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Titolo:
Autoantibodies against DNA double-strand break repair proteins
Autore:
Takeda, Y; Dynan, WS;
Indirizzi:
Med Coll Georgia, Inst Mol Med & Genet, Program Gene Regulat, Augusta, GA 30912 USA Med Coll Georgia Augusta GA USA 30912 Gene Regulat, Augusta, GA 30912 USA
Titolo Testata:
FRONTIERS IN BIOSCIENCE
, volume: 6, anno: 2001,
pagine: D1335 - D1345
SICI:
1093-9946(200111)6:<D1335:AADDBR>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
KINASE CATALYTIC SUBUNIT; SYSTEMIC LUPUS-ERYTHEMATOSUS; IONIZING-RADIATION SENSITIVITY; KU P70/P80 AUTOANTIGEN; END-BINDING-ACTIVITY; V(D)J RECOMBINATION; LIGASE-IV; XRCC4 PROTEIN; ANTINUCLEAR ANTIBODIES; ANTIGENIC DETERMINANTS;
Keywords:
autoantibodies; systemic lupus erythematosus; DNA repair; Ku protein; DNA-dependent protein kinase; review;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
91
Recensione:
Indirizzi per estratti:
Indirizzo: Takeda, Y CB-2803,1120 15th St, Augusta, GA 30912 USA CB-2803,1120 15th St Augusta GA USA 30912 Augusta, GA 30912 USA
Citazione:
Y. Takeda e W.S. Dynan, "Autoantibodies against DNA double-strand break repair proteins", FRONT BIOSC, 6, 2001, pp. D1335-D1345

Abstract

Autoantibodies against cellular components are commonly present in sera from patients with systemic rheumatic diseases and may play an important rolein pathogenesis. The Ku protein was recognized 20 years ago as a major target of autoantibodies in a subset of Japanese patients with scleroderma-polymyositis overlap syndrome, and anti-Ku antibodies have since been shown tooccur in 10-20% of patients with these and other systemic rheumatic diseases, including systemic lupus erythematosus. Ku functions physiologically inthe repair of DNA double-strand breaks, where it carries out the initial recognition of damaged DNA ends. The three dimensional structure of the Ku-DNA complex has recently been solved, and helps illuminate the relationship between the autoimmune epitopes and other features of the protein. In addition to Ku, three other polypeptides in the same DNA repair pathway have more recently been identified as autoantigens: the DNA-dependent protein kinase catalytic subunit, DNA ligase IV, and XRCC4. Two hypotheses have been invoked to explain the ability of these proteins to elicit an autoimmune response in susceptible individuals. One is that DNA damage induces formation ofnucleoprotein complexes that present novel composite or conformational epitopes. The other is that cleavage of these proteins by caspases or GranzymeB leads to presentation of immunocryptic peptides capable of stimulating autoreactive T lymphocytes. In the case of DNA double-strand break repair proteins, there is evidence that both of these mechanisms may be at work. Because of their role in the maintenance of genome stability, DNA double-strand break repair proteins have been the subject of intense study, and a wealth of new structural, biochemical and functional information makes them excellent models for investigation of the humoral autoimmune response.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 12:47:12