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Titolo:
OCT-1 ACTIVATES THE EPITHELIAL-SPECIFIC ENHANCER OF HUMAN PAPILLOMAVIRUS TYPE-16 VIA A SYNERGISTIC INTERACTION WITH NFI AT A CONSERVED COMPOSITE REGULATORY ELEMENT
Autore:
OCONNOR M; BERNARD HU;
Indirizzi:
NATL UNIV SINGAPORE,INST MOLEC & CELL BIOL,PAPILLOMAVIRUS BIOL LAB,KENT RIDGE SINGAPORE 0511 SINGAPORE NATL UNIV SINGAPORE,INST MOLEC & CELL BIOL,PAPILLOMAVIRUS BIOL LAB SINGAPORE 0511 SINGAPORE
Titolo Testata:
Virology
fascicolo: 1, volume: 207, anno: 1995,
pagine: 77 - 88
SICI:
0042-6822(1995)207:1<77:OATEEO>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEAR FACTOR-I; EUKARYOTIC TRANSCRIPTIONAL ACTIVATORS; CELL-SPECIFIC TRANSCRIPTION; CERVICAL-CARCINOMA CELLS; RNA POLYMERASE-II; HOMEO DOMAIN; BINDING-SITES; POU-DOMAIN; GLUCOCORTICOID RECEPTOR; TRANSACTIVATOR VP16;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
M. Oconnor e H.U. Bernard, "OCT-1 ACTIVATES THE EPITHELIAL-SPECIFIC ENHANCER OF HUMAN PAPILLOMAVIRUS TYPE-16 VIA A SYNERGISTIC INTERACTION WITH NFI AT A CONSERVED COMPOSITE REGULATORY ELEMENT", Virology, 207(1), 1995, pp. 77-88

Abstract

A highly conserved composite regulatory element in the epithelial-specific enhancer of human papillomaviruses (HPVs) consists of an octamermotif separated by exactly 2 bp from a nonpalindromic NFI site. Pointmutations within this composite element, created to prevent the binding of Oct-1 or NFI, result in up to a 10- to 12-fold decrease in enhancer activity. A mutation preventing the binding of both proteins does not, however, result in any further decrease in activity suggesting a cooperative interaction between these two factors. Electrophoretic mobility shift assays provide evidence that the simultaneous binding of both factors to the composite element is indeed required for efficient activation. Furthermore, evidence demonstrating the inability of Oct-1by itself to elicit a transcriptional response from this enhancer position suggests that Oct-1 does not activate transcription directly, but rather may play a crucial role in the viral enhancer by tethering NF1 to the composite element. This finding represents both a potentiallyimportant mechanism by which HPV gene expression can be regulated endan interesting model for the study of transcriptional cooperativity. (C) 1995 academic Press, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 20:21:08