Please use this identifier to cite or link to this item:
|Title:||Cyclin-dependent kinase 5 modulates nociceptive signaling through direct phosphorylation of transient receptor potential vanilloid 1|
|Citation:||Pareek, T.K., Keller, J., Kesavapany, S., Agarwal, N., Kuner, R., Pant, H.C., Iadarola, M.J., Brady, R.O., Kulkarni, A.B. (2007-01-09). Cyclin-dependent kinase 5 modulates nociceptive signaling through direct phosphorylation of transient receptor potential vanilloid 1. Proceedings of the National Academy of Sciences of the United States of America 104 (2) : 660-665. ScholarBank@NUS Repository. https://doi.org/10.1073/pnas.0609916104|
|Abstract:||Transient receptor potential vanilloid 1 (TRPV1), a ligand-gated cation channel highly expressed in small-diameter sensory neurons, is activated by heat, protons, and capsaicin. The phosphorylation of TRPV1 provides a versatile regulation of intracellular calcium levels and is critical for TRPV1 function in responding to a pain stimulus. We have previously reported that cyclin-dependent kinase 5 (Cdk5) activity regulates nociceptive signaling. In this article we report that the Cdk5-mediated phosphorylation of TRPV1 at threonine-407 can modulate agonist-induced calcium influx. Inhibition of Cdk5 activity in cultured dorsal root ganglia neurons resulted in a significant reduction of TRPV1-mediated calcium influx, and this effect could be reversed by restoring Cdk5 activity. Primary nociceptor-specific Cdk5 conditional-knockout mice showed reduced TRPV1 phosphorylation, resulting in significant hypoalgesia. Thus, the present study indicates that Cdk5-mediated TRPV1 phosphorylation is important in the regulation of pain signaling. © 2006 by The National Academy of Sciences of the USA.|
|Source Title:||Proceedings of the National Academy of Sciences of the United States of America|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Jan 17, 2019
WEB OF SCIENCETM
checked on Jan 9, 2019
checked on Jan 11, 2019
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.