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10.1016/j.ebiom.2017.03.040 http://scihub22266oqcxt.onion/10.1016/j.ebiom.2017.03.040 C5405175!5405175!28389215     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28389215&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 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EBioMedicine 2017 ; 18 (ä): 146-56 Nephropedia Template TP {{tp|p=28389215|t=2017. Clock Gene Dysregulation Induced by Chronic ER Stress Disrupts ?-cell Function |pdf=|usr=}}{{28389215}} gab.com Text Clock Gene Dysregulation Induced by Chronic ER Stress Disrupts -cell Function JO: EBioMedicine http://www.kidney.de/pget.php?&tw=1&pmid=28389215 #FOAvip In Wfs1?/?Ay/a islets, in association with endoplasmic reticulum (ER) stress, D-site-binding protein (Dbp) expression decreased and Nuclear Factor IL-3 (Nfil3)/E4 Promoter-binding protein 4 (E4bp4) expression increased, leading to reduced DBP transcriptional activity. Similar alterations were observed with chemically-induced ER stress. Transgenic mice expressing E4BP4 under the control of the mouse insulin I gene promoter (MIP), in which E4BP4 in ?-cells is expected to compete with DBP for D-box, displayed remarkable glucose intolerance with severely impaired insulin secretion. Basal ATP/ADP ratios in MIP-E4BP4 islets were elevated without the circadian oscillations observed in wild-type islets. Neither elevation of the ATP/ADP ratio nor an intracellular Ca2 + response was observed after glucose stimulation. RNA expressions of genes involved in insulin secretion gradually increase in wild-type islets early in the feeding period. In MIP-E4BP4 islets, however, these increases were not observed. Thus, molecular clock output DBP transcriptional activity, susceptible to ER stress, plays pivotal roles in ?-cell priming for insulin release by regulating ?-cell metabolism and gene expressions. Because ER stress is also involved in the ?-cell failure in more common Type-2 diabetes, understanding the currently identified ER stress-associated mechanisms warrants novel therapeutic and preventive strategies for both rare form and common diabetes. Twit Text FOAVip Clock Gene Dysregulation Induced by Chronic ER Stress Disrupts -cell Function ????EBioMedicine http://www.kidney.de/pget.php?&tw=1&pmid=28389215 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28389215 #FOAvip English Wikipedia <ref>{{Cite pmid|28389215}}</ref> Clock Gene Dysregulation Induced by Chronic ER Stress Disrupts ?-cell Function #MMPMID28389215 Ohta Y; Taguchi A; Matsumura T; Nakabayashi H; Akiyama M; Yamamoto K; Fujimoto R; Suetomi R; Yanai A; Shinoda K; Tanizawa Y EBioMedicine 2017[Apr]; 18 (ä): 146-56 PMID28389215show ga In Wfs1?/?Ay/a islets, in association with endoplasmic reticulum (ER) stress, D-site-binding protein (Dbp) expression decreased and Nuclear Factor IL-3 (Nfil3)/E4 Promoter-binding protein 4 (E4bp4) expression increased, leading to reduced DBP transcriptional activity. Similar alterations were observed with chemically-induced ER stress. Transgenic mice expressing E4BP4 under the control of the mouse insulin I gene promoter (MIP), in which E4BP4 in ?-cells is expected to compete with DBP for D-box, displayed remarkable glucose intolerance with severely impaired insulin secretion. Basal ATP/ADP ratios in MIP-E4BP4 islets were elevated without the circadian oscillations observed in wild-type islets. Neither elevation of the ATP/ADP ratio nor an intracellular Ca2 + response was observed after glucose stimulation. RNA expressions of genes involved in insulin secretion gradually increase in wild-type islets early in the feeding period. In MIP-E4BP4 islets, however, these increases were not observed. Thus, molecular clock output DBP transcriptional activity, susceptible to ER stress, plays pivotal roles in ?-cell priming for insulin release by regulating ?-cell metabolism and gene expressions. Because ER stress is also involved in the ?-cell failure in more common Type-2 diabetes, understanding the currently identified ER stress-associated mechanisms warrants novel therapeutic and preventive strategies for both rare form and common diabetes. äClock Gene Dysregulation Induced by Chronic ER Stress Disrupts ?-cell (epmc).pdf DeepDyve Pubget Overpricing