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10.1016/j.cell.2016.02.046 http://scihub22266oqcxt.onion/10.1016/j.cell.2016.02.046 C4826573!4826573!27040500     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2016 ; 165 (2): 382-95 Nephropedia Template TP {{tp|p=27040500|t=2016. The Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediated RNA Decay |pdf=|usr=}}{{27040500}} gab.com Text The Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediated RNA Decay JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=27040500 #FOAvip Gene duplication is a major evolutionary force driving adaptation and speciation, as it allows for the acquisition of new functions and can augment or diversify existing functions. Here, we report a gene duplication event that yielded another outcome ? the generation of antagonistic functions. One product of this duplication event ? UPF3B ? is critical for the nonsense-mediated RNA decay (NMD) pathway, while its autosomal counterpart ? UPF3A ? encodes an enigmatic protein previously shown to have trace NMD activity. Using loss-of-function approaches in vitro and in vivo, we discovered that UPF3A acts primarily as a potent NMD inhibitor that stabilizes hundreds of transcripts. Evidence suggests that UPF3A acquired repressor activity through simple impairment of a critical domain, a rapid mechanism that may have been widely used in evolution. Mice conditionally lacking UPF3A exhibit ?hyper? NMD and display defects in embryogenesis and gametogenesis, consistent with UPF3A serving as a molecular rheostat that directs developmental events. Twit Text FOAVip The Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediated RNA Decay ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=27040500 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27040500 #FOAvip English Wikipedia <ref>{{Cite pmid|27040500}}</ref> The Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediated RNA Decay #MMPMID27040500 Shum EY; Jones SH; Shao A; Chousal JN; Krause MD; Chan WK; Lou CH; Espinoza JL; Song HW; Phan MH; Ramaiah M; Huang L; McCarrey JR; Peterson KJ; De Rooij DG; Cook-Andersen H; Wilkinson MF Cell 2016[Apr]; 165 (2): 382-95 PMID27040500show ga Gene duplication is a major evolutionary force driving adaptation and speciation, as it allows for the acquisition of new functions and can augment or diversify existing functions. Here, we report a gene duplication event that yielded another outcome ? the generation of antagonistic functions. One product of this duplication event ? UPF3B ? is critical for the nonsense-mediated RNA decay (NMD) pathway, while its autosomal counterpart ? UPF3A ? encodes an enigmatic protein previously shown to have trace NMD activity. Using loss-of-function approaches in vitro and in vivo, we discovered that UPF3A acts primarily as a potent NMD inhibitor that stabilizes hundreds of transcripts. Evidence suggests that UPF3A acquired repressor activity through simple impairment of a critical domain, a rapid mechanism that may have been widely used in evolution. Mice conditionally lacking UPF3A exhibit ?hyper? NMD and display defects in embryogenesis and gametogenesis, consistent with UPF3A serving as a molecular rheostat that directs developmental events. äThe Antagonistic Gene Paralogs Upf3a and Upf3b Govern Nonsense-Mediate(epmc).pdf DeepDyve Pubget Overpricing