Hepatitis B virus X protein disrupts stress fiber formation and triggers apoptosis.

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題名:	Hepatitis B virus X protein disrupts stress fiber formation and triggers apoptosis.
作者:	黃光裕 Kuo, Chan-Yen Chou, Tzu-Yu Chen, Chun-Ming Tsai, Yung-Fong Hwang, Guang-Yuh Hwang, Tsong-Long
貢獻者:	Chang Gung University Department of Life Science, Tunghai University Department of Anesthesiology, Chang Gung Memorial Hospital
關鍵詞:	HBx MLCK PTEN Stress-fiber formation Apoptosis
日期:	2013-07
上傳時間:	2016-08-16
出版者:	荷蘭:Elsevier
摘要:	Cytoskeletal proteins are key participants in the cellular progression to apoptosis. In a previous study we injected nude mice with CCL13-HBx cells and identified in contrast to non-HBx transfected cells a differentially phosphorylated myosin light chain (p-MLC) by two-dimensional PAGE and mass spectrometry of the tumor material. To investigate the role of HBx in myosin light chain kinase (MLCK) signaling pathways, we analyzed the key molecules, p-MLC and MLCK, by western blotting. Immunofluorescence staining analysis showed that HBx disrupted stress fiber formation and that focal adhesion kinase (FAK) and integrin-linked kinase (ILK) were regulated by HBx-mediated phosphatase and tensin homolog (PTEN). We also used pharmacological inhibitors to explore the correlation between cytoskeletal rearrangements and HBx-mediated cell apoptosis via an MLCK and a PTEN-dependent pathway. The results showed that both ML9 and bvp restored the effects caused by HBx induction. Our findings suggest that HBx disrupts stress fiber formation and triggers apoptosis via an MLCK and a PTEN-dependent pathway.
關聯:	Virus Research, 175(1), 20-29
顯示於類別:	[生命科學系所] 期刊論文

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