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hCINAP alleviates senescence by regulating MDM2 via p14ARF and the HDAC1/CoREST complex

Xinping Huang1,2, Yan Zhao1,2, Min Wei1,2

  • 1State Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing 100871, China.

Journal of Molecular Cell Biology
|March 7, 2023
PubMed

Insights

Human coilin-interacting nuclear ATPase protein (hCINAP) negatively regulates aging. Its depletion shortens lifespan and accelerates aging in model organisms and cells, revealing new aging mechanisms.

Area of Science:

  • Molecular Biology
  • Gerontology
  • Cell Biology

Background:

  • Cellular senescence is a complex process influenced by various signals, crucial for understanding aging-related diseases.
  • Identifying novel regulators of senescence and their mechanisms is key to developing new therapeutic strategies for aging.

Purpose of the Study:

  • To identify and characterize novel regulators of cellular senescence and aging.
  • To elucidate the molecular mechanisms by which hCINAP influences aging and senescence.

Main Methods:

  • Depletion of hCINAP in Caenorhabditis elegans and primary cells.
  • Analysis of organismal aging and senescence-associated secretory phenotype in mouse models.
  • Investigation of hCINAP's role in regulating MDM2 stability and transcription.

Main Results:

  • hCINAP acts as a negative regulator of aging across different species.
  • Depletion of hCINAP accelerated aging and shortened lifespan in model organisms.
  • hCINAP influences p53 stability and MDM2 transcription through distinct molecular pathways.

Conclusions:

  • hCINAP is a novel negative regulator of the aging process.
  • hCINAP's mechanisms involve modulating p53 stability and MDM2 gene expression.
  • Understanding hCINAP's role provides insights into aging and potential therapeutic targets.
Keywords:
HDAC1/CoREST complexMDM2hCINAPp14ARFsenescencetranscription

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