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Publication year
2005Source
Trends in Microbiology, 13, 2, (2005), pp. 41-4ISSN
Publication type
Article / Letter to editor
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Organization
Medical Microbiology
Biochemistry (UMC)
Journal title
Trends in Microbiology
Volume
vol. 13
Issue
iss. 2
Page start
p. 41
Page end
p. 4
Subject
IGMD 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 metabolismAbstract
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.
This item appears in the following Collection(s)
- Academic publications [242839]
- Electronic publications [129630]
- Faculty of Medical Sciences [92293]
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