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Gigaxonin-controlled degradation of MAP1B light chain is critical to neuronal survival

Author

Listed:
  • Elizabeth Allen

    (Stanford University School of Medicine)

  • Jianqing Ding

    (Stanford University School of Medicine)

  • Wei Wang

    (Stanford University School of Medicine)

  • Suneet Pramanik

    (Stanford University School of Medicine)

  • Jonathan Chou

    (Stanford University School of Medicine)

  • Vincent Yau

    (Stanford University School of Medicine)

  • Yanmin Yang

    (Stanford University School of Medicine)

Abstract

Gigaxonin for the nerves Giant axonal neuropathy (GAN) is a rare and debilitating inherited condition that generally appears in early childhood. It is caused by mutations in the GAN gene that encodes gigaxonin, a member of the BTB/kelch superfamily of cytoskeletal proteins. Gigaxonin has now been identified as a ubiquitin-scaffolding protein that is essential for neuronal function and survival through its control of the degradation of the light chain of microtubule-associated protein 1B. This is of particular interest since alterations in the cytoskeletal network are also a feature of more common diseases such as amyotrophic lateral sclerosis, so knowledge of the function of gigaxonin may provide insights into the pathogenesis of neurodegenerative disorders in general.

Suggested Citation

  • Elizabeth Allen & Jianqing Ding & Wei Wang & Suneet Pramanik & Jonathan Chou & Vincent Yau & Yanmin Yang, 2005. "Gigaxonin-controlled degradation of MAP1B light chain is critical to neuronal survival," Nature, Nature, vol. 438(7065), pages 224-228, November.
    • Handle: RePEc:nat:nature:v:438:y:2005:i:7065:d:10.1038_nature04256
    DOI: 10.1038/nature04256
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    Cited by:

    1. Yu Guo & Minjie Shen & Qiping Dong & Natasha M. Méndez-Albelo & Sabrina X. Huang & Carissa L. Sirois & Jonathan Le & Meng Li & Ezra D. Jarzembowski & Keegan A. Schoeller & Michael E. Stockton & Vaness, 2023. "Elevated levels of FMRP-target MAP1B impair human and mouse neuronal development and mouse social behaviors via autophagy pathway," Nature Communications, Nature, vol. 14(1), pages 1-23, December.

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