Netrin-1-mediated axon outgrowth and cAMP production requires interaction with adenosine A2b receptor View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2000-10

AUTHORS

Véronique Corset, Kim Tuyen Nguyen-Ba-Charvet, Christelle Forcet, Emmanuel Moyse, Alain Chédotal, Patrick Mehlen

ABSTRACT

The netrins, a family of laminin-related secreted proteins, are critical in controlling axon elongation and pathfinding1,2,3,4. The DCC (for deleted in colorectal cancer) protein was proposed as a receptor for netrin-1 in the light of many observations including the inhibition of netrin-1-mediated axon outgrowth and attraction in the presence of an anti-DCC antiserum5,6,7, the similitude of nervous system defects in DCC and netrin-1 knockout mice4,8 and the results of receptor swapping experiments9. Previous studies have failed to show a direct interaction of DCC with netrin-1 (ref. 10), suggesting the possibility of an additional receptor or co-receptor. Here we show that DCC interacts with the membrane-associated adenosine A2b receptor, a G-protein-coupled receptor that induces cAMP accumulation on binding adenosine11. We show that A2b is actually a netrin-1 receptor and induces cAMP accumulation on binding netrin-1. Finally, we show that netrin-1-dependent outgrowth of dorsal spinal cord axons directly involves A2b. Together our results indicate that the growth-promoting function of netrin-1 may require a receptor complex containing DCC and A2b. More... »

PAGES

747-750

Journal

TITLE

Nature

ISSUE

6805

VOLUME

407

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/35037600

DOI

http://dx.doi.org/10.1038/35037600

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1040033439

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11048721


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