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The Tax oncogene enhances ELL incorporation into p300 and P-TEFb containing protein complexes to activate transcription.

Abstract：

:The eleven-nineteen lysine-rich leukemia protein (ELL) is a key regulator of RNA polymerase II mediated transcription. ELL facilitates RNA polymerase II transcription pause site entry and release by dynamically interacting with p300 and the positive transcription elongation factor b (P-TEFb). In this study, we investigated the role of ELL during the HTLV-1 Tax oncogene induced transactivation. We show that ectopic expression of Tax enhances ELL incorporation into p300 and P-TEFb containing transcriptional complexes and the subsequent recruitment of these complexes to target genes in vivo. Depletion of ELL abrogates Tax induced transactivation of the immediate early genes Fos, Egr2 and NF-kB, suggesting that ELL is an essential cellular cofactor of the Tax oncogene. Thus, our study identifies a novel mechanism of ELL-dependent transactivation of immediate early genes by Tax and provides the rational for further defining the genome-wide targets of Tax and ELL.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Fufa TD,Byun JS,Wakano C,Fernandez AG,Pise-Masison CA,Gardner K

doi

10.1016/j.bbrc.2015.07.072

subject

Has Abstract

pub_date

2015-09-11 00:00:00

pages

5-11

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)30302-8

journal_volume

465

pub_type

杂志文章

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