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10.3390/cancers8040039 http://scihub22266oqcxt.onion/10.3390/cancers8040039 C4846848!4846848!27023610     free     free     free       Cancers+(Basel) 2016 ; 8 (4): ä Nephropedia Template TP {{tp|p=27023610|t=2016. NORE1A Regulates MDM2 Via ?-TrCP |pdf=|usr=}}{{27023610}} gab.com Text NORE1A Regulates MDM2 Via -TrCP JO: Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=27023610 #FOAvip Mouse Double Minute 2 Homolog (MDM2) is a key negative regulator of the master tumor suppressor p53. MDM2 regulates p53 on multiple levels, including acting as an ubiquitin ligase for the protein, thereby promoting its degradation by the proteasome. MDM2 is oncogenic and is frequently found to be over-expressed in human tumors, suggesting its dysregulation plays an important role in human cancers. We have recently found that the Ras effector and RASSF (Ras Association Domain Family) family member RASSF5/NORE1A enhances the levels of nuclear p53. We have also found that NORE1A (Novel Ras Effector 1A) binds the substrate recognition component of the SCF-ubiquitin ligase complex ?-TrCP. Here, we now show that NORE1A regulates MDM2 protein levels by targeting it for ubiquitination by SCF-?-TrCP. We also show the suppression of NORE1A protein levels enhances MDM2 protein expression. Finally, we show that MDM2 can suppress the potent senescence phenotype induced by NORE1A over-expression. Thus, we identify a mechanism by which Ras/NORE1A can modulate p53 protein levels. As MDM2 has several important targets in addition to p53, this finding has broad implications for cancer biology in tumor cells that have lost expression of NORE1A due to promoter methylation. Twit Text FOAVip NORE1A Regulates MDM2 Via -TrCP ????Cancers (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=27023610 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27023610 #FOAvip English Wikipedia <ref>{{Cite pmid|27023610}}</ref> NORE1A Regulates MDM2 Via ?-TrCP #MMPMID27023610 Schmidt ML; Calvisi DF; Clark GJ Cancers (Basel) 2016[Apr]; 8 (4): ä PMID27023610show ga Mouse Double Minute 2 Homolog (MDM2) is a key negative regulator of the master tumor suppressor p53. MDM2 regulates p53 on multiple levels, including acting as an ubiquitin ligase for the protein, thereby promoting its degradation by the proteasome. MDM2 is oncogenic and is frequently found to be over-expressed in human tumors, suggesting its dysregulation plays an important role in human cancers. We have recently found that the Ras effector and RASSF (Ras Association Domain Family) family member RASSF5/NORE1A enhances the levels of nuclear p53. We have also found that NORE1A (Novel Ras Effector 1A) binds the substrate recognition component of the SCF-ubiquitin ligase complex ?-TrCP. Here, we now show that NORE1A regulates MDM2 protein levels by targeting it for ubiquitination by SCF-?-TrCP. We also show the suppression of NORE1A protein levels enhances MDM2 protein expression. Finally, we show that MDM2 can suppress the potent senescence phenotype induced by NORE1A over-expression. Thus, we identify a mechanism by which Ras/NORE1A can modulate p53 protein levels. As MDM2 has several important targets in addition to p53, this finding has broad implications for cancer biology in tumor cells that have lost expression of NORE1A due to promoter methylation. äNORE1A Regulates MDM2 Via ?-TrCP (epmc).pdf DeepDyve Pubget Overpricing