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Titolo:
IMPORTANCE OF A C-MYB BINDING-SITE FOR LYMPHOMAGENESIS BY THE RETROVIRUS SL3-3
Autore:
NIEVES A; LEVY LS; LENZ J;
Indirizzi:
YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MOL GENET,1300 MORRIS PK AVE BRONX NY 10461 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MOL GENET BRONX NY 10461 TULANE UNIV,SCH MED NEW ORLEANS LA 70112
Titolo Testata:
Journal of virology
fascicolo: 2, volume: 71, anno: 1997,
pagine: 1213 - 1219
SICI:
0022-538X(1997)71:2<1213:IOACBF>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
MURINE LEUKEMIA-VIRUS; LONG TERMINAL REPEAT; I TRANSCRIPTIONAL ACTIVATORS; T-CELL LYMPHOMAS; DISEASE SPECIFICITY; NONDEFECTIVE FRIEND; ENHANCER REGION; 3' END; SEQUENCES; CORE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
A. Nieves et al., "IMPORTANCE OF A C-MYB BINDING-SITE FOR LYMPHOMAGENESIS BY THE RETROVIRUS SL3-3", Journal of virology, 71(2), 1997, pp. 1213-1219

Abstract

All murine leukemia viruses (MuLVs) and related type C retroviruses contain a highly conserved binding site for the Ets family of transcription factors within the enhancer sequences in the viral long terminal repeats (LTRs), The T-cell lymphomagenic MuLV SL3-3 (SL3-3) also contains a c-Myb binding site adjacent to the Ets site, The presence of this Myb site distinguishes SL3 from most other MuLVs, We tested the importance of these two sites for the lymphomagenicity of SL3-3. Mutation of the Ets site had little effect on viral pathogenicity,, as it only slightly extended the latency period to disease onset, In contrast, mutation of the Myb site strongly inhibited pathogenicity; as only a minority of the inoculated mice developed tumors in the two mouse strainsthat were tested. All tumors that mere induced by either mutant appeared to be lymphomas, and no evidence for reversion of either mutation was detected. The effects of the Ets and Myb site mutations on transcriptional activity of the SL3 LTR were tested by inserting the viral enhancer sequences into a plasmid containing the promoter region of the c-myc gene linked to a reporter gene. Mutation the Myb site almost eliminated enhancer activity in T lymphocytes, while mutation of the Ets site had smaller effects, Thus, the effects of the enhancer mutations on transcriptional activity in T cells paralleled their effects on viral lymphomagenicity. The absence of the c-Myb site in the LTR enhancerof the weakly lymphomagenic MuLV, Akv, likely contributes to the lon pathogenicity of this virus relative to SL3-3, However, Moloney MuLV also lacks the Myb site in its LTR, although it induces T-cell lymphomas with a potency similar to that of SL3-3. Thus, it appears that SL3-3and Moloney MuLV evolved genetic determinants of T-cell lymphomagenicity that are, at least in part, distinct.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/21 alle ore 16:17:44