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Titolo:
The translesion DNA polymerase zeta plays a major role in Ig and bcl-6 somatic hypermutation
Autore:
Zan, H; Komori, A; Li, ZD; Cerutti, A; Schaffer, A; Flajnik, MF; Diaz, M; Casali, P;
Indirizzi:
Cornell Univ, Weill Med Coll, Div Mol Immunol, Dept Pathol, New York, NY 10021 USA Cornell Univ New York NY USA 10021 l, Dept Pathol, New York, NY 10021 USA Cornell Univ, Weill Med Coll, Dept Microbiol & Immunol, New York, NY 10021USA Cornell Univ New York NY USA 10021 obiol & Immunol, New York, NY 10021USA Cornell Univ, Weill Grad Sch Med Sci, Program Immunol, New York, NY 10021 USA Cornell Univ New York NY USA 10021 rogram Immunol, New York, NY 10021 USA Univ Maryland, Dept Microbiol & Immunol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 l & Immunol, Baltimore, MD 21201 USA Scripps Clin & Res Inst, Dept Immunol, La Jolla, CA 92037 USA Scripps Clin& Res Inst La Jolla CA USA 92037 nol, La Jolla, CA 92037 USA
Titolo Testata:
IMMUNITY
fascicolo: 5, volume: 14, anno: 2001,
pagine: 643 - 653
SICI:
1074-7613(200105)14:5<643:TTDPZP>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN B-CELLS; HUMAN-ANTIBODY RESPONSE; DAMAGE-INDUCED MUTAGENESIS; CYTIDINE DEAMINASE AID; THYMINE-THYMINE DIMER; BASE-EXCISION-REPAIR; DOUBLE-STRAND BREAKS; SACCHAROMYCES-CEREVISIAE; IMMUNOGLOBULIN GENES; GERMINAL CENTER;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
76
Recensione:
Indirizzi per estratti:
Indirizzo: Casali, P Cornell Univ, Weill Med Coll, Div Mol Immunol, Dept Pathol, New York, NY 10021 USA Cornell Univ New York NY USA 10021 thol, New York, NY 10021 USA
Citazione:
H. Zan et al., "The translesion DNA polymerase zeta plays a major role in Ig and bcl-6 somatic hypermutation", IMMUNITY, 14(5), 2001, pp. 643-653

Abstract

Ig somatic mutations would be introduced by a polymerase (pol) while repairing DNA outside main DNA replication. We show that human B cells constitutively express the translesion pol zeta, which effectively extends DNA past mismatched bases (mispair extender), and pol eta, which bypasses DNA lesions in an error-free fashion. Upon B cell receptor (BCR) engagement and coculture with activated CD4(+) T cells, these lymphocytes upregulated pol zeta,downregulated pol eta, and mutated the Ig and bcl-6 genes. Inhibition of the pol zeta REV3 catalytic subunit by specific phosphorothioate-modified oligonucleotides impaired Ig and bcl-6 hypermutation and UV damage-induced DNA mutagenesis, without affecting cell cycle or viability. Thus, pol zeta plays a critical role in Ig and bcl-6 hypermutation, perhaps facilitated by the downregulation of pol eta.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 23:04:10