scholarly journals Transcriptional Control of Tight Junction Proteins via a Protein Kinase C Signal Pathway in Human Telomerase Reverse Transcriptase-Transfected Human Pancreatic Duct Epithelial Cells

2010 ◽  
Vol 177 (2) ◽  
pp. 698-712 ◽  
Author(s):  
Hiroshi Yamaguchi ◽  
Takashi Kojima ◽  
Tatsuya Ito ◽  
Yasutoshi Kimura ◽  
Masafumi Imamura ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Transcriptional Control ◽  
Signal Pathway ◽  
Telomerase Reverse Transcriptase ◽  
Tight Junction Proteins ◽  
Human Telomerase Reverse Transcriptase ◽  
Kinase C ◽  
Human Telomerase ◽  
Junction Proteins

Abstract P254: Protein Kinase C Binding Protein 1 Inhibits Hypoxia-Inducible Factor 1 Action in the Heart

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Chad B Walton ◽  
David Veal ◽  
Chrisy Mafnas ◽  
Keith A MacCannell ◽  
Cynthia D Anderson ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Transcriptional Control ◽  
Binding Protein ◽  
Hypoxia Inducible Factor ◽  
Direct Interaction ◽  
Physiological Data ◽  
Stable Form ◽  
Hypoxia Inducible Factor 1 ◽  
Kinase C

The response to hypoxia in tissues is regulated by the heterodimeric transcription factor hypoxia inducible factor-1 (HIF-1). We have investigated the transcriptional effects of hypoxia-inducible factor 1 alpha (HIF-1α) in the heart by expressing an oxygen-stable form of HIF-1α in cardiac myocytes of transgenic mice. The result in most cases is regulation of an expected panoply of genes that restore homeostasis during hypoxia, with corresponding phenotypic changes including contractile dysfunction and increased capillary density. In mice that do not show this phenotype, the mRNA for protein kinase c binding protein 1 isoform 2 (PRKCBP1) was much more abundant, as was the protein, and chromatin immunoprecipitation shows a predominant binding of HIF to the promoter of this gene. Sequencing of the promoter region of the PRKCBP1 gene from the two phenotypes revealed an unexpected 480 bp insert in the HIF-resistant animals containing two canonical HIF binding sites. The protein co-immunoprecipitates with HIF and inhibits HIF transcriptional activity in cell culture. In FVB mice, that contain the promoter insert, PRKCBP is induced by ischemia and co-localizes with HIF in the infarct region. It may be responsible for the greater susceptibility of this strain to heart failure after infarction. We have confirmed with genetic, transcriptional, biochemical, and physiological data that Prkcbp1 inhibits HIF activity through direct interaction, in a mechanism mediated by transcriptional control.

scholarly journals Epidermal growth factor receptor activation by protein kinase C is necessary for FSH-induced meiotic resumption in porcine cumulus–oocyte complexes

2008 ◽  
Vol 197 (2) ◽  
pp. 409-419 ◽  
Author(s):  
Xiufen Chen ◽  
Bo Zhou ◽  
Jun Yan ◽  
Baoshan Xu ◽  
Ping Tai ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Cumulus Cells ◽  
Inhibitory Effect ◽  
Signal Pathway ◽  
Kinase C ◽  
Egfr Activation ◽  
Porcine Oocyte ◽  
Epidermal Growth

It is proved that epidermal growth factor (EGF)-like factors mediate gonadotropin-induced rodent oocyte maturation via EGF receptor (EGFR). However, the detail kinetics and signal pathway between FSH and EGF/EGFR is not clear in large animals. In the present study, we investigated the roles of EGFR and protein kinase C (PKC) in FSH-induced porcine oocyte meiotic resumption. Porcine cumulus–oocyte complexes were cultured in NCSU37 medium containing 10% porcine follicular fluid and germinal vesicle breakdown (meiotic resumption) was detected after different treatments. The results showed that EGF-like factor amphiregulin (AR) and EGFR mRNA were expressed in porcine cumulus cells, but not oocytes. FSH significantly induced AR mRNA expression with maximum at 4 h and activated EGFR phosphorylation at 8 h. AR (1–100 ng/ml) dose-dependently induced meiosis resumption of porcine oocyte. The specific EGFR inhibitor, AG1478, but not AG43 (the inactive analog of AG1478), completely blocked FSH, EGF, and AR-induced oocyte meiotic resumption; the inhibitory effect of AG1478 on FSH action gradually decreased when the inhibitor was added at 6 h or later and disappeared when it was added at 11 h; EGF reversed the inhibitory effect on FSH when AG1478 was added within 6 h. FSH triggered porcine oocyte meiotic resumption (at 20 h) later than that of EGF and AR (at 18 h). All these results supported that endogenously produced EGFR activator(s), possibly AR (maximum at 4 h) and EGFR activation (began at 6 h and finished within 11 h), in cumulus cells is necessary for FSH-induced porcine oocyte meiotic resumption (began at 18 h). Furthermore, PKC activator PMA mimicked but PKC inhibitor chelerythrine chloride inhibited FSH action, and AG1478 also suppressed PMA-induced porcine oocyte meiotic resumption. These data together suggested that EGFR activation, by PKC signal pathway, participates in FSH-induced porcine oocyte meiotic resumption.

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