Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1997-2-7
pubmed:abstractText
Genetic abnormalities in the Fas receptor or its trimeric ligand, FasL, result in massive T-cell proliferation and a lupus-like autoimmune syndrome, which was initially attributed to excessive lymphoproliferation but is now ascribed to the absence of Fas-mediated cell death. Although Fas is normally expressed on most thymocytes, negative selection seems to be unperturbed in Fas-deficient (lpr) mice. This suggests that Fas has an important function in peripheral, but not thymic, T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0960-9822
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
839-47
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Functional analysis of Fas signaling in vivo using synthetic inducers of dimerization.
pubmed:affiliation
Howard Hughes Medical Institute, Department of Developmental Biology, Stanford University Medical School, California 94305, USA. dspencer@bcm.tmc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't