Work

HSP90 is a chaperone for DLK and is required for axon injury signaling

Year: 2018

Type: article

Abstract: Significance Defining mechanisms of axon injury signaling is critical to understand axon regeneration. This knowledge can be used to develop strategies of axonal repair. Identification of such injury signals has been limited by traditional in vivo assays of proregenerative injury signaling. Here, we describe an in vitro screening platform that specifically identifies proregenerative axon injury signals in mouse neurons. We show that HSP90 is required for injury signaling and detail a mechanism by which HSP90 chaperones the essential proregenerative kinase, dual leucine zipper kinase (DLK). Thus, this work also describes HSP90 as a previously unidentified regulator of DLK, a critical neuronal stress sensor that drives axon regeneration, degeneration, and neurological disease.

Source: Proceedings of the National Academy of Sciences

DOI: 10.1073/pnas.1805351115

Authors: Scott Karney-Grobe, Alexandra Russo, Erin Frey, Jeffrey Milbrandt, Aaron DiAntonio

Institutions: Washington University in St. Louis, Hope Center for Neurological Disorders

Language: English

Topic: Nerve injury and regeneration

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: green

Funders: National Institutes of Health, National Institute of Neurological Disorders and Stroke