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Titolo:
Type B leukemogenic virus has a T-cell-specific enhancer that binds AML-1
Autore:
Mertz, JA; Mustafa, F; Meyers, S; Dudley, JP;
Indirizzi:
Univ Texas, Sect Mol Genet & Microbiol, Austin, TX 78705 USA Univ Texas Austin TX USA 78705 ol Genet & Microbiol, Austin, TX 78705 USA Univ Texas, Inst Cellular & Mol Biol, Austin, TX 78705 USA Univ Texas Austin TX USA 78705 Cellular & Mol Biol, Austin, TX 78705 USA Louisiana State Univ, Med Ctr, Dept Biochem & Mol Biol, Feist Weiller CancCtr, Shreveport, LA 71130 USA Louisiana State Univ Shreveport LA USA 71130tr, Shreveport, LA 71130 USA
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 5, volume: 75, anno: 2001,
pagine: 2174 - 2184
SICI:
0022-538X(200103)75:5<2174:TBLVHA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG TERMINAL REPEAT; MAMMARY-TUMOR VIRUS; MURINE LEUKEMIA-VIRUS; ACUTE MYELOID-LEUKEMIA; RETROVIRUS SL3-3; TRANSCRIPTIONAL ACTIVATORS; DISEASE SPECIFICITY; NONDEFECTIVE FRIEND; NEGATIVE REGULATION; THYMIC LYMPHOMAS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
70
Recensione:
Indirizzi per estratti:
Indirizzo: Dudley, JP Univ Texas, Sect Mol Genet & Microbiol, 100 W 24th St,ESB 226, Austin, TX 78705 USA Univ Texas 100 W 24th St,ESB 226 Austin TX USA 78705 78705 USA
Citazione:
J.A. Mertz et al., "Type B leukemogenic virus has a T-cell-specific enhancer that binds AML-1", J VIROLOGY, 75(5), 2001, pp. 2174-2184

Abstract

Type B leukemogenic virus (TBLV) induces rapidly appearing T-cell tumors in mice. TBLV is highly related to mouse mammary tumor virus (MMTV) except that TBLV long terminal repeats (LTRs) have a deletion of negative regulatory elements and a triplication of sequences flanking the deletion. To determine if the LTR triplication represents a viral enhancer element, we inserted the triplication upstream and downstream in either orientation relative to the thymidine kinase promoter linked to the luciferase gene. These experiments showed that upregulation of reporter gene activity by the TBLV triplication was relatively orientation independent, consistent with the activityof eukaryotic enhancer elements. TBLV enhancer activity was observed in T-cell lines but not in fibroblasts, B cells, or mammary cells, suggesting that enhancer function is cell type dependent. To analyze the transcription factor binding sites that are important for TBLV enhancer function, we prepared substitution mutations in a reconstituted C3H MMTV LTR that recapitulates the deletion observed in the TBLV LTR, Transient transfections showed that a single mutation (556M) decreased TBLV enhancer activity at least 20-fold in two different T-cell lines. This mutation greatly diminished AML-1 (recently renamed RUNX1) binding in gel shift assays with a mutant oligonucleotide, whereas AML-1 binding to a wild-type TBLV oligomer was specific, as judged by competition and supershift experiments. The 556 mutation also reduced TBLV enhancer binding of two other protein complexes, called NF-A and NF-B, that did not appear to be related to c-Myb or Ets. AML-1 overexpression in a mammary cell line enhanced expression from the TBLV LTR approximately 30-fold. These data suggest that binding of AML-1 to the TBLV enhancer, likely in combination with other factors, is necessary for optimal enhancerfunction.

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Documento generato il 20/01/21 alle ore 02:37:14