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p62/SQSTM1/A170: physiology and pathology.

Masaaki Komatsu1, Shun Kageyama, Yoshinobu Ichimura

  • 1Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan. komatsu-ms@igakuken.or.jp

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PubMed
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The stress-inducible protein p62 (also known as SQSTM1) plays a crucial role in autophagy, a cellular process for degrading damaged components. This review explores p62

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • p62/SQSTM1/A170 (p62) is a stress-inducible protein regulating cell survival and death pathways.
  • p62 is intrinsically linked to autophagy, a cellular degradation process.
  • p62 directs ubiquitinated cargo for autophagic degradation and influences autophagosome compaction.

Purpose of the Study:

  • To review the pathophysiological significance of p62.
  • To elucidate the intricate role of p62 in the regulation of autophagy.
  • To highlight p62's function as a signaling hub in cellular pathways.

Main Methods:

  • Literature review and synthesis of existing research on p62 and autophagy.
  • Analysis of signaling pathways involving p62, including NF-κB, apoptosis, and Nrf2.
  • Examination of the interplay between p62, autophagy, and mTORC1 signaling.

Main Results:

  • p62 modulates autophagy, while autophagy regulates p62 protein levels.
  • p62 can inhibit autophagy through mTORC1 activation.
  • p62 acts as a critical signaling hub, integrating pathways like NF-κB, apoptosis, and Nrf2 activation.
  • Dysregulation of p62-associated pathways is implicated in Paget disease of bone and tumorigenesis.

Conclusions:

  • p62 is a key regulator of autophagy and a central signaling node.
  • Understanding p62's role is vital for comprehending diseases like Paget disease and cancer.
  • Further research into p62's functions may reveal therapeutic targets for related pathologies.