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Induction of autophagy by anthrax lethal toxin.
Tan, Yian Kim; Kusuma, Caroline M; St John, Lena J; Vu, Hao A; Alibek, Kenneth; Wu, Aiguo.
Afiliação
  • Tan YK; Molecular and Microbiology Department, College of Sciences, George Mason University, Manassas, VA 22010, USA.
Biochem Biophys Res Commun ; 379(2): 293-7, 2009 Feb 06.
Article em En | MEDLINE | ID: mdl-19103170
Autophagy is an evolutionary conserved intracellular process whereby cells break down long-lived proteins and organelles. Accumulating evidences suggest increasing physiological significance of autophagy in pathogenesis of infectious diseases. Anthrax lethal toxin (LT) exerts its influence on numerous cells and herein, we report a novel effect of LT-induced autophagy on mammalian cells. Several autophagy biochemical markers including LC3-II conversion, increased punctuate distribution of GFP-LC3 and development of acidic vesicular organelles (AVO) were detected in cells treated with LT. Analysis of individual LT component revealed a moderate increase in LC3-II conversion for protective antigen-treated cells, whereas the LC3-II level in lethal factor-treated cells remained unchanged. In addition, our preliminary findings suggest a protective role of autophagy in LT intoxication as autophagy inhibition resulted in accelerated cell death. This study presents a hitherto undescribed effect of LT-induced autophagy on cells and provides the groundwork for future studies on the implication of autophagy in anthrax pathogenesis.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Autofagia / Toxinas Bacterianas / Antígenos de Bactérias Limite: Animals Idioma: En Revista: Biochem Biophys Res Commun Ano de publicação: 2009 Tipo de documento: Article País de afiliação: Estados Unidos País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Autofagia / Toxinas Bacterianas / Antígenos de Bactérias Limite: Animals Idioma: En Revista: Biochem Biophys Res Commun Ano de publicação: 2009 Tipo de documento: Article País de afiliação: Estados Unidos País de publicação: Estados Unidos