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10.1038/ncomms7496 http://scihub22266oqcxt.onion/10.1038/ncomms7496 C4366504!4366504 !25754093     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25754093 &cmd=llinks): Failed to open stream: HTTP request failed! 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Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy |pdf=|usr=}}{{25754093 }} gab.com Text Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25754093 #FOAvip Endoplasmic reticulum (ER) stress is associated with diabetic nephropathy (DN), but its pathophysiological relevance and the mechanisms that compromise adaptive ER signalling in podocytes remain unknown. Here we show that nuclear translocation of the transcription factor spliced X-box binding protein-1 (sXBP1) is selectively impaired in DN, inducing activating transcription factor-6 (ATF6) and C/EBP homology protein (CHOP). Podocyte-specific genetic ablation of XBP1 or inducible expression of ATF6 in mice aggravates DN. sXBP1 lies downstream of insulin signalling and attenuating podocyte insulin signalling by genetic ablation of the insulin receptor or the regulatory subunits phosphatidylinositol 3-kinase (PI3K) p85? or p85? impairs sXBP1 nuclear translocation and exacerbates DN. Corroborating our findings from murine DN, the interaction of sXBP1 with p85? and p85? is markedly impaired in the glomerular compartment of human DN. Thus, signalling via the insulin receptor, p85, and XBP1 maintains podocyte homeostasis, while disruption of this pathway impairs podocyte function in DN. Twit Text FOAVip Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25754093 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25754093 #FOAvip English Wikipedia <ref>{{Cite pmid|25754093 }}</ref> Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy #MMPMID25754093 Madhusudhan T ; Wang H ; Dong W ; Ghosh S ; Bock F ; Thangapandi VR ; Ranjan S ; Wolter J ; Kohli S ; Shahzad K ; Heidel F ; Krueger M ; Schwenger V ; Moeller MJ ; Kalinski T ; Reiser J ; Chavakis T ; Isermann B Nat Commun 2015[Mar]; 6 (ä): 6496 PMID25754093 show ga Endoplasmic reticulum (ER) stress is associated with diabetic nephropathy (DN), but its pathophysiological relevance and the mechanisms that compromise adaptive ER signalling in podocytes remain unknown. Here we show that nuclear translocation of the transcription factor spliced X-box binding protein-1 (sXBP1) is selectively impaired in DN, inducing activating transcription factor-6 (ATF6) and C/EBP homology protein (CHOP). Podocyte-specific genetic ablation of XBP1 or inducible expression of ATF6 in mice aggravates DN. sXBP1 lies downstream of insulin signalling and attenuating podocyte insulin signalling by genetic ablation of the insulin receptor or the regulatory subunits phosphatidylinositol 3-kinase (PI3K) p85? or p85? impairs sXBP1 nuclear translocation and exacerbates DN. Corroborating our findings from murine DN, the interaction of sXBP1 with p85? and p85? is markedly impaired in the glomerular compartment of human DN. Thus, signalling via the insulin receptor, p85, and XBP1 maintains podocyte homeostasis, while disruption of this pathway impairs podocyte function in DN. |Activating Transcription Factor 6/deficiency/*genetics [MESH] |Animals [MESH] |Class Ia Phosphatidylinositol 3-Kinase/deficiency/*genetics [MESH] |DNA-Binding Proteins/deficiency/*genetics [MESH] |Databases, Factual [MESH] |Diabetes Mellitus, Experimental/chemically induced/*genetics/metabolism/pathology [MESH] |Diabetic Nephropathies/chemically induced/*genetics/metabolism/pathology [MESH] |Endoplasmic Reticulum Stress/*genetics [MESH] |Endoplasmic Reticulum/genetics/metabolism/pathology [MESH] |Gene Expression Regulation [MESH] |Humans [MESH] |Insulin/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Podocytes/*metabolism/pathology [MESH] |Receptor, Insulin/deficiency/genetics [MESH] |Regulatory Factor X Transcription Factors [MESH] |Signal Transduction [MESH] |Streptozocin [MESH] |Transcription Factor CHOP/genetics/metabolism [MESH] |Transcription Factors/deficiency/*genetics [MESH]Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-d(epmc).pdf DeepDyve Pubget Overpricing