Amazing stuff! Getting closer to the fountain of youth! But it is complex!
"Now, researchers ... claim that human coilin-interacting nuclear ATPase protein (hCINAP) can do exactly that: prevent cellular senescence and, potentially, delay aging. Overexpressing the protein in worm models delayed cellular senescence—a period characterized by the absence of growth in cells—and depleting it increased senescence in human and mouse cell lines ..."
From the abstract:
"Cellular senescence is a major process affected by multiple signals and coordinated by a complex signal response network. Identification of novel regulators of cellular senescence and elucidation of their molecular mechanisms will aid the discovery of new treatment strategies for aging-related diseases. In the present study, we identified human coilin-interacting nuclear ATPase protein (hCINAP) as a negative regulator of aging. Depletion of cCINAP significantly shortened the lifespan of Caenorhabditis elegans and accelerated primary cell aging. Moreover, mCINAP deletion markedly promoted organismal aging and stimulated senescence-associated secretory phenotype in the skeletal muscle and liver from mouse models of radiation-induced senescence. Mechanistically, hCINAP functions through regulating MDM2 status by distinct mechanisms. On one hand, hCINAP decreases p53 stability by attenuating the interaction between p14ARF and MDM2; on the other hand, hCINAP promotes MDM2 transcription via inhibiting the deacetylation of H3K9ac in the MDM2 promoter by hindering HDAC1/CoREST complex integrity. Collectively, our data demonstrate that hCINAP is a negative regulator of aging and provide insight into the molecular mechanisms underlying the aging process."
hCINAP alleviates senescence by regulating MDM2 via p14ARF and the HDAC1/CoREST complex (open access)
Figure 1 hCINAP levels decrease during cellular senescence
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