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作者

Tielong Liu Yonggang Liu Jiashi Cao Xin Gao Jing Wang Guanghui Chen Yang Wang Ge Liu Guangjian Bai Yiwei Hu Jiaxiang Yang Lianfeng Dong Xinbao Quan Weiwei Zouc

作者单位

The Department of Medical Imaging Diagnosis, Changzheng Hospital, Second Military Medical University, Shanghai, China The Spinal Tumor Center, Changzheng Hospital, Second Military Medical University, Shanghai Taishan Medical University, Shandong province

刊名

Cellular Physiology & Biochemistry (Karger AG)

年份

2018

卷号

Vol.46 No.6

页码

2500-2507

ISSN

1015-8987

关键词

Apoptosis Dephosphorylation HIF-1α Hypoxia Ilkap

摘要

Background/Aims: Integrin-linked kinase-associated phosphatase , a serine/threonine phosphatase that belongs to the protein phosphatase 2C family, has a role in cell survival and apoptosis. Hypoxia-inducible factor 1α is the key transcription factor in the response to oxygen deficiency in mammals. Direct phosphorylation and dephosphorylation of HIF-1α affect its function. The present study investigated the role of ILKAP on HIF-1α dephosphorylation and cell behavior. Methods: HIF-1α was induced ...更多

Background/Aims: Integrin-linked kinase-associated phosphatase , a serine/threonine phosphatase that belongs to the protein phosphatase 2C family, has a role in cell survival and apoptosis. Hypoxia-inducible factor 1α is the key transcription factor in the response to oxygen deficiency in mammals. Direct phosphorylation and dephosphorylation of HIF-1α affect its function. The present study investigated the role of ILKAP on HIF-1α dephosphorylation and cell behavior. Methods: HIF-1α was induced by hypoxia. Physical binding between ILKAP and HIF-1α was demonstrated by a co-immunoprecipitation assay. HIF-1α transcriptional activity was investigated using a hypoxia-response element-containing luciferase reporter plasmid. Cell viability was evaluated by a trypan blue dye exclusion assay. ILKAP function was explored by a gain and loss assay with an overexpression plasmid and shRNA infection. Results: ILKAP physically interacted with HIF-1α and induced its dephosphorylation. Both the HIF-1α-p53 interaction and apoptosis relied on ILKAP. Conclusion: The results indicated that the ILKAP directly binds and dephosphorylates HIF-1α and responsible for severe hypoxiainduced cell apoptosis.收起

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