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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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BMAL1 modulates senescence programming via AP-1.

Sarah K Jachim1,2, Jian Zhong3, Tamas Ordog4,5

  • 1Mayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN 55905, USA.

Aging
|October 11, 2023
PubMed
Summary
This summary is machine-generated.

The core circadian clock component BMAL1 is upregulated in senescent cells and influences their survival pathways. This study reveals a novel link between circadian regulation and cellular senescence, impacting aging research.

Keywords:
AP-1cellular senescencecircadian clocksenolytictranscription regulation

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Area of Science:

  • Molecular Biology
  • Chronobiology
  • Aging Research

Background:

  • Cellular senescence and circadian dysregulation are key aging hallmarks.
  • The interplay between these processes remains largely unexplored.
  • BMAL1, a core circadian regulator, is hypothesized to influence senescence.

Purpose of the Study:

  • To investigate the role of BMAL1 in cellular senescence.
  • To determine if BMAL1 is coordinately regulated with senescence.
  • To elucidate BMAL1's contribution to the senescent phenotype.

Main Methods:

  • Analysis of BMAL1 expression and rhythmicity in senescent vs. non-senescent cells.
  • BMAL1 Chromatin Immunoprecipitation sequencing (ChIP-seq) in senescent cells.
  • Integration of ChIP-seq with RNA sequencing (RNA-seq) data.
  • Functional studies on BMAL1's role in senescence-associated pathways.

Main Results:

  • BMAL1 is significantly upregulated and exhibits altered rhythmicity in senescent cells.
  • BMAL1 uniquely binds to AP-1 motifs in senescent cells, correlating with active transcription.
  • BMAL1 regulates key senescence features, including cell survival and apoptosis resistance.

Conclusions:

  • BMAL1 plays a significant, previously unrecognized role in the molecular phenotype of senescent cells.
  • The circadian clock component BMAL1 impacts cellular senescence, offering new therapeutic targets for aging.
  • Findings highlight the coordinated regulation between circadian rhythm and cellular senescence.