A point mutation in the putative ATP binding site of the pseudorabies virus US3 protein kinase prevents Bad phosphorylation and cell survival following apoptosis induction-Reference-Cited by-同舟云学术

A point mutation in the putative ATP binding site of the pseudorabies virus US3 protein kinase prevents Bad phosphorylation and cell survival following apoptosis induction

Published:2007-09 Issue:1-2 Volume:128 Page:65-70
ISSN:0168-1702
Container-title:Virus Research
language:en
Short-container-title:Virus Research

Author:

Deruelle Matthias,Geenen Kristin,Nauwynck Hans J.,Favoreel Herman W.

Publisher

Elsevier BV

Subject

Cancer Research,Infectious Diseases,Virology

Reference26 articles.

1. Varicella-Zoster virus retains major histocompatibility complex class I proteins in the golgi compartment of infected cells;Abendroth;J. Virol.,2001

2. The herpes simplex virus 1 US3 protein kinase blocks caspase-dependent double cleavage and activation of the proapoptotic protein Bad;Benetti;J. Virol.,2003

3. Herpes simplex virus protein kinase US3 activates and functionally overlaps protein kinase A to block apoptosis;Benetti;Proc. Natl. Acad. Sci. U.S.A.,2004

4. The pseudorabies virus serine/threonine kinase Us3 contains mitochondrial, nuclear and membrane localization signals;Calton;Virus Genes,2004

5. The Us3 protein kinase of herpes simplex virus 1 blocks apoptosis and induces phosporylation of the Bcl-2 family member Bad;Cartier;Exp. Cell. Res.,2003

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