https://transhumanist.ru/index.php?action=history&feed=atom&title=SRSF3 2026-06-07T12:23:34Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=SRSF3&diff=4047&oldid=prev 2021-04-29T18:58:00Z

<p>Новая страница: «Serine/arginine-rich splicing factor 3 (Pre-mRNA-splicing factor SRP20) (Splicing factor, arginine/serine-rich 3) [SFRS3] [SRP20] ==Publications== {{medline-ent...»</p> <p><b>Новая страница</b></p><div>Serine/arginine-rich splicing factor 3 (Pre-mRNA-splicing factor SRP20) (Splicing factor, arginine/serine-rich 3) [SFRS3] [SRP20]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Alternative polyadenylation dependent function of splicing factor [[SRSF3]] contributes to cellular senescence.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30835716<br /> |abstract=Down-regulated splicing factor [[SRSF3]] is known to promote cellular senescence, an important biological process in preventing cancer and contributing to individual aging, via its alternative splicing dependent function in human cells. Here we discovered alternative polyadenylation (APA) dependent function of [[SRSF3]] as a novel mechanism explaining [[SRSF3]] downregulation induced cellular senescence. Knockdown of [i][[SRSF3]][/i] resulted in preference usage of proximal poly(A) sites and thus global shortening of 3&#039; untranslated regions (3&#039; UTRs) of mRNAs. [i][[SRSF3]][/i]-depletion also induced senescence-related phenotypes in both human and mouse cells. These 3&#039; UTR shortened genes were enriched in senescence-associated pathways. Shortened 3&#039; UTRs tended to produce more proteins than the longer ones. Simulating the effects of 3&#039; UTR shortening by overexpression of three candidate genes ([i]PTEN, PIAS1[/i] and [i]DNMT3A[/i]) all led to senescence-associated phenotypes. Mechanistically, [[SRSF3]] has higher binding density near proximal poly(A) site than distal one in 3&#039; UTR shortened genes. Further, upregulation of [i]PTEN[/i] by either ectopic overexpression or [i][[SRSF3]][/i]-knockdown induction both led to reduced phosphorylation of AKT and ultimately senescence-associated phenotypes. We revealed for the first time that reduced [[SRSF3]] expression could promote cellular senescence through its APA-dependent function, largely extending our mechanistic understanding in splicing factor regulated cellular senescence.<br /> |mesh-terms=* Animals<br /> * Cell Line<br /> * Cell Proliferation<br /> * Cellular Senescence<br /> * Computational Biology<br /> * Down-Regulation<br /> * Gene Expression Regulation<br /> * Human Umbilical Vein Endothelial Cells<br /> * Humans<br /> * Polyadenylation<br /> * RNA Interference<br /> * Serine-Arginine Splicing Factors<br /> |keywords=* 3′UTR<br /> * PTEN<br /> * SRSF3<br /> * alternative polyadenylation<br /> * senescence<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428108<br /> }}</div>

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