IMR Press / FBL / Volume 17 / Issue 6 / DOI: 10.2741/4053

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


PDCD10 interacts with STK25 to accelerate cell apoptosis under oxidative stress

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1 Department of Immunology , School of Basic Medical Sciences, Peking University, Beijing, PR China
2 Department of Medical Genetics, School of Basic Medical Sciences, Peking University, No. 38 Xueyuan Road, Beijing 100191, PR China
3 Human Disease Genomics Center, Peking University No. 38 Xueyuan Road, Beijing 100191, PR China
4 Central Laboratory, Peking University School and Hospital of Stomatology, No. 22 Zhongguancun Nandajie, Beijing 100081, PR China
5 State Key Lab of Animal Nutrition, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, PR China
Front. Biosci. (Landmark Ed) 2012, 17(6), 2295–2305;
Published: 1 June 2012

An apoptosis-related protein, cerebral cavernous malformation 3 (CCM3 or PDCD10), has recently been implicated in mutations associated with cerebral cavernous malformation. Herein, we show that PDCD10 interacts with serine/threonine kinase 25 (STK25), an oxidant stress response kinase related to sterile-20 (Ste20) that is activated by oxidative stress and induces apoptotic cell death. Functional investigations indicate that PDCD10 and STK25 protein are up-regulated by H2O2 stimulation, and that co-expression of the proteins accelerates cell apoptosis. The induction of small interfering PDCD10 (siPDCD10) or siSTK25 results in decreased endogenous PDCD10 and STK25 expression, which is accompanied by attenuated cell apoptosis. Interaction between PDCD10 and STK25 modulates ERK activity under oxidative stress. PDCD10 stabilizes STK25 protein through a proteasome-dependent pathway. Our findings suggest that PDCD10 might be a regulatory adaptor required for STK25 functions, which differ distinctly depending on the redox status of the cells that may be potentially related to tumor progression.

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