Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Lack of responsiveness of a nuclear factor-kappa B-regulated promoter to transactivation by human immunodeficiency virus 1 Tat in HeLa cells
Autore:
Kelly, GD; Morris, CB; Offermann, MK;
Indirizzi:
Emory Univ, Winship Canc Ctr, Atlanta, GA 30322 USA Emory Univ Atlanta GAUSA 30322 , Winship Canc Ctr, Atlanta, GA 30322 USA Emory Univ, Program Genet & Mol Biol, Atlanta, GA 30322 USA Emory Univ Atlanta GA USA 30322 m Genet & Mol Biol, Atlanta, GA 30322 USA Emory Univ, Dept Med, Div Hematol Oncol, Atlanta, GA 30322 USA Emory UnivAtlanta GA USA 30322 Div Hematol Oncol, Atlanta, GA 30322 USA Tulane Univ, Med Ctr, Tulane Canc Ctr, Dept Pathol & Lab Med, New Orleans,LA 70112 USA Tulane Univ New Orleans LA USA 70112 & Lab Med, New Orleans,LA 70112 USA
Titolo Testata:
VIROLOGY
fascicolo: 1, volume: 263, anno: 1999,
pagine: 128 - 138
SICI:
0042-6822(19991010)263:1<128:LOROAN>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEINS SPECIFICALLY ASSOCIATE; KAPOSIS-SARCOMA CELLS; CREB-BINDING-PROTEIN; HIV-1 TAT; TYPE-1 TAT; TRANSCRIPTIONAL ACTIVATION; P-TEFB; FLK-1/KDR RECEPTOR; GENE-EXPRESSION; TERMINAL DOMAIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Offermann, MK Emory Univ, Winship Canc Ctr, 1365-B Clifton Rd NE, Atlanta,GA 30322 USA Emory Univ 1365-B Clifton Rd NE Atlanta GA USA 30322 322 USA
Citazione:
G.D. Kelly et al., "Lack of responsiveness of a nuclear factor-kappa B-regulated promoter to transactivation by human immunodeficiency virus 1 Tat in HeLa cells", VIROLOGY, 263(1), 1999, pp. 128-138

Abstract

Transcriptional activation by Tat protein is in large part, dependent on interactions with the TAR RNA element located in the 5'-untranslated region of all human immunodeficiency virus type 1 (HIV-1) transcripts. In addition, Wt has been shown to induce nuclear translocation of nuclear factor-kappaB (NF-kappa B), potentially contributing to gene induction. The NF-KB responsive reporter construct, (PRDII)(4)-CAT, was used to explore transcription resulting from NF-kappa B activated by Wt. Wt did not activate (PRDII)(4)-CAT, whereas (PRDII)(4)-CAT was highly responsive to either transfected Rel A or to turner necrosis factor-alpha (TNF-alpha). Despite its inability to directly induce, Tat enhanced the responsiveness of (PRDII)(4)-CAT toeither transfected Rel A or to TNF-alpha by similar to 2.5-fold. High levels ofCAT activity were seen with HIV-LTR-derived reporters that contained kappaB and TAR elements in response to transfected Tat in the absence of eithertransfected Rel A or exogenous TNF-alpha, and overexpression of I kappa B alpha with Tat inhibited CAT activity by 60% to 80%, suggesting that some activation of NF-kappa B by Wt was occurring. HIV-LTR reporter activities were enhanced three fold to sixfold compared with Tat alone when additional NF-kappa B was provided by transfection or by activation with TNF-alpha. These data indicate that Wt is unable to activate some NF-kappa B-responsive promoters but is able to synergize with NF-kappa B in the activation of bothHIV-derived and non-HIV-derived promoters, (C) 1999 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 06:29:37