https://transhumanist.ru/index.php?action=history&feed=atom&title=SND1 2026-07-31T07:47:02Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=SND1&diff=4109&oldid=prev 2021-04-29T19:01:15Z

<p>Новая страница: «Staphylococcal nuclease domain-containing protein 1 (EC 3.1.31.1) (100 kDa coactivator) (EBNA2 coactivator p100) (Tudor domain-containing protein 11) (p100 co-act...»</p> <p><b>Новая страница</b></p><div>Staphylococcal nuclease domain-containing protein 1 (EC 3.1.31.1) (100 kDa coactivator) (EBNA2 coactivator p100) (Tudor domain-containing protein 11) (p100 co-activator) [TDRD11]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=[Downregulation of [[SND1]] Expression Accelerates Cell Senescence of Human Diploid Fibroblasts 2BS via Modulating the SASP].<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32543144<br /> |abstract=To investigate the effect of down-regulation of [[SND1]] expression on senescence of human diploid fibroblasts. Western blot and immunohistochemistry were used to detect the expression of [[SND1]] in young or senescent 2BS cells and aged tissues. Immunofluorescence was conducted to detect the localization of [[SND1]] in young 2BS cells. CCK8 and EDU were performed to detect the proliferation of 2BS. Colony formation analysis was used to evaluate the capacity of colony formation of 2BS. Expression chip and RT-qPCR analysis were performed to detect the change of SASP expression level. β-galactosidase staining was employed to indicate the senescent 2BS cells. The expression of [[SND1]] in the senescent 2BS cells was significantly down-regulated compared with in the younger 2BS cells, and in human colon adenomas, its expression was also significantly down-regulated compared with in non-lesion colon tissues. In young 2BS, knockdown of [i]SND[/i]1 inhibited the proliferation and colony formation of 2BS, and led to stronger senescence-associated beta-galactosidase staining (SA-β-gal). Expression chip and RT-qPCR analysis indicated that knockdown of [i]SND[/i]1 up-regulated the expression of senescence-associated secretory phenotype components (SASP). Our data indicated that down-regulation of [[SND1]] regulated human diploid cell senescence by up-regulating the expression of SASP components.<br /> |mesh-terms=* Cellular Senescence<br /> * Diploidy<br /> * Down-Regulation<br /> * Endonucleases<br /> * Fibroblasts<br /> * Humans<br /> * Nuclear Proteins<br /> |keywords=* Aging<br /> * Cellular senescent<br /> * SND1<br /> * Senescence-associated-secretory-phenotype<br /> |full-text-url=https://sci-hub.do/10.12182/20200560504<br /> }}</div>

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