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Titolo:
2ND-SITE PROVIRAL ENHANCER ALTERATIONS IN LYMPHOMAS INDUCED BY ENHANCER MUTANTS OF SL3-3 MURINE LEUKEMIA-VIRUS - NEGATIVE EFFECT OF NUCLEARFACTOR-1 BINDING-SITE
Autore:
ETHELBERG S; HALLBERG B; LOVMAND J; SCHMIDT J; LUZ A; GRUNDSTROM T; PEDERSEN FS;
Indirizzi:
AARHUS UNIV,DEPT MOL & STRUCT BIOL,CF MOLLERS ALLE,BLDG 130 DK-8000 AARHUS C DENMARK AARHUS UNIV,DEPT MOL & STRUCT BIOL DK-8000 AARHUS C DENMARK AARHUS UNIV,DEPT MED MICROBIOL & IMMUNOL DK-8000 AARHUS C DENMARK UMEA UNIV,DEPT APPL CELL & MOL BIOL S-90187 UMEA SWEDEN GSF,INST MOL VIROL D-85758 OBERSCHLEISSHEIM GERMANY GSF,INST PATHOL D-85758 OBERSCHLEISSHEIM GERMANY
Titolo Testata:
Journal of virology
fascicolo: 2, volume: 71, anno: 1997,
pagine: 1196 - 1206
SICI:
0022-538X(1997)71:2<1196:2PEAIL>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG TERMINAL REPEAT; ACUTE MYELOID-LEUKEMIA; I TRANSCRIPTIONAL ACTIVATORS; POLYMERASE CHAIN-REACTION; MOUSE RETROVIRUS SL3-3; REGULATORY ELEMENTS; VECTOR PROVIRUSES; MOLECULAR-CLONING; POINT MUTATIONS; RUNT DOMAIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
72
Recensione:
Indirizzi per estratti:
Citazione:
S. Ethelberg et al., "2ND-SITE PROVIRAL ENHANCER ALTERATIONS IN LYMPHOMAS INDUCED BY ENHANCER MUTANTS OF SL3-3 MURINE LEUKEMIA-VIRUS - NEGATIVE EFFECT OF NUCLEARFACTOR-1 BINDING-SITE", Journal of virology, 71(2), 1997, pp. 1196-1206

Abstract

SL3-3 is a highly T-lymphomagenic murine retrovirus. Previously, mutation of binding sites in the U3 repeat region for the AML1 transcription Factor family (also known as core binding factor [CBF], polyomavirus enhancer binding protein 2 [PEBP2], and SL3-3 enhancer factor 1 [SEF1]) were found to strongly reduce the pathogenicity of SW-3 (B. Hallberg, J. Schmidt, A. Luz, F. S. Pedersen, and T. Grundstrom, J. Virol. 65:4177-4181, 1991). We have now examined the fem cases in which tumorsdeveloped harboring proviruses that besides the AML1 (core) site mutations carried second-site alterations in their U3 repeat structures. In three distinct cases we observed the same type of alteration which involved deletions of regions known to contain binding sites for nuclear factor 1 (NF1) and the addition of extra enhancer repeat elements. In transient-expression experiments in T-lymphoid cells, these new U3 regions acted as stronger enhancers than the U3 regions of the originalviruses, This suggests that the altered proviruses represent more-pathogenic variants selected for in the process of tumor formation. To analyze the proviral alterations, we generated a series of different enhancer-promoter reporter constructs, These constructs showed that the additional repeat elements are not critical for enhancer strength, whereas the NF1 sites down-regulate the level of transcription in T-lymphoid cells whether or not the AML1 (core) sites are functional, We therefore also tested SW-3 viruses with mutated NF1 sites. These viruses have unimpaired pathogenic properties and thereby distinguish SW-3 from Moloney murine leukemia virus.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 03:45:29