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Critical roles of FAM134B in ER-phagy and diseases

Jie Mo1, Jin Chen1, Bixiang Zhang2

  • 1Hubei Key Laboratory of Hepato-Pancreato-Biliary Diseases; Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Clinical Medicine Research Center for Hepatic Surgery of Hubei Province; Key Laboratory of Organ Transplantation, Ministry of Education and Ministry of Public Health, Wuhan, Hubei, 430030, P.R. China.

Cell Death & Disease
|November 17, 2020
PubMed

Insights

Family with sequence similarity 134B (FAM134B) is a key receptor regulating endoplasmic reticulum (ER)-phagy. Its dysfunction links to neuropathy, viral replication, inflammation, and cancer, highlighting its critical biological roles.

Area of Science:

  • Molecular biology
  • Cellular biology
  • Pathophysiology

Background:

  • FAM134B, also known as JK-1 or RETREG1, was initially identified as an oncogene.
  • Its primary recognized role is as a receptor that regulates ER-phagy (endoplasmic reticulum autophagy).
  • Growing evidence links FAM134B dysfunction to various diseases, including neuropathy, viral infections, inflammatory conditions, and cancer.

Purpose of the Study:

  • To comprehensively review the biological functions of FAM134B.
  • To emphasize its crucial role in the process of ER-phagy.
  • To summarize the spectrum of diseases associated with FAM134B and elucidate the underlying pathogenic mechanisms.

Main Methods:

  • Literature review of existing studies on FAM134B.
  • Analysis of research focusing on ER-phagy mechanisms.
  • Synthesis of data linking FAM134B to various pathophysiological conditions.

Main Results:

  • FAM134B is a critical regulator of ER-phagy, a cellular process for clearing damaged ER.
  • Dysregulation of FAM134B is implicated in diverse diseases, affecting cellular homeostasis.
  • The review consolidates current knowledge on FAM134B's functions and disease associations.

Conclusions:

  • FAM134B plays a vital role in cellular quality control through ER-phagy.
  • Understanding FAM134B's mechanisms is crucial for developing therapeutic strategies for related diseases.
  • Further research into FAM134B is warranted to fully explore its potential in medicine.

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