https://transhumanist.ru/index.php?action=history&feed=atom&title=IMMP2L 2026-04-06T22:57:23Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=IMMP2L&diff=4431&oldid=prev 2021-04-29T19:17:49Z

<p>Новая страница: «Mitochondrial inner membrane protease subunit 2 (EC 3.4.21.-) (IMP2-like protein) ==Publications== {{medline-entry |title=Switching off <a href="/IMMP2L" title="IMMP2L">IMMP2L</a> signaling dri...»</p> <p><b>Новая страница</b></p><div>Mitochondrial inner membrane protease subunit 2 (EC 3.4.21.-) (IMP2-like protein)<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Switching off [[IMMP2L]] signaling drives senescence via simultaneous metabolic alteration and blockage of cell death.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29808012<br /> |abstract=Cellular senescence is a fundamental cell fate playing a significant role throughout the natural aging process. However, the molecular determinants distinguishing senescence from other cell-cycle arrest states such as quiescence and post-mitotic state, and the specified mechanisms underlying cell-fate decisions towards senescence versus cell death in response to cellular stress stimuli remain less understood. Employing multi-omics approaches, we revealed that switching off the specific mitochondrial processing machinery involving the peptidase [[IMMP2L]] serves as the foundation of the senescence program, which was also observed during the mammalian aging process. Mechanistically, we demonstrate that [[IMMP2L]] processes and thus activates at least two substrates, mitochondrial metabolic enzyme glycerol-3-phosphate dehydrogenase ([[GPD2]]) and cell death regulator apoptosis-inducing factor (AIF). For cells destined to senesce, concerted shutdown of the [[IMMP2L]]-[[GPD2]] and [[IMMP2L]]-AIF signaling axes collaboratively drives the senescent process by reprogramming mitochondria-associated redox status, phospholipid metabolism and signaling network, and simultaneously blocking cell death under oxidative stress conditions.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Apoptosis Inducing Factor<br /> * Cell Death<br /> * Cell Line<br /> * Cellular Senescence<br /> * Endopeptidases<br /> * Glycerolphosphate Dehydrogenase<br /> * HEK293 Cells<br /> * HeLa Cells<br /> * Humans<br /> * Mice, Inbred C57BL<br /> * Oxidative Stress<br /> * Signal Transduction<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5993829<br /> }}</div>

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