TRPA1 is a substrate for de-ubiquitination by the tumor suppressor CYLD.

Abstract:

:Certain TRP cation channels confer the ability to sense environmental stimuli (heat, cold, pressure, osmolarity) across physiological and pathophysiological ranges. TRPA1 is a TRP-related channel that responds to cold temperatures, and pungent compounds that include the cold-mimetic icilin and cannabinoids. The initial report of TRPA1 as a transformation-associated gene product in lung epithelia is at odds with subsequent descriptions of a tissue distribution for TRPA1 that is restricted to sensory neurons. Here, we report that the human TRPA1 protein is widely expressed outside the CNS, and is indeed dys-regulated during oncogenic transformation. We describe that TRPA1 associates with the tumor-suppressor protein CYLD. TRPA1 is a novel substrate for the de-ubiquitinating activity of CYLD, and this de-ubiquitination has the net effect of increasing the cellular pool of TRPA1 proteins. Oncogenic mutations in the CYLD gene may therefore be predicted to alter cellular levels of TRPA1.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Stokes A,Wakano C,Koblan-Huberson M,Adra CN,Fleig A,Turner H

doi

10.1016/j.cellsig.2005.12.009

subject

Has Abstract

pub_date

2006-10-01 00:00:00

pages

1584-94

issue

10

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(06)00002-7

journal_volume

18

pub_type

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