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VPS37C facilitates erythroid differentiation by promoting EKLF stability.

Ying Lu1, Wen-Bing Ma2, Guang-Ming Ren3

  • 1College of Life Science and Bioengineering, Faculty of Environmental and Life Sciences, Beijing University of Technology, Beijing, 100124, China; State Key Laboratory of Proteomics, National Center for Protein Sciences (Beijing), Beijing Institute of Radiation Medicine, Beijing, 100850, China.

Biochemical and Biophysical Research Communications
|June 12, 2023
PubMed
Summary

Vacuolar protein sorting 37 C (VPS37C) stabilizes the master regulator Erythroid Krüppel-like factor (EKLF/KLF1) by preventing its degradation. This finding reveals VPS37C

Keywords:
EKLFErythroid differentiationProtein stabilityUbiquitinationVPS37C

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Area of Science:

  • Molecular Biology
  • Cellular Differentiation
  • Protein Regulation

Background:

  • Erythroid differentiation is a complex process controlled by transcription factors.
  • Erythroid Krüppel-like factor (EKLF/KLF1) is a key regulator of erythroid differentiation.
  • Mechanisms controlling EKLF protein stability remain largely unelucidated.

Purpose of the Study:

  • To identify novel regulators of EKLF protein stability.
  • To investigate the role of Vacuolar protein sorting 37 C (VPS37C) in EKLF regulation and erythroid differentiation.

Main Methods:

  • Identified VPS37C as an EKLF interacting protein.
  • Assessed the effect of VPS37C on EKLF ubiquitination and degradation.
  • Utilized murine erythroleukemia (MEL) cells to study erythroid differentiation.

Main Results:

  • VPS37C interacts with EKLF, preventing its K48-linked polyubiquitination and proteasomal degradation.
  • VPS37C overexpression enhances EKLF stability and transcriptional activity, promoting erythroid differentiation in MEL cells.
  • VPS37C knockdown inhibits erythroid differentiation, which can be rescued by restoring EKLF expression.

Conclusions:

  • VPS37C is a novel regulator of EKLF ubiquitination and degradation.
  • VPS37C enhances EKLF protein stability, positively impacting erythroid differentiation.
  • VPS37C represents a potential therapeutic target for modulating erythropoiesis.