Редактирование: IMMP2L (раздел)

==Publications==

{{medline-entry
|title=Switching off [[IMMP2L]] signaling drives senescence via simultaneous metabolic alteration and blockage of cell death.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29808012
|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.
|mesh-terms=* Aging
* Animals
* Apoptosis Inducing Factor
* Cell Death
* Cell Line
* Cellular Senescence
* Endopeptidases
* Glycerolphosphate Dehydrogenase
* HEK293 Cells
* HeLa Cells
* Humans
* Mice, Inbred C57BL
* Oxidative Stress
* Signal Transduction

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5993829
}}