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UXT-V1 protects cells against TNF-induced apoptosis through modulating complex II formation

Yuefeng Huang1, Liang Chen, Yi Zhou

  • 1Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

Molecular Biology of the Cell
|February 11, 2011
PubMed

Insights

UXT-V1, a novel protein, regulates tumor necrosis factor (TNF)-induced apoptosis by interacting with TNF receptor signaling components. Its degradation promotes cell death, revealing a new mechanism in apoptosis regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Tumor necrosis factor (TNF) signaling is crucial for cell death and survival.
  • Ubiquitously expressed transcript (UXT) isoforms play roles in cellular regulation.
  • UXT-V2 regulates nuclear factor-κB in the nucleus.

Purpose of the Study:

  • To investigate the role of UXT-V1, a cytoplasmic isoform of UXT, in TNF-induced apoptosis.
  • To elucidate the molecular mechanism by which UXT-V1 regulates TNF signaling.

Main Methods:

  • Cellular localization studies of UXT-V1.
  • Knockdown experiments to assess sensitivity to TNF.
  • Co-immunoprecipitation assays to identify binding partners.
  • Analysis of protein degradation and complex formation.

Main Results:

  • UXT-V1 localizes in the cytoplasm and regulates TNF-induced apoptosis.
  • UXT-V1 knockdown increases sensitivity to TNF-induced cell death.
  • UXT-V1 binds to TNF receptor-associated factor 2 (TRAF2).
  • UXT-V1 prevents the recruitment of TNF receptor-associated death domain (TRADD) to the TNF receptor.
  • Degradation of UXT-V1 facilitates the formation of apoptotic receptor complex II.

Conclusions:

  • UXT-V1 is a novel cytoplasmic regulator of TNF-induced apoptosis.
  • UXT-V1 acts as a negative regulator by preventing early signaling complex assembly.
  • The degradation of UXT-V1 is a key step in initiating TNF-induced apoptosis.

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