Linked Life Data

19591957

Source:http://linkedlifedata.com/resource/pubmed/id/19591957

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2009-9-1
pubmed:abstractText
Many viruses have evolved strategies to either evade or hijack host cell immune programs, as a means of promoting their own reproduction. For example, the human cytomegalovirus (HCMV) immediate-early protein vMIA/UL37ex1 inhibits host cell apoptosis, and its expression during infection aids virus replication. Here it is shown that stable expression of vMIA/UL37ex1 reduces cleavage of the innate immune response-proteins MAVS and RIG-I by caspases during apoptosis. Unexpectedly, it is demonstrated that RIG-I, but not MAVS, is degraded during HCMV infection. This process occurs in a non-apoptotic manner, and provides new evidence that HCMV may have evolved a unique strategy to evade RIG-I-mediated immune responses.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1769-714X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
973-9
pubmed:dateRevised
2011-9-29
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Degradation of RIG-I following cytomegalovirus infection is independent of apoptosis.
pubmed:affiliation
Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA. scotti@mail.nih.gov
pubmed:publicationType
Journal Article, Research Support, N.I.H., Intramural