We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Protein kinase WNK3 increases cell survival in a caspase-3-dependent pathway.
- Authors
Veríssimo, F.; Silva, E.; Morris, J. D.; Pepperkok, R.; Jordan, P.
- Abstract
The subfamily of WNK (with no K=lysine) protein kinases has four human members and germline mutations in the WNK1 and WNK4 genes were recently found to cause pseudohypoaldosteronism type II, a familial hypertension disease. Here, we describe cloning and functional analysis of a further WNK member, human WNK3. Endogenous WNK3 protein is an active protein kinase when immunoprecipitated from cells and its overexpression increases the survival of HeLa cells by delaying the onset of apoptosis. Suppression of endogenous WNK3 protein by RNA interference accelerates the apoptotic response and promotes the activation of caspase-3. The mechanism of WNK3 action involves interaction with procaspase-3 and heat-shock protein 70. These results demonstrate a role for WNK3 in promoting cell survival and suggest a mechanism at the level of procaspase-3 activation.Oncogene (2006) 25, 4172–4182. doi:10.1038/sj.onc.1209449; published online 27 February 2006
- Subjects
PROTEIN kinases; GENETIC mutation; HYPERTENSION; CLONING; FUNCTIONAL analysis; HELA cells; APOPTOSIS
- Publication
Oncogene, 2006, Vol 25, Issue 30, p4172
- ISSN
0950-9232
- Publication type
Article
- DOI
10.1038/sj.onc.1209449