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10.1038/s41419-018-0353-z http://scihub22266oqcxt.onion/10.1038/s41419-018-0353-z C5832796!5832796 !29497040     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29497040 &cmd=llinks): Failed to open stream: HTTP request failed! 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Podocyte-specific Rac1 deficiency ameliorates podocyte damage and proteinuria in STZ-induced diabetic nephropathy in mice |pdf=|usr=}}{{29497040 }} gab.com Text Podocyte-specific Rac1 deficiency ameliorates podocyte damage and proteinuria in STZ-induced diabetic nephropathy in mice JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29497040 #FOAvip Activation of Ras-related C3 botulinum toxin substrate 1 (Rac1) has been implicated in diverse kidney diseases, yet its in vivo significance in diabetic nephropathy (DN) is largely unknown. In the present study, we demonstrated a podocyte-specific Rac1-deficient mouse strain and showed that specific inhibition of Rac1 was able to attenuate diabetic podocyte injury and proteinuria by the blockade of Rac1/PAK1/p38/?-catenin signaling cascade, which reinstated the integrity of podocyte slit diaphragms (SD), rectified the effacement of foot processes (FPs), and prevented the dedifferentiation of podocytes. In vitro, we showed Rac1/PAK1 physically bound to ?-catenin and had a direct phosphorylation modification on its C-terminal Ser675, leading to less ubiquitylated ?-catenin, namely more stabilized ?-catenin, and its nuclear migration under high-glucose conditions; further, p38 activation might be responsible for ?-catenin nuclear accumulation via potentiating myocyte-specific enhancer factor 2C (MEF2c) phosphorylation. These findings provided evidence for a potential renoprotective and therapeutic strategy of cell-specific Rac1 deficiency for DN and other proteinuric diseases. Twit Text FOAVip Podocyte-specific Rac1 deficiency ameliorates podocyte damage and proteinuria in STZ-induced diabetic nephropathy in mice ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29497040 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29497040 #FOAvip English Wikipedia <ref>{{Cite pmid|29497040 }}</ref> Podocyte-specific Rac1 deficiency ameliorates podocyte damage and proteinuria in STZ-induced diabetic nephropathy in mice #MMPMID29497040 Lv Z ; Hu M ; Fan M ; Li X ; Lin J ; Zhen J ; Wang Z ; Jin H ; Wang R Cell Death Dis 2018[Mar]; 9 (3 ): 342 PMID29497040 show ga Activation of Ras-related C3 botulinum toxin substrate 1 (Rac1) has been implicated in diverse kidney diseases, yet its in vivo significance in diabetic nephropathy (DN) is largely unknown. In the present study, we demonstrated a podocyte-specific Rac1-deficient mouse strain and showed that specific inhibition of Rac1 was able to attenuate diabetic podocyte injury and proteinuria by the blockade of Rac1/PAK1/p38/?-catenin signaling cascade, which reinstated the integrity of podocyte slit diaphragms (SD), rectified the effacement of foot processes (FPs), and prevented the dedifferentiation of podocytes. In vitro, we showed Rac1/PAK1 physically bound to ?-catenin and had a direct phosphorylation modification on its C-terminal Ser675, leading to less ubiquitylated ?-catenin, namely more stabilized ?-catenin, and its nuclear migration under high-glucose conditions; further, p38 activation might be responsible for ?-catenin nuclear accumulation via potentiating myocyte-specific enhancer factor 2C (MEF2c) phosphorylation. These findings provided evidence for a potential renoprotective and therapeutic strategy of cell-specific Rac1 deficiency for DN and other proteinuric diseases. |Animals [MESH] |Diabetic Nephropathies/chemically induced/genetics/*metabolism [MESH] |Humans [MESH] |MEF2 Transcription Factors/genetics/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Neuropeptides/deficiency/*genetics [MESH] |Podocytes/*metabolism [MESH] |Protein Binding [MESH] |Proteinuria/genetics/*metabolism [MESH] |Signal Transduction [MESH] |Streptozocin/adverse effects [MESH] |beta Catenin/genetics/metabolism [MESH] |p21-Activated Kinases/genetics/metabolism [MESH] |p38 Mitogen-Activated Protein Kinases/genetics/metabolism [MESH]Podocyte-specific Rac1 deficiency ameliorates podocyte damage and prot(epmc).pdf DeepDyve Pubget Overpricing