Enterovirus protein 2B po(u)res out the calcium: a viral strategy to survive?
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.
van Kuppeveld
Frank J M
FJ
Department of Medical Microbiology, Radboud University Nijmegen Medical Center, Nijmegen Center for Molecular Life Sciences, PO Box 9101, 6500 HB Nijmegen, The Netherlands. f.vankuppeveld@ncmls.kun.nl
de Jong
Arjan S
AS
Melchers
Willem J G
WJ
Willems
Peter H G M
PH
D000595:Amino Acid Sequence; D017209:Apoptosis / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000821:virology; D004770:Enterovirus / Q000235:genetics / Q000378:metabolism*; D004769:Enterovirus Infections / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D006056:Golgi Apparatus / Q000378:metabolism / Q000821:virology; D006801:Humans; D008969:Molecular Sequence Data; D014764:Viral Proteins / Q000378:metabolism*
D014764:Viral Proteins; D002118:Calcium