Truncation of cytoplasmic tail of EIAV Env increases the pathogenic necrosis

Virus Research

Volumn 133, Issue 2, 2008, Pages 201-210

  Meng, Qinglai ^a,b,d   Li, Shenwei ^b   Liu, Lianxing ^a,b,d   Xu, Jianqing ^b   Liu, Yong ^b   Zhang, Yaozhou ^c   Zhang, Xiaoyan ^b   Shao, Yiming ^a,b  

^a WUHAN INSTITUTE OF VIROLOGY   (China)

^b CHINESE CENTER FOR DISEASE CONTROL AND PREVENTION   (China)

^c ZHEJIANG SCI TECH UNIVERSITY   (China)

^d UNIVERSITY OF CHINESE ACADEMY OF SCIENCES   (China)

Author keywords

Apoptosis; EIAV; Envelope; Mitochondrial depolarization; Necrosis; Truncation

Indexed keywords

BETA TUBULIN; CASPASE; ENVELOPE PROTEIN;

ARTICLE; CELL DEATH; CELL MEMBRANE DEPOLARIZATION; CONTROLLED STUDY; CYTOPLASM; ENZYME ACTIVATION; EQUINE INFECTIOUS ANEMIA VIRUS; FLOW CYTOMETRY; HUMAN; HUMAN CELL; NECROSIS; NONHUMAN; NUCLEOTIDE SEQUENCE; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN EXPRESSION; VIRUS ENVELOPE;

ANIMALS; APOPTOSIS; CASPASES; CELL LINE; ENZYME ACTIVATION; GENE PRODUCTS, ENV; HUMANS; INFECTIOUS ANEMIA VIRUS, EQUINE; MEMBRANE POTENTIALS; MITOCHONDRIA; NECROSIS; PROTEINS; TRANSFECTION;

EQUINE INFECTIOUS ANEMIA VIRUS;

EID: 41149142794     PISSN: 01681702     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.virusres.2008.01.004     Document Type: Article

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