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10.1101/gr.224451.117 http://scihub22266oqcxt.onion/10.1101/gr.224451.117 C5848608!5848608!29440281     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       Genome+Res 2018 ; 28 (3): 285-94 Nephropedia Template TP {{tp|p=29440281|t=2018. 3? UTR lengthening as a novel mechanism in regulating cellular senescence |pdf=|usr=}}{{29440281}} gab.com Text 3 UTR lengthening as a novel mechanism in regulating cellular senescence JO: Genome Res http://www.kidney.de/pget.php?&tw=1&pmid=29440281 #FOAvip Cellular senescence has been viewed as a tumor suppression mechanism and also as a contributor to individual aging. Widespread shortening of 3? untranslated regions (3? UTRs) in messenger RNAs (mRNAs) by alternative polyadenylation (APA) has recently been discovered in cancer cells. However, the role of APA in the process of cellular senescence remains elusive. Here, we found that hundreds of genes in senescent cells tended to use distal poly(A) (pA) sites, leading to a global lengthening of 3? UTRs and reduced gene expression. Genes that harbor longer 3? UTRs in senescent cells were enriched in senescence-related pathways. Rras2, a member of the Ras superfamily that participates in multiple signal transduction pathways, preferred longer 3? UTR usage and exhibited decreased expression in senescent cells. Depletion of Rras2 promoted senescence, while rescue of Rras2 reversed senescence-associated phenotypes. Mechanistically, splicing factor TRA2B bound to a core ?AGAA? motif located in the alternative 3? UTR of Rras2, thereby reducing the RRAS2 protein level and causing senescence. Both proximal and distal poly(A) signals showed strong sequence conservation, highlighting the vital role of APA regulation during evolution. Our results revealed APA as a novel mechanism in regulating cellular senescence. Twit Text FOAVip 3 UTR lengthening as a novel mechanism in regulating cellular senescence ????Genome Res http://www.kidney.de/pget.php?&tw=1&pmid=29440281 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29440281 #FOAvip English Wikipedia <ref>{{Cite pmid|29440281}}</ref> 3? UTR lengthening as a novel mechanism in regulating cellular senescence #MMPMID29440281 Chen M; Lyu G; Han M; Nie H; Shen T; Chen W; Niu Y; Song Y; Li X; Li H; Chen X; Wang Z; Xia Z; Li W; Tian XL; Ding C; Gu J; Zheng Y; Liu X; Hu J; Wei G; Tao W; Ni T Genome Res 2018[Mar]; 28 (3): 285-94 PMID29440281show ga Cellular senescence has been viewed as a tumor suppression mechanism and also as a contributor to individual aging. Widespread shortening of 3? untranslated regions (3? UTRs) in messenger RNAs (mRNAs) by alternative polyadenylation (APA) has recently been discovered in cancer cells. However, the role of APA in the process of cellular senescence remains elusive. Here, we found that hundreds of genes in senescent cells tended to use distal poly(A) (pA) sites, leading to a global lengthening of 3? UTRs and reduced gene expression. Genes that harbor longer 3? UTRs in senescent cells were enriched in senescence-related pathways. Rras2, a member of the Ras superfamily that participates in multiple signal transduction pathways, preferred longer 3? UTR usage and exhibited decreased expression in senescent cells. Depletion of Rras2 promoted senescence, while rescue of Rras2 reversed senescence-associated phenotypes. Mechanistically, splicing factor TRA2B bound to a core ?AGAA? motif located in the alternative 3? UTR of Rras2, thereby reducing the RRAS2 protein level and causing senescence. Both proximal and distal poly(A) signals showed strong sequence conservation, highlighting the vital role of APA regulation during evolution. Our results revealed APA as a novel mechanism in regulating cellular senescence. ä3? UTR lengthening as a novel mechanism in regulating cellular senesce(epmc).pdf DeepDyve Pubget Overpricing