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Receptor-interacting protein 140 attenuates endoplasmic reticulum stress in neurons and protects against cell death

Author

Listed:
  • Xudong Feng

    (University of Minnesota Medical School)

  • Kelly A. Krogh

    (University of Minnesota Medical School)

  • Cheng-Ying Wu

    (University of Minnesota Medical School)

  • Yi-Wei Lin

    (University of Minnesota Medical School)

  • Hong-Chieh Tsai

    (University of Minnesota Medical School
    Chang-Gung Memorial Hospital and University, Tao-Yuan 333)

  • Stanley A. Thayer

    (University of Minnesota Medical School)

  • Li-Na Wei

    (University of Minnesota Medical School)

Abstract

Inositol 1, 4, 5-trisphosphate receptor (IP3R)-mediated Ca2+ release from the endoplasmic reticulum (ER) triggers many physiological responses in neurons, and when uncontrolled can cause ER stress that contributes to neurological disease. Here we show that the unfolded protein response (UPR) in neurons induces rapid translocation of nuclear receptor-interacting protein 140 (RIP140) to the cytoplasm. In the cytoplasm, RIP140 localizes to the ER by binding to the IP3R. The carboxyl-terminal RD4 domain of RIP140 interacts with the carboxyl-terminal gate-keeping domain of the IP3R. This molecular interaction disrupts the IP3R’s ‘head–tail’ interaction, thereby suppressing channel opening and attenuating IP3R-mediated Ca2+ release. This contributes to a rapid suppression of the ER stress response and provides protection from apoptosis in both hippocampal neurons in vitro and in an animal model of ER stress. Thus, RIP140 translocation to the cytoplasm is an early response to ER stress and provides protection against neuronal death.

Suggested Citation

  • Xudong Feng & Kelly A. Krogh & Cheng-Ying Wu & Yi-Wei Lin & Hong-Chieh Tsai & Stanley A. Thayer & Li-Na Wei, 2014. "Receptor-interacting protein 140 attenuates endoplasmic reticulum stress in neurons and protects against cell death," Nature Communications, Nature, vol. 5(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5487
    DOI: 10.1038/ncomms5487
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