Adenovirus E3 10.4K/14.5kD Protein

A protein encoded by the nonessential E3 early multi-gene transcription unit of various adenovirus serotypes. It is a heterodimer of 10.4 kD and 14.5 kD cytoplasmic membrane proteins, and involved in viral interaction with the host immune system: it downregulates cell surface expression of EGF receptors in virus-infected cells, inhibits TNF-alpha-induced inflammation and TNF activation of cytosolic phospholipase A2, which cleaves arachidonic acid from membrane phospholipids, preventing leukotriene and prostaglandin formation from arachidonic acid, thereby dampening the inflammatory response. E3 10.4K/14.5 kD synthesis is upregulated by TNF-alpha by transcription of factor NF-kappa-B, and protects adenovirus-infected fibroblasts against TNF-alpha induced cytolysis and apoptosis. It induces loss of FAS antigen surface expression and blocks FAS induced apoptosis of virus-infected cells. It also causes the loss of TRAIL DR4 (death receptor-4) and prevents TRAIL-induced apoptosis of virus-infected human cells.

单词	adenovirus e3 10.4k/14.5kd protein
释义	DictionarySeerid Adenovirus E3 10.4K/14.5kD Protein Adenovirus E3 10.4K/14.5kD Protein A protein encoded by the nonessential E3 early multi-gene transcription unit of various adenovirus serotypes. It is a heterodimer of 10.4 kD and 14.5 kD cytoplasmic membrane proteins, and involved in viral interaction with the host immune system: it downregulates cell surface expression of EGF receptors in virus-infected cells, inhibits TNF-alpha-induced inflammation and TNF activation of cytosolic phospholipase A2, which cleaves arachidonic acid from membrane phospholipids, preventing leukotriene and prostaglandin formation from arachidonic acid, thereby dampening the inflammatory response. E3 10.4K/14.5 kD synthesis is upregulated by TNF-alpha by transcription of factor NF-kappa-B, and protects adenovirus-infected fibroblasts against TNF-alpha induced cytolysis and apoptosis. It induces loss of FAS antigen surface expression and blocks FAS induced apoptosis of virus-infected cells. It also causes the loss of TRAIL DR4 (death receptor-4) and prevents TRAIL-induced apoptosis of virus-infected human cells.
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