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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Qi, Zhilin Shen, Lei Qi, Shimei Gui, Lin |
| Description | Author Affiliation: Qi Z ( Department of Biochemistry, Wannan Medical College, Wuhu, Anhui 241002, P.R. China.); Qi S ( Department of Biochemistry, Wannan Medical College, Wuhu, Anhui 241002, P.R. China.); Gui L ( Department of Microbiology and Immunology, Wannan Medical College, Wuhu, Anhui 241002, P.R. China.); Shen L ( Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing, Jiangsu 210023, P.R. China.) |
| Abstract | ß-arrestins, including ß-arrestin1 and ßarrestin2, two ubiquitously expressed members of the arrestin family in various types of tissue, are adaptor proteins that modulate the desensitization and trafficking of seven membranespanning receptors. Recently, ßarrestins have been shown to bind to numerous signaling molecules, including cSrc and mitogenactivated protein kinase family members. In addition, accumulating evidence has suggested that ßarrestins are involved in the antiapoptosis signaling pathway by associating with kinases, such as Akt and ERK, and altering their activities. However, the role of ßarrestins in tumor necrosis factorrelated apoptosisinducing ligand (TRAIL)induced apoptosis remains unclear. In the present study, ßarrestin2, but not ßarrestin1, was observed to modulate TRAILtriggered HepG2 cell apoptosis by regulating activation of the Srcextracellular signalregulated kinase (ERK) signaling pathway. Using overexpression and RNA interference experiments, ßarrestin2 was demonstrated to prevent TRAILinduced HepG2 cell apoptosis. Additionally, ßarrestin2 exerted an additive effect on TRAILinduced activation of Src and ERK. Furthermore, downregulating ßarrestin2 expression attenuated the TRAILinduced activation of Src and ERK survival signaling and enhanced TRAILinduced apoptosis. PP2, a pharmacological inhibitor of Src, reduced activation of the SrcERK signaling pathway and enhanced TRAILinduced HepG2 cell apoptosis. Co-immunoprecipitation experiments demonstrated a physical association between ßarrestin2 and Src, and TRAIL stimulation resulted in enhanced quantities of the ßarrestin2/Src complex. A notable interaction was identified between ßarrestin2 and death receptors (DR)4 and 5, but only in the presence of TRAIL stimulation. To the best of our knowledge, these findings are the first to demonstrate that ßarrestin2 mediates TRAILinduced apoptosis by combing with DRs and Src, and regulates the activation of SrcERK signaling in HepG2 cells. It is hypothesized that the formation of a signaling complex comprising DR, ßarrestin2 and Src is required for the action of TRAIL on HepG2 cell apoptosis, which provides a novel insight into analyzing the effects of ßarrestin2 on protecting cells from TRAILinduced apoptosis. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| Journal | Molecular Medicine Reports |
| Issue Number | 1 |
| Volume Number | 14 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2016-07-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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