Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
32
|
| pubmed:dateCreated |
1997-9-5
|
| pubmed:databankReference | |
| pubmed:abstractText |
Cytotoxic lymphocytes contain granules that have the ability to induce apoptosis in susceptible target cells. The granule contents include perforin, a pore-forming molecule, and several granzymes, including A and B, which are the most abundant serine proteases in these granules. Granzyme B-deficient cytotoxic T lymphocytes (CTL) have a severe defect in their ability to rapidly induce apoptosis in their targets, but have an intact late cytotoxicity pathway that is in part perforin-dependent. In this report, we have created mice that are deficient for granzyme A and characterized their phenotype. These mice have normal growth and development and normal lymphocyte development, activation, and proliferation. Granzyme A-deficient CTL have a small but reproducible defect in their ability to induce 51Cr and 125I-UdR release from susceptible allogeneic target cells. Since other granzyme A-like tryptases could potentially account for the residual cytotoxicity in granzyme A-deficient CTL, we cloned the murine granzyme K gene, which is linked to granzyme A in humans, and proved that it is also tightly linked with murine granzyme A. The murine granzyme K gene (which encodes a tryptase similar to granzyme A) is expressed at much lower levels than granzyme A in CTL and LAK cells, but its expression is unaltered in granzyme A-/- mice. The minimal cytotoxic defect in granzyme A-/- CTL could be due to the existence of an intact, functional early killing pathway (granzyme B dependent), or to the persistent expression of additional granzyme tryptases like granzyme K.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chymases,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/GZMA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Granzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Mcpt6 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Mcpt6 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Serine Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/TPSB1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Tpsab1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tryptases,
http://linkedlifedata.com/resource/pubmed/chemical/chymase 2
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0021-9258
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
8
|
| pubmed:volume |
272
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
20236-44
|
| pubmed:dateRevised |
2010-11-18
|
| pubmed:meshHeading |
pubmed-meshheading:9242702-Amino Acid Sequence,
pubmed-meshheading:9242702-Animals,
pubmed-meshheading:9242702-Chromosome Mapping,
pubmed-meshheading:9242702-Chymases,
pubmed-meshheading:9242702-Cytotoxicity, Immunologic,
pubmed-meshheading:9242702-DNA, Complementary,
pubmed-meshheading:9242702-Exons,
pubmed-meshheading:9242702-Genetic Linkage,
pubmed-meshheading:9242702-Granzymes,
pubmed-meshheading:9242702-Humans,
pubmed-meshheading:9242702-Mice,
pubmed-meshheading:9242702-Molecular Sequence Data,
pubmed-meshheading:9242702-RNA, Messenger,
pubmed-meshheading:9242702-Rats,
pubmed-meshheading:9242702-Restriction Mapping,
pubmed-meshheading:9242702-Sequence Alignment,
pubmed-meshheading:9242702-Serine Endopeptidases,
pubmed-meshheading:9242702-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:9242702-Tryptases
|
| pubmed:year |
1997
|
| pubmed:articleTitle |
Residual cytotoxicity and granzyme K expression in granzyme A-deficient cytotoxic lymphocytes.
|
| pubmed:affiliation |
Department of Internal Medicine, Washington University School of Medicine, Campus Box 8007, St. Louis, Missouri 63110-1093, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|