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10.1093/hmg/ddu077 http://scihub22266oqcxt.onion/10.1093/hmg/ddu077 C4065145!4065145!24556217     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hum+Mol+Genet 2014 ; 23 (14): 3681-94 Nephropedia Template TP {{tp|p=24556217|t=2014. Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis |pdf=|usr=}}{{24556217}} gab.com Text Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis JO: Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=24556217 #FOAvip Inclusion body myositis (IBM), a degenerative and inflammatory disorder of skeletal muscle, and Alzheimer's disease share protein derangements and attrition of postmitotic cells. Overexpression of cyclins and proliferating cell nuclear antigen (PCNA) and evidence for DNA replication is reported in Alzheimer's disease brain, possibly contributing to neuronal death. It is unknown whether aberrant cell cycle reentry also occurs in IBM. We examined cell cycle markers in IBM compared with normal control, polymyositis (PM) and non-inflammatory dystrophy sample sets. Next, we tested for evidence of reentry and DNA synthesis in C2C12 myotubes induced to express ?-amyloid (A?42). We observed increased levels of Ki-67, PCNA and cyclins E/D1 in IBM compared with normals and non-inflammatory conditions. Interestingly, PM samples displayed similar increases. Satellite cell markers did not correlate with Ki-67-affected myofiber nuclei. DNA synthesis and cell cycle markers were induced in A?-bearing myotubes. Cell cycle marker and cyclin protein expressions were also induced in an experimental allergic myositis-like model of PM in mice. Levels of p21 (Cip1/WAF1), a cyclin-dependent kinase inhibitor, were decreased in affected myotubes. However, overexpression of p21 did not rescue cells from A?-induced toxicity. This is the first report of cell cycle reentry in human myositis. The absence of rescue and evidence for reentry in separate models of myodegeneration and inflammation suggest that new DNA synthesis may be a reactive response to either or both stressors. Twit Text FOAVip Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis ????Hum Mol Genet http://www.kidney.de/pget.php?&tw=1&pmid=24556217 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24556217 #FOAvip English Wikipedia <ref>{{Cite pmid|24556217}}</ref> Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis #MMPMID24556217 Kwon B; Kumar P; Lee HK; Zeng L; Walsh K; Fu Q; Barakat A; Querfurth HW Hum Mol Genet 2014[Jul]; 23 (14): 3681-94 PMID24556217show ga Inclusion body myositis (IBM), a degenerative and inflammatory disorder of skeletal muscle, and Alzheimer's disease share protein derangements and attrition of postmitotic cells. Overexpression of cyclins and proliferating cell nuclear antigen (PCNA) and evidence for DNA replication is reported in Alzheimer's disease brain, possibly contributing to neuronal death. It is unknown whether aberrant cell cycle reentry also occurs in IBM. We examined cell cycle markers in IBM compared with normal control, polymyositis (PM) and non-inflammatory dystrophy sample sets. Next, we tested for evidence of reentry and DNA synthesis in C2C12 myotubes induced to express ?-amyloid (A?42). We observed increased levels of Ki-67, PCNA and cyclins E/D1 in IBM compared with normals and non-inflammatory conditions. Interestingly, PM samples displayed similar increases. Satellite cell markers did not correlate with Ki-67-affected myofiber nuclei. DNA synthesis and cell cycle markers were induced in A?-bearing myotubes. Cell cycle marker and cyclin protein expressions were also induced in an experimental allergic myositis-like model of PM in mice. Levels of p21 (Cip1/WAF1), a cyclin-dependent kinase inhibitor, were decreased in affected myotubes. However, overexpression of p21 did not rescue cells from A?-induced toxicity. This is the first report of cell cycle reentry in human myositis. The absence of rescue and evidence for reentry in separate models of myodegeneration and inflammation suggest that new DNA synthesis may be a reactive response to either or both stressors. äAberrant cell cycle reentry in human and experimental inclusion body m(epmc).pdf DeepDyve Pubget Overpricing