Linked Life Data

18158115

Source:http://linkedlifedata.com/resource/pubmed/id/18158115

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-12-25
pubmed:abstractText
Ras is a guanine nucleotide-binding protein that plays a major role in regulating the proliferation of T cells. To investigate the mechanism of the Ras/mitogen-activated protein kinase pathway, one of the downstream signal-transduction pathways of T-cell receptors, in the response to alloantigen, we performed full-thickness skin grafting in the major histocompatibility complex (MHC) incompatible strain BALB/c (H-2Kd) (donor) and T-cell-specific H-Ras dominant-negative (dnRas) transgenic (tg) C57BL/6 (H-2Kb) (recipient) male mice. In vitro and in vivo dnRas tg mouse T-cell proliferation and cytotoxic T lymphocyte (CTL) activity assay were also performed. The median graft survival time in control B6/wild type (wt) mouse allografts was seven days. Conversely, the dnRas tg mouse group exhibited a significant (p<0.01) prolongation of graft survival to 15 days. However, all grafts were eventually rejected after one month. Mixed lymphocyte reaction and popliteal lymph node assay revealed that T-cell proliferation was decreased in response to alloantigen, but CTL activity was not changed in the dnRas tg mice. These results suggested that Ras is essential for peripheral T lymphocytes to respond to allo-MHC antigens, and Ras may be a molecular target for controlling transplant rejection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0966-3274
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
302-6
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Survival of skin allografts is prolonged in mice with a dominant-negative H-Ras.
pubmed:affiliation
Laboratory of Transplantation Immunology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't