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Apoptosis repressor with caspase recruitment domain, a multifunctional modulator of cell death

Agnieszka H Ludwig-Galezowska1, Lorna Flanagan, Markus Rehm

  • 1Department of Physiology & Medical Physics, Royal College of Surgeons in Ireland, Dublin, Ireland.

Journal of Cellular and Molecular Medicine
|December 7, 2010
PubMed

Insights

Apoptosis repressor with caspase recruitment domain (ARC) is a potent apoptosis inhibitor found in post-mitotic cells and tumors. It blocks cell death signaling from various stresses, impacting physiological and pathological processes.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Apoptosis repressor with caspase recruitment domain (ARC) is a key inhibitor of programmed cell death.
  • Physiologically, ARC is predominantly expressed in post-mitotic cells like neurons and cardiomyocytes.
  • ARC is frequently upregulated in various malignant tumors, suggesting a role in cancer progression.

Purpose of the Study:

  • To review and synthesize current knowledge on ARC's function.
  • To elucidate ARC's role in modulating apoptosis in both normal and disease states.
  • To structure and comment on ARC's transcriptional and post-translational regulation.

Main Methods:

  • Literature review and synthesis of published research on ARC.
  • Analysis of ARC's molecular interactions with apoptosis signaling pathways.
  • Examination of ARC's expression patterns in physiological and pathological contexts.

Main Results:

  • ARC inhibits apoptosis induced by diverse stimuli including death receptor ligands, ER stress, genotoxic drugs, radiation, oxidative stress, and hypoxia.
  • ARC's function is regulated at both transcriptional and post-translational levels.
  • ARC interacts with multiple upstream signaling molecules to block apoptosis.

Conclusions:

  • ARC is a critical regulator of apoptosis, impacting cell survival in various cellular contexts.
  • Understanding ARC's multifaceted roles is essential for comprehending physiological cell death and pathological conditions like cancer.
  • Further research into ARC's regulatory mechanisms and interactions may reveal therapeutic targets.

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