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      Membrane cholesterol is required for activity of Vibrio vulnificus cytolysin

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      https://www.riss.kr/link?id=A75070233

      • 저자

        Yu, Hong-Nu (Department of Biochemistry,Institute of Medical Science,Chungbuk National University Medical School) ;  Lee, Young-Rae (Department of Biochemistry,Institute of Medical Science,Chungbuk National University Medical School) ;  Park, Kwang-Hyun (Department of Biochemistry,Institute of Medical Science,Chungbuk National University Medical School) ;  Rah, So-Young (Department of Biochemistry,Institute of Medical Science,Chungbuk National University Medical School) ;  Noh, Eun-Mi (Department of Biochemistry,Institute of Medical Science,Chungbuk National University Medical School) ;  Song, Eun-Kyung (Department of Microbiology and Immunology,Institute of Medical Science,Chungbuk National University Medical School) ;  Han, Myung-Kwan (Department of Microbiology and Immunology,Institute of Medical Science,Chungbuk National University Medical School) ;  Kim, Byeong-Soo (Department of Companion and Laboratory Animal Science,Research Center for Transgenic Cloned Pigs,Kongju National University) ;  Lee, Sung-Ho (Department of Companion and Laboratory Animal Science,Research Center for Transgenic Cloned Pigs,Kongju National University) ;  Kim, Jong-Suk (Department of Biochemistry,Institute of Medical Science,Chungbuk National University Medical School)

      • 발행기관
      • 학술지명
      • 권호사항
      • 발행연도

        2007

      • 작성언어

        English

      • 주제어
      • KDC

        630

      • 자료형태

        학술저널

      • 수록면

        393-399(7쪽)

      • 제공처
      • 중단사유

        ※ 저작자의 요청에 따라 해당 논문은 원문이 제공되지 않습니다.

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      다국어 초록 (Multilingual Abstract)

      Vibrio vulnificus cytolysin (VVC) forms a pore in the plasma membrane and induces cytolysis of various cells including erythrocytes, neutrophil and endothelial cells. The cytolytic activity of VVC is inhibited by exogenously added cholesterol, suggest...

      Vibrio vulnificus cytolysin (VVC) forms a pore in the plasma membrane and induces cytolysis of various cells including erythrocytes, neutrophil and endothelial cells. The cytolytic activity of VVC is inhibited by exogenously added cholesterol, suggesting that membrane cholesterol might be required for VVC cytolytic activity. However, there is no direct evidence that membrane cholesterol is involved in VVC-induced cytolysis. Herein we demonstrate that membrane cholesterol is required for binding of VVC to the plasma membrane. Membrane cholesterol depletion with methyl-β-cyclodextrin inhibited VVC-induced K^(+) release, 2-deoxy glucose release and Ca^(2+) influx, which are indicators of VVC pore formation. The cholesterol depletion-induced blockage of VVC cytolysis was due to the inhibition of VVC binding to membrane. These findings suggest that interaction with cholesterol is required for activity of VVC.

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