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10.1002/bies.201600115 http://scihub22266oqcxt.onion/10.1002/bies.201600115 C5142446!5142446 !27644006     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27644006 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27644006 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Bioessays 2016 ; 38 (11 ): 1111-1116 Nephropedia Template TP {{tp|p=27644006 |t=2016. p53 in the game of transposons |pdf=|usr=}}{{27644006 }} gab.com Text p53 in the game of transposons JO: Bioessays http://www.kidney.de/pget.php?&tw=1&pmid=27644006 #FOAvip Throughout the animal kingdom, p53 genes function to restrain mobile elements and recent observations indicate that transposons become derepressed in human cancers. Together, these emerging lines of evidence suggest that cancers driven by p53 mutations could represent "transpospoathies," i.e. disease states linked to eruptions of mobile elements. The transposopathy hypothesis predicts that p53 acts through conserved mechanisms to contain transposon movement, and in this way, prevents tumor formation. How transposon eruptions provoke neoplasias is not well understood but, from a broader perspective, this hypothesis also provides an attractive framework to explore unrestrained mobile elements as inciters of late-onset idiopathic disease. Also see the video abstract here. Twit Text FOAVip p53 in the game of transposons ????Bioessays http://www.kidney.de/pget.php?&tw=1&pmid=27644006 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27644006 #FOAvip English Wikipedia <ref>{{Cite pmid|27644006 }}</ref> p53 in the game of transposons #MMPMID27644006 Wylie A ; Jones AE ; Abrams JM Bioessays 2016[Nov]; 38 (11 ): 1111-1116 PMID27644006 show ga Throughout the animal kingdom, p53 genes function to restrain mobile elements and recent observations indicate that transposons become derepressed in human cancers. Together, these emerging lines of evidence suggest that cancers driven by p53 mutations could represent "transpospoathies," i.e. disease states linked to eruptions of mobile elements. The transposopathy hypothesis predicts that p53 acts through conserved mechanisms to contain transposon movement, and in this way, prevents tumor formation. How transposon eruptions provoke neoplasias is not well understood but, from a broader perspective, this hypothesis also provides an attractive framework to explore unrestrained mobile elements as inciters of late-onset idiopathic disease. Also see the video abstract here. |*DNA Transposable Elements [MESH] |Animals [MESH] |Humans [MESH] |Mutation [MESH] |Neoplasms/*genetics/metabolism [MESH]p53 in the game of transposons (epmc).pdf DeepDyve Pubget Overpricing