English  |  正體中文  |  简体中文  |  Items with full text/Total items : 90437/105768 (86%)
Visitors : 10963612      Online Users : 581
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version


    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/112848


    Title: CHIP attenuates lipopolysaccharide-induced cardiac hypertrophy and apoptosis by promoting NFATc3 proteasomal degradation
    Authors: 趙崇男;La, Chao?Hung;Lai, Chao?Hung;Farheen, Khan;Badrealam, Khan Farheen;Lo, Jeng?Fan;Lo, Jeng?Fan;She, Chia?Yao;Shen, Chia?Yao;Che, Chia?Hua;Chen, Chia?Hua;Che, Ray?Jade;Chen, Ray?Jade;Padma, Vijaya;Viswanadha, Vijaya Padma;Kuo, Wei?Wen;Kuo, Wei?Wen;黃志揚;Huang, Chih-Yang
    Contributors: 醫學檢驗暨生物技術學系
    Keywords: CHIP;NFATc3;apoptosis;hypertrophy;lipopolysaccharide.
    Date: 2019-11
    Issue Date: 2020-09-01 13:59:21 (UTC+8)
    Publisher: 亞洲大學
    Abstract: Carboxyl-terminus of Hsc70 interacting protein (CHIP) is a chaperone-dependent E3-ubiquitin ligase with important function in protein quality control system. In the current research endeavor, we have investigated the putative role of CHIP in lipopolysaccharides (LPS)-induced cardiomyopathies. Basically, H9c2 cardiomyoblasts were transfected with CHIP for 24 hr, and thereafter, treated with LPS for 12 hr. Concomitantly, western blot analysis, actin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and coimmunoprecipitation studies were performed to investigate the underlying intricacies. Interestingly, western blot analysis revealed that the expression of hypertrophy and apoptosis-related proteins were considerably reduced following overexpression of CHIP. Moreover, Actin staining and TUNEL assay further ascertained the attenuation of cardiac hypertrophy and apoptosis following overexpression of CHIP respectively. These aspects instigate the role of CHIP in attenuation of LPS-induced cardiomyopathies. Additionally and importantly, co-immunoprecipitation and western blot studies revealed that CHIP plausibly promotes degradation of nuclear factor of activated T cells 3 (NFATc3) through ubiquitin-proteasomal pathway. Taken together, our study reveals that CHIP attenuates LPS-induced cardiac hypertrophy and apoptosis perhaps by promoting NFATc3 proteasomal degradation.
    Relation: JOURNAL OF CELLULAR PHYSIOLOGY
    Appears in Collections:[醫學檢驗暨生物技術學系] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML5View/Open


    All items in ASIAIR are protected by copyright, with all rights reserved.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback