Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1158/2159-8290.CD-14-0625 http://scihub22266oqcxt.onion/10.1158/2159-8290.CD-14-0625 C4355177!4355177!25582697     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Discov 2015 ; 5 (3): 288-303 Nephropedia Template TP {{tp|p=25582697|t=2015. PRMT5 is required for lymphomagenesis triggered by multiple oncogenic drivers |pdf=|usr=}}{{25582697}} gab.com Text PRMT5 is required for lymphomagenesis triggered by multiple oncogenic drivers JO: Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=25582697 #FOAvip Protein arginine transferase 5(PRMT5) has been implicated as a key modulator of lymphomagenesis. Whether PRMT5 has overt oncogenic function in the context of leukemia/lymphoma and whether it represents a therapeutic target remains to be established. We demonstrate that inactivation of PRMT5 inhibits colony-forming activity by multiple oncogenic-drivers including cyclin D1, c-MYC, NOTCH1 and MLL-AF9. Furthermore, we demonstrate that PRMT5 overexpression specifically cooperates with cyclin D1 to drive lymphomagenesis in a mouse model revealing inherent neoplastic activity. Molecular analysis of lymphomas, revealed that arginine methylation of p53 selectively suppresses expression of crucial proapoptotic and anti-proliferative target genes thereby sustaining tumor cell self-renewal and proliferation and bypassing the need for the acquisition of inactivating p53 mutations. Critically, analysis of human tumor specimen reveal a strong correlation between cyclin D1 overexpression and p53 methylation supporting the biomedical relevance of this pathway. Twit Text FOAVip PRMT5 is required for lymphomagenesis triggered by multiple oncogenic drivers ????Cancer Discov http://www.kidney.de/pget.php?&tw=1&pmid=25582697 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25582697 #FOAvip English Wikipedia <ref>{{Cite pmid|25582697}}</ref> PRMT5 is required for lymphomagenesis triggered by multiple oncogenic drivers #MMPMID25582697 Li Y; Chitnis N; Nakagawa H; Kita Y; Natsugoe S; Yang Y; Li Z; Wasik M; Klein-Szanto AJP; Rustgi AK; Diehl JA Cancer Discov 2015[Mar]; 5 (3): 288-303 PMID25582697show ga Protein arginine transferase 5(PRMT5) has been implicated as a key modulator of lymphomagenesis. Whether PRMT5 has overt oncogenic function in the context of leukemia/lymphoma and whether it represents a therapeutic target remains to be established. We demonstrate that inactivation of PRMT5 inhibits colony-forming activity by multiple oncogenic-drivers including cyclin D1, c-MYC, NOTCH1 and MLL-AF9. Furthermore, we demonstrate that PRMT5 overexpression specifically cooperates with cyclin D1 to drive lymphomagenesis in a mouse model revealing inherent neoplastic activity. Molecular analysis of lymphomas, revealed that arginine methylation of p53 selectively suppresses expression of crucial proapoptotic and anti-proliferative target genes thereby sustaining tumor cell self-renewal and proliferation and bypassing the need for the acquisition of inactivating p53 mutations. Critically, analysis of human tumor specimen reveal a strong correlation between cyclin D1 overexpression and p53 methylation supporting the biomedical relevance of this pathway. äPRMT5 is required for lymphomagenesis triggered by multiple oncogenic (epmc).pdf DeepDyve Pubget Overpricing