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Titolo:
RESIDUE-231 TO RESIDUE-280 OF THE EPSTEIN-BARR-VIRUS NUCLEAR-PROTEIN-2 ARE NOT ESSENTIAL FOR PRIMARY B-LYMPHOCYTE GROWTH TRANSFORMATION
Autore:
HARADA S; YALAMANCHILI R; KIEFF E;
Indirizzi:
HARVARD UNIV,SCH MED,DEPT MED,181 LONGWOOD AVE BOSTON MA 02115 HARVARD UNIV,SCH MED,DEPT MED BOSTON MA 02115 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOL GENET BOSTON MA 02115 BRIGHAM & WOMENS HOSP BOSTON MA 02115
Titolo Testata:
Journal of virology (Print)
fascicolo: 12, volume: 72, anno: 1998,
pagine: 9948 - 9954
SICI:
0022-538X(1998)72:12<9948:RTROTE>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
SIGNAL-BINDING-PROTEIN; RBP-J-KAPPA; LATENT MEMBRANE-PROTEIN; SPLIT COMPLEX GENES; TRANSCRIPTIONAL ACTIVATION; CIS-ELEMENT; DOMAIN; TRANSACTIVATION; EBNA-2; NOTCH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
S. Harada et al., "RESIDUE-231 TO RESIDUE-280 OF THE EPSTEIN-BARR-VIRUS NUCLEAR-PROTEIN-2 ARE NOT ESSENTIAL FOR PRIMARY B-LYMPHOCYTE GROWTH TRANSFORMATION", Journal of virology (Print), 72(12), 1998, pp. 9948-9954

Abstract

Epstein-Barr virus (EBV) nuclear protein 2 (EBNA-2) is a transcriptional transactivator of cellular and viral gene expression and is essential for the transformation of resting human B lymphocytes into long-term lymphoblastoid cell lines (LCLs). Previous molecular genetic analyses identified three domains that are critical for transformation and showed that the rest of EBNA-2 is not critical. We now find that codons231 to 280 that were part of one of the critical domains (J. I. Cohen, F. Wang, and E. Kieff, J. Virol. 65:2545-2554, 1991) can be deleted with only a small effect on the ability of EBNA-2 to transactivate gene expression. In transient transfection assays, EBNA-2 deleted for codons 231 to 280 accumulated to higher levels and was similar to wild-type EBNA-2 in activation of the BamC promoter and in association with RBPJk, a cellular transcription factor that is important for EBNA-2 interaction with promoter regulatory elements. However, EBNA-2 d231-280 activated the viral latent membrane protein 1 (LMP1) promoter with only60% of wild-type efficiency. Recombinant EBVs specifically deleted for EBNA-2 codons 231 to 280 were efficient in initiating the transformation of resting primary human B lymphocytes into LCLs. However, these LCLs grew less well than wild-type EBV-transformed LCLs, and 4- to 10-fold more cells were required for outgrowth following limit dilution. EBNA-2 d231-280 accumulated to unusually high levels in the recombinant transformed LCLs, and this was associated with somewhat higher EBNA-1 and lower LMP1 expression, consistent with the near-wild-type activation of the BamC EBNA promoter and the abnormally low activation of the LMP1 promoter in transient transfection assays. Thus, EBNA-2 d231-280 modestly perturbed the regulation of viral gene expression and resulted in less LMP1, while having surprisingly subtle effects on LCL outgrowth. Deletion of EBNA-2 codons 292 to 310, which are closer to the site that specifies interaction with RBPJk, was more disruptive of RBPJk association and of the ability to transform B lymphocytes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 01:08:59