Enterovirus protein 2B po(u)res out the calcium: a viral strategy to survive?
until further notice
SourceTrends in Microbiology, 13, 2, (2005), pp. 41-44
Article / Letter to editor
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Trends in Microbiology
SubjectIGMD 8: Mitochondrial medicine; N4i 1: Pathogenesis and modulation of inflammation; N4i 2: Invasive mycoses and compromised host; N4i 3: Poverty-related infectious diseases; NCMLS 1: Infection and autoimmunity; NCMLS 4: Energy and redox metabolism; UMCN 4.1: Microbial pathogenesis and host defense; UMCN 5.3: Cellular energy metabolism
Enteroviruses modify several cellular functions to ensure efficient replication. However, some of these alterations can trigger a defensive apoptotic host-cell program. To prevent premature abortion of their productive cycle, enteroviruses have developed anti-apoptotic countermeasures. Here, we discuss recent evidence that the enterovirus 2B protein exerts an anti-apoptotic activity that is related to its ability to form pores in endoplasmic reticulum (ER) and Golgi membranes, thereby reducing their Ca(2+) content and perturbing ER-mitochondrial Ca(2+) signaling.
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