File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Calcium signals and calpain-dependent necrosis are essential for release of coxsackievirus B from polarized intestinal epithelial cells

TitleCalcium signals and calpain-dependent necrosis are essential for release of coxsackievirus B from polarized intestinal epithelial cells
Authors
Issue Date2011
PublisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/
Citation
Molecular Biology of the Cell, 2011, v. 22 n. 17, p. 3010-3021 How to Cite?
AbstractCoxsackievirus B (CVB), a member of the enterovirus family, targets the polarized epithelial cells lining the intestinal tract early in infection. Although the polarized epithelium functions as a protective barrier, this barrier is likely exploited by CVB to promote viral entry and subsequent egress. Here we show that, in contrast to nonpolarized cells, CVB-infected polarized intestinal Caco-2 cells undergo nonapoptotic necrotic cell death triggered by inositol 1,4,5-trisphosphate receptor-dependent calcium release. We further show that CVB-induced cellular necrosis depends on the Ca 2+-activated protease calpain-2 and that this protease is involved in CVB-induced disruption of the junctional complex and rearrangements of the actin cytoskeleton. Our study illustrates the cell signaling pathways hijacked by CVB, and perhaps other viral pathogens, to promote their replication and spread in polarized cell types. © 2011 Bozym et al.
Persistent Identifierhttp://hdl.handle.net/10722/152816
ISSN
2015 Impact Factor: 4.037
2015 SCImago Journal Rankings: 3.665
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of HealthR01AI081759
R01AI52281
Funding Information:

We are grateful to Kevin Foskett for helpful advice and suggestions. This work was supported by funding from the National Institutes of Health (R01AI081759 to C.B.C. and R01AI52281 to J.M.B.).

References

 

DC FieldValueLanguage
dc.contributor.authorBozym, RAen_HK
dc.contributor.authorPatel, Ken_HK
dc.contributor.authorWhite, Cen_HK
dc.contributor.authorCheung, KHen_HK
dc.contributor.authorBergelson, JMen_HK
dc.contributor.authorMorosky, SAen_HK
dc.contributor.authorCoyne, CBen_HK
dc.date.accessioned2012-07-16T09:49:25Z-
dc.date.available2012-07-16T09:49:25Z-
dc.date.issued2011en_HK
dc.identifier.citationMolecular Biology of the Cell, 2011, v. 22 n. 17, p. 3010-3021en_HK
dc.identifier.issn1059-1524en_HK
dc.identifier.urihttp://hdl.handle.net/10722/152816-
dc.description.abstractCoxsackievirus B (CVB), a member of the enterovirus family, targets the polarized epithelial cells lining the intestinal tract early in infection. Although the polarized epithelium functions as a protective barrier, this barrier is likely exploited by CVB to promote viral entry and subsequent egress. Here we show that, in contrast to nonpolarized cells, CVB-infected polarized intestinal Caco-2 cells undergo nonapoptotic necrotic cell death triggered by inositol 1,4,5-trisphosphate receptor-dependent calcium release. We further show that CVB-induced cellular necrosis depends on the Ca 2+-activated protease calpain-2 and that this protease is involved in CVB-induced disruption of the junctional complex and rearrangements of the actin cytoskeleton. Our study illustrates the cell signaling pathways hijacked by CVB, and perhaps other viral pathogens, to promote their replication and spread in polarized cell types. © 2011 Bozym et al.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/en_HK
dc.relation.ispartofMolecular Biology of the Cellen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCalcium Signaling-
dc.subject.meshCalpain - metabolism-
dc.subject.meshEnterovirus Infections - virology-
dc.subject.meshIntestinal Mucosa - enzymology - pathology - virology-
dc.subject.meshNecrosis - metabolism - virology-
dc.titleCalcium signals and calpain-dependent necrosis are essential for release of coxsackievirus B from polarized intestinal epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, KH: kingho.cheung@hku.hken_HK
dc.identifier.authorityCheung, KH=rp01463en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1091/mbc.E11-02-0094en_HK
dc.identifier.pmid21737691-
dc.identifier.pmcidPMC3164450-
dc.identifier.scopuseid_2-s2.0-80052252539en_HK
dc.identifier.hkuros200563en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80052252539&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue17en_HK
dc.identifier.spage3010en_HK
dc.identifier.epage3021en_HK
dc.identifier.eissn1939-4586-
dc.identifier.isiWOS:000294419300003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridBozym, RA=6506295661en_HK
dc.identifier.scopusauthoridPatel, K=41361690100en_HK
dc.identifier.scopusauthoridWhite, C=7404153650en_HK
dc.identifier.scopusauthoridCheung, KH=14007487800en_HK
dc.identifier.scopusauthoridBergelson, JM=7005085403en_HK
dc.identifier.scopusauthoridMorosky, SA=26531551400en_HK
dc.identifier.scopusauthoridCoyne, CB=7005683822en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats