Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
STABILITY OF AML1 (CORE) SITE ENHANCER MUTATIONS IN T-LYMPHOMAS INDUCED BY ATTENUATED SL3-3 MURINE LEUKEMIA-VIRUS MUTANTS
Autore:
AMTOFT HW; SORENSEN AB; BAREIL C; SCHMIDT J; LUZ A; PEDERSEN FS;
Indirizzi:
AARHUS UNIV,DEPT BIOL MOL & STRUCT,CF MOLLERS ALLE,BLDG 130 DK-8000 AARHUS C DENMARK AARHUS UNIV,DEPT BIOL MOL & STRUCT DK-8000 AARHUS C DENMARK AARHUS UNIV,DEPT MED MICROBIOL & IMMUNOL DK-8000 AARHUS C DENMARK GSF MUNICH,NATL RES CTR ENVIRONM & HLTH,INST MOL VIROL D-85758 NEUHERBERG GERMANY GSF MUNICH,NATL RES CTR ENVIRONM & HLTH,INST PATHOL D-85758 NEUHERBERG GERMANY
Titolo Testata:
Journal of virology
fascicolo: 7, volume: 71, anno: 1997,
pagine: 5080 - 5087
SICI:
0022-538X(1997)71:7<5080:SOA(SE>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG TERMINAL REPEAT; I TRANSCRIPTIONAL ACTIVATORS; MOUSE RETROVIRUS SL3-3; RECEPTOR-DELTA; CELL LYMPHOMAS; C-MYC; SEQUENCES; BINDING; GENE; PROVIRUSES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
H.W. Amtoft et al., "STABILITY OF AML1 (CORE) SITE ENHANCER MUTATIONS IN T-LYMPHOMAS INDUCED BY ATTENUATED SL3-3 MURINE LEUKEMIA-VIRUS MUTANTS", Journal of virology, 71(7), 1997, pp. 5080-5087

Abstract

Murine retrovirus SL3-3 is highly T lymphomagenic. Its pathogenic properties are determined by the transcriptional enhancer of the U3 repeat region which shows preferential activity in T cells, Within the U3 repeats, the major determinant of T-cell specificity has been mapped tobinding sites for the AML1 transcription factor family (also known asthe core binding factor [CBF], polyomavirus enhancer binding protein 2 [PEBP2], and SL3-3 enhancer factor 1 [SEF-1]). SL3-3 viruses with AML1 site mutations have lost a major determinant of T-cell-specific enhancer function but have been found to retain a lymphomagenic potential, although disease induction is slower than for the SL3-3 wild type. To compare the specificities and mechanisms of disease induction of wild-type and mutant viruses, we have examined lymphomas induced by mutant viruses harboring transversions of three consecutive base pairs critical to AML1 site function (B. Hallberg, J. Schmidt, A. Luz, F. S. Pedersen, and T. Grundstrom. J. Virol. 65:4177-4181, 1991). Our results show that the mutated AML1 sites are genetically stable during lymphomagenesis and that ecotropic provirus numbers in DNA. of tumors induced by wild-type and mutant viruses fall within the same range, Moreover, proviruses were found to be integrated at the e-myc locus in similar proportions of wild-type and mutant SL3-3-indured tumors, and the mutated AML1 sites of proviruses at c-myc are unaltered, In some cases, however, including one c-myc-integrated provirus, a single-base pair change mas detected in a second, weaker AML1 binding site, By DNA rearrangement analysis of the T-cell receptor p-locus, tumors induced by the AML1 site mutants are found to be of the T-cell type, Thus, although the AML1 site mutants have weakened T-cell-specific enhancers they are T-lymphomagenic, and wild-type- and mutant-virus-induccd tumor DNAs aresimilar with respect to the number of overall ecotropic and c-myc-integrated clonal proviruses. The SL3-3 wild-type and AML1 site mutant viruses may therefore induce disease by similar mechanisms.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/01/21 alle ore 22:31:33