fos mRNA accumulation.
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17 |
10799542
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Thus, the two LRb tyrosine residues that are phosphorylated during receptor activation mediate distinct signaling pathways as follows: SHP-2 binding to Tyr(985) positively regulates the ERK --> c-fos pathway, and STAT3 binding to Tyr(1138) mediates the inhibitory SOCS3 pathway.
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18 |
10748122
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FGF-1, FGF-2, and FGF-4 enhanced mitogen-activated protein kinase (MAPK) activity, increased steady-state c-fos mRNA levels, and stimulated proliferation through either receptor, whereas KGF was without effect.
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19 |
11147774
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We investigated activation of orexin and other neurons during insulin-induced hypoglycemia using the immediate early gene product Fos.
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20 |
11937295
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Promoter assay showed that the induction of VEGF was dependent on AP-1.
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21 |
12368225
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Cerivastatin, a hydroxymethylglutaryl CoA reductase inhibitor; pyrrolidinedithiocarbamate; or curcumin was found to completely prevent the AGE-induced increase in NF-kB and AP-1 activity, VEGF mRNA up-regulation, and the resultant increase in DNA synthesis in microvascular EC.
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22 |
12388107
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HG, PKC activators, and ETs (ET-1 and ET-3) that increased FN expression also caused activation of NF-kappaB and AP-1.
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23 |
12582013
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Bosentan treatment prevented NF-kappaB activation in the retina and heart and AP-1 activation in the retina and kidney.
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24 |
12811469
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This interaction activated endothelial tyrosine kinase(s) but not NFkappaB and AP-1, while SOD prevented tyrosine kinase stimulation but facilitated NFkappaB and AP-1 activation.
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25 |
12815381
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The c-Jun NH(2)-terminal kinases (JNKs) phosphorylate and activate members of the activator protein-1 (AP-1) transcription factor family and other cellular factors implicated in regulating altered gene expression, cellular survival and proliferation in response to cytokines and growth factors, noxious stimuli and oncogenic transformation.
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26 |
12941765
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Finally, these above responses as well as expression of c-Fos-like immunohistochemistry in the hypothalamus were not induced by central application of adiponectin (0-15 micro g/kg).
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27 |
12947315
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Viability was analyzed by a colorimetric assay, islet mass by DNA content, JNK activity by Western blots, AP-1 nuclear activity with a promoter-Luciferase AP-1 responsive construct, and c-Fos, Jun-D, and ATF-2 nuclear activities by an enzyme-linked immunosorbent assay.
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28 |
12947315
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These effects were associated with reduction in JNK targets, including the nuclear activities of transcription factors AP-1, c-Jun, c-Fos, Jun-D and ATF-2, involved in apoptosis in beta-cells.
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29 |
12878589
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Here we demonstrate that LDL(-) increases tumor necrosis factor alpha (TNFalpha)-induced inflammatory responses through NF kappa B and AP-1 activation with corresponding increases in vascular cell adhesion molecule-1 (VCAM1) expression.
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30 |
12878589
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LPL-treated LDL(-) suppressed NF kappa B and AP-1 activation, increasing expression of the PPAR alpha target gene I kappa B alpha, although only in the genetic presence of PPAR alpha and with intact LPL hydrolysis.
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31 |
14504138
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At 10 nm, E-Hb stimulated both AP-1 and NF-kappaB activity, as assessed by transient transfection, electromobility shift assays or immunofluorescence staining.
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32 |
15069077
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Mutational analysis of the PAI-1 promoter revealed that oxidative stress acted at an AP-1 site at -60/52 of the promoter.
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33 |
15145956
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Thus, glucose-stimulated monocyte adhesion is primarily regulated through phosphorylation of p38 with subsequent activation of AP-1, leading to IL-8 production.
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34 |
15591499
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The authors measured food intake, gastric emptying, c-Fos expression in the hypothalamus, and gene expression of hypothalamic neuropeptides in mice after administration of desacyl ghrelin.
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35 |
15772901
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Abundances of the transcription factors Elk-1 and SRF being major players in coupling of MAPKs to cfos promoter activation were not altered.
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36 |
16505217
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In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons.
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37 |
16848894
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Cultured MVECs, exposed either to glucose or glucose and varying concentrations of curcumin, were assessed for alterations of NOS expression and activation of nuclear factor-kappaB (NF-kappaB) and activating protein-1 (AP-1).
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38 |
17264162
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Insulin activates the glucokinase gene from plasma membrane-standing IR-B, while c-fos gene activation is dependent on clathrin-mediated IR-B-endocytosis and signaling from early endosomes.
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39 |
17264162
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Moreover, glucokinase gene up-regulation requires the integrity of the juxtamembrane IR-B NPEY-motif and signaling via PI3K-C2alpha-like/PDK1/PKB, while c-fos gene activation requires the intact C-terminal YTHM-motif and signaling via PI3K Ia/Shc/MEK1/ERK.
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40 |
17653206
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Increased production of ROS, mainly from mitochondria and NAD(P)H oxidase, stimulates signaling cascades including protein kinase C and mitogen-activated protein kinase pathway leading to nuclear translocation of transcription factors such as nuclear factor-kappaB (NF-kappaB), activator protein 1, and specificity protein 1.
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41 |
17666488
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We investigated FN mRNA, EDB(+)FN mRNA, and transforming growth factor (TGF)-beta mRNA expression, Akt phosphorylation, Akt kinase activity, and NF-kappaB and AP-1 activation in the retina, heart, and kidney.
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42 |
17916333
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Furthermore, intracerebroventricular injection of PrRP did not induce a significant increase of c-fos-like immunoreactivity in the paraventricular nucleus of the mutant rats compared to the control rats.
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43 |
18187539
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Intracerebroventricular administration of the MAPK inhibitor, PD98059, prevented LPS-induced ERK1/2 phosphorylation, c-fos activation, and the increase of CRH gene expression in the PVN but had no effect on c-fos activation in brainstem A2-C1/C2 regions.
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44 |
18519802
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Gut-glucose-sensitive c-Fos-positive cells of the arcuate nucleus colocalized with neuropeptide Y-positive neurons but not with proopiomelanocortin-positive neurons.
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45 |
19132243
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The MAPK inhibitors blocked the phosphorylation of IkBalpha and c-jun, indicating the role of MAPK in NF-kappaB and AP-1 activation in SMC under HG conditions.
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46 |
19132243
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In conclusion, HG upregulates the expression of fractalkine and MCP-1 in SMC leading to increased monocyte-SMC adhesive interactions by a mechanism involving activation of MAPK, activator protein-1 (AP-1) and NF-kappaB.
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47 |
19699734
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When bone marrow cells were cultured with macrophage colony stimulating factor and receptor activator NF-kappaB ligand (RANKL), the increased activity to form TRAP-positive multinucleated cells and the increased levels of mRNA and protein of c-fos and c-jun in the cultured cells from diabetic rats decreased to control levels in the curcumin-supplemented rats.
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48 |
19805233
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Furthermore, E2 treatment suppresses fasting-induced c-Fos activation in AgRP and NPY neurons and blunts the refeeding response.
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49 |
19931518
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Transfection of hCOX-2, as well as of deletion and mutation promoter constructs, revealed that the CCAAT/enhancer-binding protein (C/EBP) and activator protein-1 (AP-1) predominantly contributed to the effects of CDCQ.
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50 |
19933997
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ICV administration of PK2 increased c-fos expression in proopiomelanocortin neurons of the arcuate nucleus (ARC) of the hypothalamus.
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51 |
20034466
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Co-stimulation with resistin and HG increased P-selectin and fractalkine mRNA and protein and induced monocyte adhesion, generated an increase in NADPH oxidase activity and of the intracellular reactive oxygen species and activated the NF-kB and AP-1 transcription factors at similar values as those of each activator.
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52 |
20445124
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AP-1, the downstream transcription factor of ERK1/2, was also activated, and VEGF became highly regulated in a similar trend.
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53 |
20445124
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U0126, an inhibitor of ERK1/2, also downregulated VEGF expression, in addition to ERK1/2 and AP-1 activity.
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54 |
20542118
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Quercetin was found to attenuate HG induced increased NF-kappaB and AP-1 DNA binding activity in electrophoretic mobility shift assay.
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55 |
20693579
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Additionally, attempts to elucidate a possible mechanism underlying the UVA-mediated effects revealed that UVA induced migration inhibitory factor (MIF) gene expression, and this was mediated through activation of AP-1 (especially JNK and p42/44 MAPK) and nuclear factor-?B.
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56 |
20923696
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Here we show that the melanocortin agonist Melanotan II (MTII) potently suppresses food intake and activates the hypothalamic paraventricular nuclei (PVN) in SDC-3(-/-) mice based on c-fos immunoreactivity.
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57 |
20946955
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Consistent with this synergy, PRL and PDGF also synergized for c-fos-dependent transactivation of a luciferase reporter gene in T47D cells, indicating that events downstream of ERK activation reflect this signaling synergy.
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58 |
21252113
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Furthermore, troxerutin significantly inhibited the activation of c-jun N-terminal kinase 1 and I?B kinase ?/nuclear factor-?B induced by endoplasmic reticulum stress and enhanced insulin signalling pathway, which prevented obesity, restored normal levels of blood glucose, fatty acids and cholesterol and increased the phosphorylation of cyclic adenosine monophosphate response element-binding protein and the expression levels of c-fos in the hippocampus.
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59 |
20225236
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We also observed that IL-6 and high glucose stimulated the expression of c-Jun, a key subunit of AP-1 known to be essential for MMP-1 transcription.
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60 |
11457715
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These studies suggest that EGF potentiates the ANP glomerular effects in diabetes by inhibition of its degradation by mesangial NPR-C via a mechanism involving AP-1.
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61 |
20044046
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In vitro analysis corroborated a negative effect of insulin on osteoclast recruitment, maturation and the expression levels of c-fos and RANK transcripts.
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62 |
21076077
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Depletion of PPARG using a lentivirally encoded short hairpin RNA abolishes the effect of rosiglitazone to suppress activation of JNKs and induction of the transcription factors EGR1 and FOS as well as the gonadotropin genes Lhb and Fshb.
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63 |
21474329
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In summary, BEX inhibits lipotoxicity-induced IL-6 overproduction in muscle and adipose cell lines through the NF-?B and AP-1 pathways, implicating a potential application of this natural product as a cost-effective anti-inflammation nutraceutical.
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64 |
16522740
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Analysis of the INGAP promoter suggested that candidate regulators of INGAP expression include the transcription factors PDX-1, NeuroD, PAN-1, STAT and AP-1.
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65 |
21589925
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MCP-1 failed to induce amylin expression in pancreatic islets isolated from Fos knockout mice.
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66 |
19833897
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GLO1 knockdown mimicked the effect of high glucose, and in high glucose, overexpression of GLO1 normalized increased binding of NFkappaB p65 and AP-1.
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67 |
15507471
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Induction of the matrix metalloprotease MMP-7 (matrilysin) gene and protein by Wnt-2 was abolished by inactivation of the AP-1 binding site in the promoter.
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68 |
15507471
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Thus, the proinvasive activity of Wnt-2 is mediated by a noncanonical Wnt pathway using GSK-3beta and the AP-1 oncogene.
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69 |
18036354
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Our findings indicate that atorvastatin treatment for 15 days inhibited pressure overload-induced cardiac hypertrophy and prevented nuclear translocation of GATA4 and c-Jun and AP-1 DNA-binding activity.
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