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10.1038/s41419-018-0603-0 http://scihub22266oqcxt.onion/10.1038/s41419-018-0603-0 C5964068!5964068!29789539     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29789539&cmd=llinks): Failed to open stream: HTTP request failed! 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Proteasomal degradation of the histone acetyl transferase p300 contributes to beta-cell injury in a diabetes environment |pdf=|usr=}}{{29789539}} gab.com Text Proteasomal degradation of the histone acetyl transferase p300 contributes to beta-cell injury in a diabetes environment JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29789539 #FOAvip In type 2 diabetes, amyloid oligomers, chronic hyperglycemia, lipotoxicity, and pro-inflammatory cytokines are detrimental to beta-cells, causing apoptosis and impaired insulin secretion. The histone acetyl transferase p300, involved in remodeling of chromatin structure by epigenetic mechanisms, is a key ubiquitous activator of the transcriptional machinery. In this study, we report that loss of p300 acetyl transferase activity and expression leads to beta-cell apoptosis, and most importantly, that stress situations known to be associated with diabetes alter p300 levels and functional integrity. We found that proteasomal degradation is the mechanism subserving p300 loss in beta-cells exposed to hyperglycemia or pro-inflammatory cytokines. We also report that melatonin, a hormone produced in the pineal gland and known to play key roles in beta-cell health, preserves p300 levels altered by these toxic conditions. Collectively, these data imply an important role for p300 in the pathophysiology of diabetes. Twit Text FOAVip Proteasomal degradation of the histone acetyl transferase p300 contributes to beta-cell injury in a diabetes environment ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29789539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29789539 #FOAvip English Wikipedia <ref>{{Cite pmid|29789539}}</ref> Proteasomal degradation of the histone acetyl transferase p300 contributes to beta-cell injury in a diabetes environment #MMPMID29789539 Ruiz L; Gurlo T; Ravier MA; Wojtusciszyn A; Mathieu J; Brown MR; Broca C; Bertrand G; Butler PC; Matveyenko AV; Dalle S; Costes S Cell Death Dis 2018[Jun]; 9 (6): � PMID29789539show ga In type 2 diabetes, amyloid oligomers, chronic hyperglycemia, lipotoxicity, and pro-inflammatory cytokines are detrimental to beta-cells, causing apoptosis and impaired insulin secretion. The histone acetyl transferase p300, involved in remodeling of chromatin structure by epigenetic mechanisms, is a key ubiquitous activator of the transcriptional machinery. In this study, we report that loss of p300 acetyl transferase activity and expression leads to beta-cell apoptosis, and most importantly, that stress situations known to be associated with diabetes alter p300 levels and functional integrity. We found that proteasomal degradation is the mechanism subserving p300 loss in beta-cells exposed to hyperglycemia or pro-inflammatory cytokines. We also report that melatonin, a hormone produced in the pineal gland and known to play key roles in beta-cell health, preserves p300 levels altered by these toxic conditions. Collectively, these data imply an important role for p300 in the pathophysiology of diabetes. �Proteasomal degradation of the histone acetyl transferase p300 contrib(epmc).pdf DeepDyve Pubget Overpricing