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10.1038/cddis.2013.535 http://scihub22266oqcxt.onion/10.1038/cddis.2013.535 C4040660!4040660!24481442     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2014 ; 5 (1): e1028- Nephropedia Template TP {{tp|p=24481442|t=2014. GLI2 induces genomic instability in human keratinocytes by inhibiting apoptosis |pdf=|usr=}}{{24481442}} gab.com Text GLI2 induces genomic instability in human keratinocytes by inhibiting apoptosis JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24481442 #FOAvip Abnormal Sonic Hedgehog signalling leads to increased transcriptional activation of its downstream effector, glioma 2 (GLI2), which is implicated in the pathogenesis of a variety of human cancers. However, the mechanisms underlying the tumorigenic role of GLI2 remain elusive. We demonstrate that overexpression of GLI2-? isoform, which lacks the N-terminal repressor domain (GLI2?N) in human keratinocytes is sufficient to induce numerical and structural chromosomal aberrations, including tetraploidy/aneuploidy and chromosomal translocations. This is coupled with suppression of cell cycle regulators p21WAF1/CIP1 and 14-3-3?, and strong induction of anti-apoptotic signalling, resulting in a reduction in the ability to eliminate genomically abnormal cells. Overexpression of GLI2?N also rendered human keratinocytes resistant to UVB-mediated apoptosis, whereas inhibition of B-cell lymphoma 2 (BCL-2) restored endogenous (genomic instability (GIN)) and exogenous (UVB) DNA damage-induced apoptosis. Thus, we propose that ectopic expression of GLI2 profoundly affects the genomic integrity of human epithelial cells and contributes to the survival of progenies with genomic alterations by deregulating cell cycle proteins and disabling the apoptotic mechanisms responsible for their elimination. This study reveals a novel role for GLI2 in promoting GIN, a hallmark of human tumors, and identifies potential mechanisms that may provide new opportunities for the design of novel forms of cancer therapeutic strategies. Twit Text FOAVip GLI2 induces genomic instability in human keratinocytes by inhibiting apoptosis ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24481442 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24481442 #FOAvip English Wikipedia <ref>{{Cite pmid|24481442}}</ref> GLI2 induces genomic instability in human keratinocytes by inhibiting apoptosis #MMPMID24481442 Pantazi E; Gemenetzidis E; Trigiante G; Warnes G; Shan L; Mao X; Ikram M; Teh MT; Lu YJ; Philpott MP Cell Death Dis 2014[Jan]; 5 (1): e1028- PMID24481442show ga Abnormal Sonic Hedgehog signalling leads to increased transcriptional activation of its downstream effector, glioma 2 (GLI2), which is implicated in the pathogenesis of a variety of human cancers. However, the mechanisms underlying the tumorigenic role of GLI2 remain elusive. We demonstrate that overexpression of GLI2-? isoform, which lacks the N-terminal repressor domain (GLI2?N) in human keratinocytes is sufficient to induce numerical and structural chromosomal aberrations, including tetraploidy/aneuploidy and chromosomal translocations. This is coupled with suppression of cell cycle regulators p21WAF1/CIP1 and 14-3-3?, and strong induction of anti-apoptotic signalling, resulting in a reduction in the ability to eliminate genomically abnormal cells. Overexpression of GLI2?N also rendered human keratinocytes resistant to UVB-mediated apoptosis, whereas inhibition of B-cell lymphoma 2 (BCL-2) restored endogenous (genomic instability (GIN)) and exogenous (UVB) DNA damage-induced apoptosis. Thus, we propose that ectopic expression of GLI2 profoundly affects the genomic integrity of human epithelial cells and contributes to the survival of progenies with genomic alterations by deregulating cell cycle proteins and disabling the apoptotic mechanisms responsible for their elimination. This study reveals a novel role for GLI2 in promoting GIN, a hallmark of human tumors, and identifies potential mechanisms that may provide new opportunities for the design of novel forms of cancer therapeutic strategies. äGLI2 induces genomic instability in human keratinocytes by inhibiting (epmc).pdf DeepDyve Pubget Overpricing