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PMID |
Sentence |
1 |
2521209
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We studied the growth effects of insulin and IGF-I as measured by stimulation of c-myc, DNA synthesis, and cellular proliferation in the presence and absence of these antibodies.
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2 |
2474397
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Peripheral blood mononuclear cells (MNC) of patients with systemic lupus erythematosus (SLE) have increased expression of the c-myc protooncogene.
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3 |
1708099
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Cycloheximide treatment resulted in a superinduction of both c-fos and c-myc and prevented any further stimulation by IGF-I.
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4 |
1730782
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The exact relationship between EGF-stimulated tyrosine phosphorylation, induction of the cellular proto-oncogenes c-myc and c-fos, and DNA synthesis remains uncertain.
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5 |
1730782
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They also suggest that, in MDCK cells, the EGF dependent induction of the c-fos and c-myc genes is not strictly correlated to the extent of EGF receptor autophosphorylation or EGF-stimulated DNA synthesis, and that EGF stimulation of DNA synthesis likely involves additional rate-limiting intermediate steps.
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6 |
8468460
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Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1.
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7 |
11714718
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The expression of the basic helix-loop-helix transcription factor c-Myc is induced in pancreatic islets of several different diabetic model animals and is possibly involved in suppression of the insulin gene transcription.
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8 |
11714718
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In this study, we found that activity of protein kinase C is increased by high glucose, preceding the induction of c-myc expression and that PKC beta2 specifically regulates c-myc expression in pancreatic beta-cells.
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9 |
11714718
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Moreover, c-myc induction by high glucose was suppressed by adenovirus-mediated overexpression of DN PKC beta2 but not by other DN PKC isoforms.
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10 |
11714718
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These results suggest that at least some of the reduction of insulin gene transcription found in the diabetic state is mediated by PKC beta2 regulation of c-myc expression.
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11 |
11799123
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In gel-shift assays c-Myc bound to the E-box in the insulin gene promoter region.
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12 |
11799123
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Furthermore, in betaTC1, MIN6, and HIT-T15 cells and primary rat islets, wild type insulin gene promoter activity was dramatically decreased by c-Myc overexpression, whereas the activity of an E-box mutated insulin promoter was not affected.
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13 |
11799123
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In HeLa and HepG2 cells c-Myc exerted a suppressive effect on the insulin promoter activity only in the presence of NeuroD/BETA2 but not PDX-1.
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14 |
11799123
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Both c-Myc and NeuroD can bind the E-box element in the insulin promoter, but unlike NeuroD, the c-Myc transactivation domain lacked the ability to activate insulin gene expression.
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15 |
11799123
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In conclusion, increased expression of c-Myc in beta-cells suppresses the insulin gene transcription by inhibiting NeuroD-mediated transcriptional activation.
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16 |
12393479
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Additional studies showed that HDAC-i treatment inhibited c-Myc expression, which was further shown to be important for CD154 gene activation.
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17 |
16283526
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Furthermore, a substantial decrease in the expression of c-myc, an established endogenous transcriptional repressor of gadd45alpha and gadd153 genes, was noted.
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18 |
16887799
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Using a Myc-tagged PDX-1 construct, we showed that the translocation of PDX-1 from the nucleus to the cytoplasm during glucotoxic conditions was prevented when CDK5 was inhibited.
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19 |
18302196
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In addition to its recently recognized role in diabetes, aberrant TCF7L2 expression has been implicated in cancer through regulation of cell proliferation and apoptosis by c-MYC and cyclin D.
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20 |
18987311
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We show here that RNA interference with the expression of parafibromin or Paf1 stimulates cell proliferation and increases levels of the c-myc proto-oncogene product, a DNA-binding protein and established regulator of cell growth.
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21 |
18987311
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Knockdown of c-myc blocks the proliferative effect of RNA interference with parafibromin or Paf1 expression.
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22 |
18987311
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These experiments provide a previously uncharacterized mechanism for the anti-proliferative action of the parafibromin tumor suppressor protein resulting from PAF1 complex-mediated inhibition of the c-myc proto-oncogene.
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23 |
20442404
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Rspo1 activated cWnt signaling in MIN6 beta-cells by increasing nuclear beta-catenin and c-myc, a cWnt target gene.
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24 |
20566667
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Wounds were assessed for collagen content, thickness and vascularity of granulation tissue, apoptosis, reepithelialization, and expression of c-myc and beta-catenin.
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25 |
20923823
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This was concomitant with increased E2F1 binding to the c-myc promoter.
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26 |
21205112
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It regulated c-myc gene expression through the JAK2/STAT system and c-fos and AgRP (agouti-related peptide) gene expression through the ERK1/2 pathway simultaneously and independently.
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27 |
17270172
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Our results suggest that quiescence of small cells correlates with up-regulation of Cdk inhibitors p27(Kip1), p16(INK4a) and p21(CIP1), PTEN, Hep27 and Foxo1a and with down-regulation of c-Myc and the receptors for EGF, FGF2 and HGF.
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28 |
17317781
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Here we demonstrated that Pdx1 could suppress c-Myc promoter activity, which relied on T cell factor (Tcf) binding elements harbored in c-Myc promoter.
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29 |
17317781
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Moreover, adenovirus-mediated Pdx1 interference caused cell proliferation and cytokine-induced apoptosis via the dysregulation of c-Myc transcription.
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30 |
21521872
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Bcl-2, Cdk4, and c-myc expression levels were increased in Pax4 islets while MafA, insulin, and GLUT2 transcript levels were suppressed in both animal models.
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31 |
21719578
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To this end, we examined the role of cytochrome c in pancreatic ?-cells under homeostatic conditions and in diabetes models, including those induced by streptozotocin (STZ) and c-Myc.
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32 |
21719578
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Previous studies have shown that both STZ- and c-Myc-induced ?-cell apoptosis is mediated through caspase-3 activation; however, the precise mechanism in these modes of cell death was not characterized.
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33 |
21719578
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We also observed that the extrinsic apoptotic pathway mediated through caspase-8 was not essential in c-Myc-induced ?-cell destruction.
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34 |
21719578
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These findings suggest that cytochrome c is not required for STZ-induced ?-cell apoptosis and, together with the caspase-8-mediated extrinsic pathway, plays a redundant role in c-Myc-induced ?-cell apoptosis.
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35 |
21829621
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Using HIT-T15 and primary adult islet cells as cell models, we show that ISL1 promoted adult pancreatic islet cell proliferation with increased c-Myc and CyclinD1 transcription, while knockdown of ISL1 increased the proportion of cells in G(1) phase and decreased the proportion of cells in G(2)/M and S phases.
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36 |
21829621
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Further investigation shows that ISL1 activated both c-Myc and CyclinD1 transcription through direct binding on their promoters.
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37 |
21494254
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With confirmation using RNA and protein analyses, GSI-I blocked nuclear accumulation of cleaved Notch1 and Notch2, and inhibited Notch targets Hey2 and Myc.
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