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10.1124/jpet.115.229377 http://scihub22266oqcxt.onion/10.1124/jpet.115.229377 C4767392!4767392!26699146     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26699146&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26699146.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Pharmacol+Exp+Ther 2016 ; 356 (3): 525-33 Nephropedia Template TP {{tp|p=26699146|t=2016. 20-HETE Activates the Transcription of Angiotensin-Converting Enzyme via Nuclear Factor-?B Translocation and Promoter Binding |pdf=|usr=}}{{26699146}} gab.com Text 20-HETE Activates the Transcription of Angiotensin-Converting Enzyme via Nuclear Factor- B Translocation and Promoter Binding JO: J Pharmacol Exp Ther http://www.kidney.de/pget.php?&tw=1&pmid=26699146 #FOAvip Increased vascular 20-hydroxyeicosatetraenoic acid (20-HETE), a cytochrome P450 arachidonic acid metabolite, promotes vascular dysfunction, injury, and hypertension that is dependent, in part, on the renin angiotensin system (RAS). We have shown that, in human microvascular endothelial cells, 20-HETE increases angiotensin-converting enzyme (ACE) mRNA, protein, and ACE activity via an epidermal growth factor receptor (EGFR)/tyrosine kinase/mitogen-activated protein kinase (MAPK)/inhibitor of ?B kinase (IKK)??mediated signaling pathway. In this work, we show that, similar to epidermal growth factor (EGF), 20-HETE (10 nM) activates EGFR by stimulating tyrosine phosphorylation; however, unlike 20-HETE, EGF does not induce ACE expression, and pretreatment with a neutralizing antibody against EGF does not prevent the 20-HETE?mediated ACE induction. Inhibition of nuclear factor ?B (NF-?B) activation prevented the 4.58-fold (±0.78; P < 0.05) 20-HETE?mediated induction of ACE. The 20-HETE increased NF-?B?binding activity in nuclear extracts and the activity of both the somatic and germinal ACE promoters by 4.37-fold (±0.18; P < 0.05) and 2.53-fold (± 0.24; P < 0.05), respectively. The 20-HETE?stimulated ACE promoter activity was abrogated by the 20-HETE antagonist 20-hydroxy-6,15-eicosadienoic acid and by inhibitors of EGFR, MAPK, IKK?, and NF-?B activation. Sequence analysis demonstrated the presence of two and one putative NF-?B binding sites on the human somatic and germinal ACE promoters, respectively. Chromatin immunoprecipitation assay indicated that 20-HETE stimulates the translocation and subsequent binding of NF-?B to each of the putative binding sites (S1, 3.43 ± 0.3-fold enrichment versus vehicle; S2, 3.72 ± 0.68-fold enrichment versus vehicle; S3, 3.20 ± 0.18-fold enrichment versus vehicle; P < 0.05). This is the first study to identify NF-?B as a transcriptional factor for ACE and to implicate a distinct EGFR/MAPK/IKK/NF-?B signaling cascade underlying 20-HETE?mediated transcriptional activation of ACE mRNA and stimulation of ACE activity. Twit Text FOAVip 20-HETE Activates the Transcription of Angiotensin-Converting Enzyme via Nuclear Factor- B Translocation and Promoter Binding ????J Pharmacol Exp Ther http://www.kidney.de/pget.php?&tw=1&pmid=26699146 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26699146 #FOAvip English Wikipedia <ref>{{Cite pmid|26699146}}</ref> 20-HETE Activates the Transcription of Angiotensin-Converting Enzyme via Nuclear Factor-?B Translocation and Promoter Binding #MMPMID26699146 Garcia V; Shkolnik B; Milhau L; Falck JR; Schwartzman ML J Pharmacol Exp Ther 2016[Mar]; 356 (3): 525-33 PMID26699146show ga Increased vascular 20-hydroxyeicosatetraenoic acid (20-HETE), a cytochrome P450 arachidonic acid metabolite, promotes vascular dysfunction, injury, and hypertension that is dependent, in part, on the renin angiotensin system (RAS). We have shown that, in human microvascular endothelial cells, 20-HETE increases angiotensin-converting enzyme (ACE) mRNA, protein, and ACE activity via an epidermal growth factor receptor (EGFR)/tyrosine kinase/mitogen-activated protein kinase (MAPK)/inhibitor of ?B kinase (IKK)??mediated signaling pathway. In this work, we show that, similar to epidermal growth factor (EGF), 20-HETE (10 nM) activates EGFR by stimulating tyrosine phosphorylation; however, unlike 20-HETE, EGF does not induce ACE expression, and pretreatment with a neutralizing antibody against EGF does not prevent the 20-HETE?mediated ACE induction. Inhibition of nuclear factor ?B (NF-?B) activation prevented the 4.58-fold (±0.78; P < 0.05) 20-HETE?mediated induction of ACE. The 20-HETE increased NF-?B?binding activity in nuclear extracts and the activity of both the somatic and germinal ACE promoters by 4.37-fold (±0.18; P < 0.05) and 2.53-fold (± 0.24; P < 0.05), respectively. The 20-HETE?stimulated ACE promoter activity was abrogated by the 20-HETE antagonist 20-hydroxy-6,15-eicosadienoic acid and by inhibitors of EGFR, MAPK, IKK?, and NF-?B activation. Sequence analysis demonstrated the presence of two and one putative NF-?B binding sites on the human somatic and germinal ACE promoters, respectively. Chromatin immunoprecipitation assay indicated that 20-HETE stimulates the translocation and subsequent binding of NF-?B to each of the putative binding sites (S1, 3.43 ± 0.3-fold enrichment versus vehicle; S2, 3.72 ± 0.68-fold enrichment versus vehicle; S3, 3.20 ± 0.18-fold enrichment versus vehicle; P < 0.05). This is the first study to identify NF-?B as a transcriptional factor for ACE and to implicate a distinct EGFR/MAPK/IKK/NF-?B signaling cascade underlying 20-HETE?mediated transcriptional activation of ACE mRNA and stimulation of ACE activity. ä20-HETE Activates the Transcription of Angiotensin-Converting Enzyme v(epmc).pdf DeepDyve Pubget Overpricing