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Titolo:
Hemolytic uremic syndrome: how do factor H mutants mediate endothelial damage?
Autore:
Zipfel, PF;
Indirizzi:
Hans Knoell Inst Nat Prod Res, Dept Infect Biol, D-07745 Jena, Germany Hans Knoell Inst Nat Prod Res Jena Germany D-07745 D-07745 Jena, Germany
Titolo Testata:
TRENDS IN IMMUNOLOGY
fascicolo: 7, volume: 22, anno: 2001,
pagine: 345 - 348
SICI:
1471-4906(200107)22:7<345:HUSHDF>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
COMPLEMENT FACTOR-H; ALTERNATIVE PATHWAY; BINDING-SITES; DEFICIENCY; PROTEINS; CELLS; C3B;
Tipo documento:
Editorial Material
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
21
Recensione:
Indirizzi per estratti:
Indirizzo: Zipfel, PF Hans Knoell Inst Nat Prod Res, Dept Infect Biol, Beutenbergstr 11, D-07745Jena, Germany Hans Knoell Inst Nat Prod Res Beutenbergstr 11 Jena Germany D-07745
Citazione:
P.F. Zipfel, "Hemolytic uremic syndrome: how do factor H mutants mediate endothelial damage?", TRENDS IMMU, 22(7), 2001, pp. 345-348

Abstract

Hemolytic uremic syndrome is characterized by microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. Data from recent genetic analyses reveal a clear association between the complement regulator factor H and the atypical form of this fatal human disease. The clustering of the identified mutations in the C-terminus of factor H identifies a 'hot spot' that is central to the pathogenesis of the disease. What are the possible biological and functional consequences of the identified mutations for the disease process and mechanisms of disease progression?.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/02/20 alle ore 04:09:49