IR@PKUHSC  > 北京大学基础医学院  > 医学遗传学系
学科主题基础医学
PDCD10 interacts with STK25 to accelerate cell apoptosis under oxidative stress
Zhang, Heyu2,3,4; Ma, Xi5; Deng, Xuan2,3; Chen, Yiyu2,3; Mo, Xiaoning3; Zhang, Yingmei2,3; Zhao, Hongshan1,3; Ma, Dalong2,3
关键词PDCD10 STK25 Apoptosis ERK Oxidative stress
刊名FRONTIERS IN BIOSCIENCE-LANDMARK
2012-06-01
DOI10.2741/4053
17页:2295-2305
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]CEREBRAL CAVERNOUS MALFORMATIONS ; 20-LIKE KINASE-3 MST3 ; OXIDANT STRESS ; CARDIOVASCULAR EVENTS ; STE20-RELATED KINASE ; STE20-LIKE KINASE ; GENE-EXPRESSION ; CHEMICAL ANOXIA ; PROTEIN-KINASE ; CANCER-CELLS
英文摘要

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.

语种英语
WOS记录号WOS:000311885100020
项目编号30872940 ; 2009ZX09503-004
资助机构National Natural Science Foundation of China ; National Key New Drug Creation Program of China
引用统计
被引频次:14[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61529
专题北京大学基础医学院_医学遗传学系
北京大学基础医学院
北京大学口腔医学院_中心实验室
作者单位1.Peking Univ, Sch Basic Med Sci, Dept Med Genet, Beijing 100191, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Dept Immunol, Beijing 100191, Peoples R China
3.Peking Univ, Human Dis Genom Ctr, Beijing 100191, Peoples R China
4.Peking Univ Sch & Hosp Stomatol, Cent Lab, Beijing 100081, Peoples R China
5.China Agr Univ, State Key Lab Anim Nutr, Beijing 100193, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Heyu,Ma, Xi,Deng, Xuan,et al. PDCD10 interacts with STK25 to accelerate cell apoptosis under oxidative stress[J]. FRONTIERS IN BIOSCIENCE-LANDMARK,2012,17:2295-2305.
APA Zhang, Heyu.,Ma, Xi.,Deng, Xuan.,Chen, Yiyu.,Mo, Xiaoning.,...&Ma, Dalong.(2012).PDCD10 interacts with STK25 to accelerate cell apoptosis under oxidative stress.FRONTIERS IN BIOSCIENCE-LANDMARK,17,2295-2305.
MLA Zhang, Heyu,et al."PDCD10 interacts with STK25 to accelerate cell apoptosis under oxidative stress".FRONTIERS IN BIOSCIENCE-LANDMARK 17(2012):2295-2305.
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