https://transhumanist.ru/index.php?action=history&feed=atom&title=RRAD 2026-05-15T18:29:14Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=RRAD&diff=4095&oldid=prev 2021-04-29T19:00:23Z

<p>Новая страница: «GTP-binding protein RAD (RAD1) (Ras associated with diabetes) [RAD] ==Publications== {{medline-entry |title=Pan-senescence transcriptome analysis identified R...»</p> <p><b>Новая страница</b></p><div>GTP-binding protein RAD (RAD1) (Ras associated with diabetes) [RAD]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Pan-senescence transcriptome analysis identified [[RRAD]] as a marker and negative regulator of cellular senescence.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30391675<br /> |abstract=Cellular senescence, an irreversible proliferative arrest, functions in tissue remodeling during development and is implicated in multiple aging-associated diseases. While senescent cells often manifest an array of senescence-associated phenotypes, such as cell cycle arrest, altered heterochromatin architecture, reprogrammed metabolism and senescence-associated secretory phenotype (SASP), the identification of senescence cells has been hindered by lack of specific and universal biomarkers. To systematically identify universal biomarkers of cellular senescence, we integrated multiple transcriptome data sets of senescent cells obtained through different in vitro manipulation modes as well as age-related gene expression data of human tissues. Our analysis showed that [[RRAD]] (Ras-related associated with diabetes) expression is up-regulated in all the manipulation modes and increases with age in human skin and adipose tissues. The elevated [[RRAD]] expression was then confirmed in senescent human fibroblasts that were induced by Ras, H O , ionizing radiation, hydroxyurea, etoposide and replicative passage, respectively. Further functional study suggests that [[RRAD]] up-regulation acts as a negative feedback mechanism to counter cellular senescence by reducing the level of reactive oxygen species. Finally, we found both p53 and NF-κB bind to [[RRAD]] genomic regions and modulate [[RRAD]] transcription. This study established [[RRAD]] to be a biomarker as well as a novel negative regulator of cellular senescence.<br /> |mesh-terms=* Aging<br /> * Biomarkers<br /> * Cellular Senescence<br /> * Fibroblasts<br /> * Humans<br /> * Hydrogen Peroxide<br /> * NF-kappa B<br /> * Oxidative Stress<br /> * Protein Binding<br /> * Radiation, Ionizing<br /> * Reactive Oxygen Species<br /> * Skin<br /> * Transcription Factor RelA<br /> * Transcriptome<br /> * Tumor Suppressor Protein p53<br /> * ras Proteins<br /> <br /> |full-text-url=https://sci-hub.do/10.1016/j.freeradbiomed.2018.10.457<br /> }}</div>

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