Human T-cell leukemia virus oncoprotein tax represses nuclear receptor-dependent transcription by targeting coactivator TAX1BP1.

Abstract	Human T-cell leukemia virus type 1 oncoprotein Tax is a transcriptional regulator that interacts with a large number of host cell factors. Here, we report the novel characterization of the interaction of Tax with a human cell protein named Tax1-binding protein 1 (TAX1BP1). We show that TAX1BP1 is a nuclear receptor coactivator that forms a complex with the glucocorticoid receptor. TAX1BP1 and Tax colocalize into intranuclear speckles that partially overlap with but are not identical to the PML oncogenic domains. Tax binds TAX1BP1 directly, induces the dissociation of TAX1BP1 from the glucocorticoid receptor-containing protein complex, and represses the coactivator function of TAX1BP1. Genetic knockout of Tax1bp1 in mice abrogates the influence of Tax on the activation of nuclear receptors. We propose that Tax-TAX1BP1 interaction mechanistically explains the previously reported repression of nuclear receptor activity by Tax.
Authors	King-Tung Chin, Abel C S Chun, Yick-Pang Ching, Kuan-Teh Jeang, Dong-Yan Jin
Journal	Cancer research (Cancer Res) Vol. 67 Issue 3 Pg. 1072-81 (Feb 01 2007) ISSN: 0008-5472 [Print] United States
PMID	17283140 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Gene Products, tax Intracellular Signaling Peptides and Proteins Neoplasm Proteins Nuclear Proteins Promyelocytic Leukemia Protein Receptors, Cytoplasmic and Nuclear Receptors, Glucocorticoid TAX1BP1 protein, human Transcription Factors Tumor Suppressor Proteins PML protein, human
Topics	Animals Cell Nucleus (metabolism) Gene Products, tax (metabolism) HeLa Cells Humans Intracellular Signaling Peptides and Proteins (antagonists & inhibitors, metabolism) Mice Mice, Knockout Neoplasm Proteins (antagonists & inhibitors, metabolism) Nuclear Proteins (metabolism) Promyelocytic Leukemia Protein Protein Binding Receptors, Cytoplasmic and Nuclear (antagonists & inhibitors, metabolism) Receptors, Glucocorticoid (antagonists & inhibitors, metabolism) Signal Transduction Transcription Factors (metabolism) Transcription, Genetic (physiology) Tumor Suppressor Proteins (metabolism)

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