https://transhumanist.ru/index.php?action=history&feed=atom&title=TERF2IP 2026-06-15T21:07:04Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=TERF2IP&diff=4425&oldid=prev 2021-04-29T19:17:33Z

<p>Новая страница: «Telomeric repeat-binding factor 2-interacting protein 1 (TERF2-interacting telomeric protein 1) (TRF2-interacting telomeric protein 1) (Dopamine receptor-interact...»</p> <p><b>Новая страница</b></p><div>Telomeric repeat-binding factor 2-interacting protein 1 (TERF2-interacting telomeric protein 1) (TRF2-interacting telomeric protein 1) (Dopamine receptor-interacting protein 5) (Repressor/activator protein 1 homolog) (RAP1 homolog) (hRap1) [DRIP5] [RAP1] [PP8000]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Endothelial senescence-associated secretory phenotype (SASP) is regulated by Makorin-1 ubiquitin E3 ligase.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31476350<br /> |abstract=Disturbed flow (d-flow)-induced senescence and activation of endothelial cells (ECs) have been suggested to have critical roles in promoting atherosclerosis. Telomeric repeat-binding factor 2 ([[TERF2]])-interacting protein ([[[[TERF2]]IP]]), a member of the shelterin complex at the telomere, regulates the senescence-associated secretory phenotype (SASP), in which EC activation and senescence are engendered simultaneously by p90RSK-induced phosphorylation of [[[[TERF2]]IP]] S205 and subsequent nuclear export of the [[[[TERF2]]IP]]-[[TERF2]] complex. In this study, we investigated [[[[TERF2]]IP]]-dependent gene expression and its role in regulating d-flow-induced SASP. A principal component analysis and hierarchical clustering were used to identify genes whose expression is regulated by [[[[TERF2]]IP]] in ECs under d-flow conditions. Senescence was determined by reduced telomere length, increased p53 and p21 expression, and increased apoptosis; EC activation was detected by NF-κB activation and the expression of adhesion molecules. The involvement of [[[[TERF2]]IP]] S205 phosphorylation in d-flow-induced SASP was assessed by depletion of [[[[TERF2]]IP]] and mutation of the phosphorylation site. Our unbiased transcriptome analysis showed that [[[[TERF2]]IP]] caused alteration in the expression of a distinct set of genes, including rapamycin-insensitive companion of mTOR ([[RICTOR]]) and makorin-1 ([[MKRN1]]) ubiquitin E3 ligase, under d-flow conditions. In particular, both depletion of [[[[TERF2]]IP]] and overexpression of the [[[[TERF2]]IP]] S205A phosphorylation site mutant in ECs increased the d-flow and p90RSK-induced [[MKRN1]] expression and subsequently inhibited apoptosis, telomere shortening, and NF-κB activation in ECs via suppression of p53, p21, and telomerase (TERT) induction. [[MKRN1]] and [[RICTOR]] belong to a distinct reciprocal gene set that is both negatively and positively regulated by p90RSK. [[[[TERF2]]IP]] S205 phosphorylation, a downstream event of p90RSK activation, uniquely inhibits [[MKRN1]] expression and contributes to EC activation and senescence, which are key events for atherogenesis.<br /> |mesh-terms=* Cellular Senescence<br /> * Endothelial Cells<br /> * Human Umbilical Vein Endothelial Cells<br /> * Humans<br /> * MicroRNAs<br /> * Nerve Tissue Proteins<br /> * Phosphorylation<br /> * Protein Binding<br /> * Rapamycin-Insensitive Companion of mTOR Protein<br /> * Ribonucleoproteins<br /> * Telomeric Repeat Binding Protein 2<br /> * Ubiquitin-Protein Ligases<br /> |keywords=* Inflammation<br /> * MKRN1<br /> * Senescence<br /> * Senescence-associated secretory phenotype (SASP)<br /> * Telomeric repeat binding factor 2-interacting protein (TERF2IP)<br /> * p90RSK<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059097<br /> }}</div>

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