• DocumentCode
    3151407
  • Title

    Apop-1 Induces Caspase-Dependent Apoptosis

  • Author

    Sun, Xin ; Lv, Gang ; Gao, Ling ; Kong, Fanli ; Zhu, Xiaotao ; Tian, Dan ; Tong, Haibin ; Chu, Xiaodan ; Xie, Yu

  • Author_Institution
    Life Sci. Center, Beihua Univ. China, China
  • fYear
    2010
  • fDate
    18-20 June 2010
  • Firstpage
    1
  • Lastpage
    4
  • Abstract
    Apoptosis is a form of genetically programmed cell death, which plays a pivotal role in normal development and the maintenance of homeostasis of a variety of tissues including cardiovascular system. Apop-1 is a soluble protein consisting of 194 amino acids with a mitochondrial localization signal at its N-terminus. RT-PCR data revealed that Apop-1 is expressed in all the organs tested. Immunofluorescence study showed that Apop-1 protein is localized in mitochondria. Transient transfection experiment showed Apop-1 induces apoptosis of cultured VSMC, and this apoptosis is inhibited by a pan-caspase inhibitor Z-VAD. The apoptosis induced by Apop-1 may contribute to the loss of VSMC in atherosclerosis, which will influence the stability of atherosclerotic plaques.
  • Keywords
    blood vessels; cardiovascular system; cellular biophysics; enzymes; fluorescence; molecular biophysics; molecular configurations; Apop-1; N-terminus; RT-PCR data; amino acids; atherosclerosis; atherosclerotic plaques; biological tissues; cardiovascular system; caspase-dependent apoptosis; genetically programmed cell death; homeostasis; immunofluorescence; mitochondrial localization signal; pan-caspase inhibitor Z-VAD; protein; Amino acids; Fluorescence; Hospitals; Microscopy; Muscles; Proteins; Sliding mode control; Statistical analysis; Sun; Surgery;
  • fLanguage
    English
  • Publisher
    ieee
  • Conference_Titel
    Bioinformatics and Biomedical Engineering (iCBBE), 2010 4th International Conference on
  • Conference_Location
    Chengdu
  • ISSN
    2151-7614
  • Print_ISBN
    978-1-4244-4712-1
  • Electronic_ISBN
    2151-7614
  • Type

    conf

  • DOI
    10.1109/ICBBE.2010.5518003
  • Filename
    5518003