Commentary 10.1172/JCI136162

(H)Elping nerve growth factor: Elp1 inhibits TrkA’s phosphatase to maintain retrograde signaling

David R. Kaplan1,2 and William C. Mobley3

1Program in Neurosciences and Mental Health, Hospital for Sick Children, Toronto, Ontario, Canada.

2Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.

3Department of Neurosciences, UCSD, La Jolla, California, USA.

Address correspondence to: David R. Kaplan, Hospital for Sick Children, PGCRL Building, 686 Bay Street, Room 18.9715, Toronto, Ontario M5G 0A4 Canada. Phone: 416.813.7654 ext. 301433; Email: dkaplan@sickkids.ca.

Find articles by Kaplan, D. in: JCI | PubMed | Google Scholar

1Program in Neurosciences and Mental Health, Hospital for Sick Children, Toronto, Ontario, Canada.

2Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.

3Department of Neurosciences, UCSD, La Jolla, California, USA.

Address correspondence to: David R. Kaplan, Hospital for Sick Children, PGCRL Building, 686 Bay Street, Room 18.9715, Toronto, Ontario M5G 0A4 Canada. Phone: 416.813.7654 ext. 301433; Email: dkaplan@sickkids.ca.

Find articles by Mobley, W. in: JCI | PubMed | Google Scholar

First published April 13, 2020 - More info

Published in Volume 130, Issue 5 on May 1, 2020
J Clin Invest. 2020;130(5):2195–2198. https://doi.org/10.1172/JCI136162.
© 2020 American Society for Clinical Investigation
First published April 13, 2020 - Version history

Nerve growth factor (NGF) regulates many aspects of neuronal biology by retrogradely propagating signals along axons to the targets of those axons. How this occurs when axons contain a plethora of proteins that can silence those signals has long perplexed the neurotrophin field. In this issue of the JCI, Li et al. suggest an answer to this vexing problem, while exploring why the Elp1 gene that is mutated in familial dysautonomia (FD) causes peripheral neuropathy. They describe a distinctive function of Elp1 as a protein that is required to sustain NGF signaling by blocking the activity of its phosphatase that shuts off those signals. This finding helps explain the innervation deficits prominent in FD and reveals a unique role for Elp1 in the regulation of NGF-dependent TrkA activity.

Preview pages

Reset
Page preview
2196 Page 2195 Back

Continue reading with a subscription.

A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.

Already subscribed?

Click here to sign into your account.

Don't have a subscription?

Please select one of the subscription options, which includes a low-cost option just for this article.

At an institution or library?

If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).

Problems?

Please try these troubleshooting tips.

  • Purchase this article
  • $10
  • Purchasing this article will give you full access for the calendar year.
  • Purchase article
  • Purchase Site Pass
  • $25
  • This will give you access to every article on the site for 24 hours.
  • Order site pass
  • Online subscription
  • $95
  • Individual online subscriptions give you full online access for the calendar year.
  • Individual online subscriptions ordered from September 1st on will receive access for the remainder of current year as well as for the full following year subscription term.
  • Order Online
  • JCI This Month subscription
  • $135
  • JCI This Month is a 16- to 20-page overview of the articles published each month
  • Subscribing to JCI This Month also gives subscribers full online access for the calendar year.
  • *Price outside U.S. and Canada: $195.
  • JCI This Month + Online
Advertisement