Source:http://linkedlifedata.com/resource/pubmed/id/18947875
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2009-2-9
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pubmed:abstractText |
The rodent-specific complement regulator complement receptor 1-related gene/protein-y (Crry) is critical for complement homeostasis. Gene deletion is 100% embryonically lethal; Crry-deficient (Crry(-/-)) mice were rescued by back-crossing onto C3 deficiency, confirming that embryo loss was complement mediated. In order to rescue viable Crry(-/-) mice without deleting C3, we have tested inhibition of C5 during gestation. Crry(+/-) females were given neutralizing anti-C5 mAb immediately prior to mating with Crry(+/-) males and C5 inhibition maintained through pregnancy. A single, healthy Crry(-/-) female was obtained and mating with Crry(+/-) males yielded healthy litters containing equal numbers of Crry(+/-) and Crry(-/-) pups. Inter-crossing Crry(-/-) mice yielded healthy litters of expected size. Although the mice were not anemic, exposure of Crry(-/-) erythrocytes to normal mouse serum caused C3 deposition and lysis, while transfusion into normal or C6(-/-) mice resulted in rapid clearance. Complement activity and C3 levels in Crry(-/-) mice were markedly reduced. Comparison with factor H deficient (CfH(-/-)) mice revealed similar levels of residual C3; however, unlike the CfH(-/-) mice, Crry(-/-) mice showed no evidence of renal injury, demonstrating distinct roles for these regulators in protecting the kidney.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C5,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C6,
http://linkedlifedata.com/resource/pubmed/chemical/Complement Factor H,
http://linkedlifedata.com/resource/pubmed/chemical/Crry protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0161-5890
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
46
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
803-11
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pubmed:meshHeading |
pubmed-meshheading:18947875-Animals,
pubmed-meshheading:18947875-Antibodies, Monoclonal,
pubmed-meshheading:18947875-Complement C3,
pubmed-meshheading:18947875-Complement C5,
pubmed-meshheading:18947875-Complement C6,
pubmed-meshheading:18947875-Complement Factor H,
pubmed-meshheading:18947875-Crosses, Genetic,
pubmed-meshheading:18947875-Embryo Loss,
pubmed-meshheading:18947875-Female,
pubmed-meshheading:18947875-Homeostasis,
pubmed-meshheading:18947875-Kidney,
pubmed-meshheading:18947875-Male,
pubmed-meshheading:18947875-Mice,
pubmed-meshheading:18947875-Mice, Knockout,
pubmed-meshheading:18947875-Pregnancy,
pubmed-meshheading:18947875-Receptors, Complement
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pubmed:year |
2009
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pubmed:articleTitle |
Crry deficiency in complement sufficient mice: C3 consumption occurs without associated renal injury.
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pubmed:affiliation |
Complement Biology Group, Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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