Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Mutations truncating the EP300 acetylase in human cancers
Autore:
Gayther, SA; Batley, SJ; Linger, L; Bannister, A; Thorpe, K; Chin, SF; Daigo, Y; Russell, P; Wilson, A; Sowter, HM; Delhanty, JDA; Ponder, BAJ; Kouzarides, T; Caldas, C;
Indirizzi:
Univ Cambridge, Dept Oncol, Cambridge, England Univ Cambridge Cambridge England bridge, Dept Oncol, Cambridge, England Univ Cambridge, Dept Pathol, Cambridge, England Univ Cambridge CambridgeEngland ridge, Dept Pathol, Cambridge, England Univ Cambridge, Strangeways Res Labs, Cambridge, England Univ Cambridge Cambridge England rangeways Res Labs, Cambridge, England Univ Cambridge, Canbridge Inst Med Res, Wellcome Trust Ctr Study Mol Mechanisms Dis, Cambridge, England Univ Cambridge Cambridge England Mol Mechanisms Dis, Cambridge, England Univ Cambridge, Wellcome CRC Inst, Cambridge, England Univ Cambridge Cambridge England Wellcome CRC Inst, Cambridge, England Derby City Gen Hosp, Oncol Res Lab, Derby, England Derby City Gen Hosp Derby England n Hosp, Oncol Res Lab, Derby, England Univ Cambridge, Rosie Hosp, Dept Obstet & Gynaecol, Cambridge, England Univ Cambridge Cambridge England Obstet & Gynaecol, Cambridge, England Univ Coll London, London Sch Med, Dept Obstet & Gynaecol, London, England Univ Coll London London England Dept Obstet & Gynaecol, London, England
Titolo Testata:
NATURE GENETICS
fascicolo: 3, volume: 24, anno: 2000,
pagine: 300 - 303
SICI:
1061-4036(200003)24:3<300:MTTEAI>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
E1A-ASSOCIATED PROTEIN P300; COACTIVATORS P300; CBP; GENE; P53; BINDING; FAMILY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
18
Recensione:
Indirizzi per estratti:
Indirizzo: Caldas, C Univ Cambridge, Dept Oncol, Cambridge, England Univ Cambridge Cambridge England pt Oncol, Cambridge, England
Citazione:
S.A. Gayther et al., "Mutations truncating the EP300 acetylase in human cancers", NAT GENET, 24(3), 2000, pp. 300-303

Abstract

The EP300 protein is a histone acetyltransferase(1.2) that regulates transcription via chromatin remodelling(3) and is important in the processes of cell proliferation(4) and differentiation(5). EP300 acetylation of TP53 in response to DNA damage regulates its DNA-binding and transcription functions(6-9). A role for EP300 in cancer has been implied by the fact that it is targeted by viral oncoproteins, it is fused to MLL in leukaemia and two missense sequence alterations in EP300 were identified in epithelial malignancies(10-13). Nevertheless, direct demonstration of the role of EP300 in tumorigenesis by inactivating mutations in human cancers has been lacking. Herewe describe EP300 mutations, which predict a truncated protein, in 6 (3%) of 193 epithelial cancers analysed. Of these six mutations, two were in primary tumours (a colorectal cancer and a breast cancer) and four were in cancer cell lines (colorectal, breast and pancreatic). In addition, we identified a somatic in-frame insertion in a primary breast cancer and missense alterations in a primary colorectal cancer and two cell lines (breast and pancreatic). Inactivation of the second allele was demonstrated in five of sixcases with truncating mutations and in two other cases. Our data show thatEP300 is mutated in epithelial cancers and provide the first evidence thatit behaves as a classical tumour-suppressor gene.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/09/20 alle ore 17:21:53