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

Elizabeth Allen, Jianqing Ding, Wei Wang, Suneet Pramanik, Jonathan Chou, Vincent Yau and Yanmin Yang ()
Additional contact information
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

Nature, 2005, vol. 438, issue 7065, 224-228

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.

Date: 2005
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DOI: 10.1038/nature04256

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