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- Publisher Website: 10.1038/74689
- Scopus: eid_2-s2.0-0033622010
- PMID: 10742150
- WOS: WOS:000165474100037
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Article: The tyrosine kinase p56(lck) is essential in coxsackievirus B3-mediated heart disease
Title | The tyrosine kinase p56(lck) is essential in coxsackievirus B3-mediated heart disease |
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Authors | |
Issue Date | 2000 |
Citation | Nature Medicine, 2000, v. 6, n. 4, p. 429-434 How to Cite? |
Abstract | Infections are thought to be important in the pathogenesis of many heart diseases. Coxsackievirus B3 (CVB3) has been linked to chronic dilated cardiomyopathy, a common cause of progressive heart disease, heart failure and sudden death. We show here that the sarcoma (Src) family kinase Lck (p56(lck)) is required for efficient CVB3 replication in T-cell lines and for viral replication and persistence in vivo. Whereas infection of wild-type mice with human pathogenic CVB3 caused acute and very severe myocarditis, meningitis, hepatitis, pancreatitis and dilated cardiomyopathy, mice lacking the p56(lck) gene were completely protected from CVB3-induced acute pathogenicity and chronic heart disease. These data identify a previously unknown function of Src family kinases and indicate that p56(lck) is the essential host factor that controls the replication and pathogenicity of CVB3. |
Persistent Identifier | http://hdl.handle.net/10722/291509 |
ISSN | 2021 Impact Factor: 87.241 2020 SCImago Journal Rankings: 19.536 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Liu, Peter | - |
dc.contributor.author | Aitken, Karen | - |
dc.contributor.author | Kong, Young Yun | - |
dc.contributor.author | Opavsky, Mary Anne | - |
dc.contributor.author | Martino, Tammy | - |
dc.contributor.author | Dawood, Fayez | - |
dc.contributor.author | Wen, Wen Hu | - |
dc.contributor.author | Kozeiradzki, Ivona | - |
dc.contributor.author | Bachmaier, Kurt | - |
dc.contributor.author | Straus, David | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Penninger, Josef M. | - |
dc.date.accessioned | 2020-11-17T14:54:31Z | - |
dc.date.available | 2020-11-17T14:54:31Z | - |
dc.date.issued | 2000 | - |
dc.identifier.citation | Nature Medicine, 2000, v. 6, n. 4, p. 429-434 | - |
dc.identifier.issn | 1078-8956 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291509 | - |
dc.description.abstract | Infections are thought to be important in the pathogenesis of many heart diseases. Coxsackievirus B3 (CVB3) has been linked to chronic dilated cardiomyopathy, a common cause of progressive heart disease, heart failure and sudden death. We show here that the sarcoma (Src) family kinase Lck (p56(lck)) is required for efficient CVB3 replication in T-cell lines and for viral replication and persistence in vivo. Whereas infection of wild-type mice with human pathogenic CVB3 caused acute and very severe myocarditis, meningitis, hepatitis, pancreatitis and dilated cardiomyopathy, mice lacking the p56(lck) gene were completely protected from CVB3-induced acute pathogenicity and chronic heart disease. These data identify a previously unknown function of Src family kinases and indicate that p56(lck) is the essential host factor that controls the replication and pathogenicity of CVB3. | - |
dc.language | eng | - |
dc.relation.ispartof | Nature Medicine | - |
dc.title | The tyrosine kinase p56(lck) is essential in coxsackievirus B3-mediated heart disease | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1038/74689 | - |
dc.identifier.pmid | 10742150 | - |
dc.identifier.scopus | eid_2-s2.0-0033622010 | - |
dc.identifier.volume | 6 | - |
dc.identifier.issue | 4 | - |
dc.identifier.spage | 429 | - |
dc.identifier.epage | 434 | - |
dc.identifier.isi | WOS:000165474100037 | - |
dc.identifier.issnl | 1078-8956 | - |