Mechanisms of persistent NF-κB activation by HTLV-I tax

Edward Harhaj, Nicole S. Harhaj

Research output: Contribution to journalReview article

35 Citations (Scopus)

Abstract

Human T cell leukemia virus type I (HTLV-I) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL). The HTLV-I Tax protein is thought to play a significant role in the initiation and pathogenesis of HTLV-I-mediated disease. Tax is a potent oncogene that deregulates cellular gene expression by persistently activating signaling pathways such as NF-κB. Tax activation of NF-κB is critical for the immortalization and survival of HTLV-I-infected T cells. In this review, we describe recent insights into the mechanisms employed by Tax to activate the canonical and noncanonical NF-κB signaling pathways. The adaptor function of Tax appears to be a common and important mechanism for the pathological activation of both NF-κB pathways.

Original languageEnglish (US)
Pages (from-to)83-91
Number of pages9
JournalIUBMB Life
Volume57
Issue number2
DOIs
StatePublished - Feb 1 2005

Fingerprint

Human T-lymphotropic virus 1
T-cells
Taxation
Viruses
Chemical activation
Adult T Cell Leukemia Lymphoma
Oncogenes
T-Lymphocytes
Gene Expression
Gene expression
Neoplasms

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Genetics
  • Clinical Biochemistry
  • Cell Biology

Cite this

Harhaj, Edward ; Harhaj, Nicole S. / Mechanisms of persistent NF-κB activation by HTLV-I tax. In: IUBMB Life. 2005 ; Vol. 57, No. 2. pp. 83-91.
@article{51c88b36e0154733bd38e9c8c94d6316,
title = "Mechanisms of persistent NF-κB activation by HTLV-I tax",
abstract = "Human T cell leukemia virus type I (HTLV-I) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL). The HTLV-I Tax protein is thought to play a significant role in the initiation and pathogenesis of HTLV-I-mediated disease. Tax is a potent oncogene that deregulates cellular gene expression by persistently activating signaling pathways such as NF-κB. Tax activation of NF-κB is critical for the immortalization and survival of HTLV-I-infected T cells. In this review, we describe recent insights into the mechanisms employed by Tax to activate the canonical and noncanonical NF-κB signaling pathways. The adaptor function of Tax appears to be a common and important mechanism for the pathological activation of both NF-κB pathways.",
author = "Edward Harhaj and Harhaj, {Nicole S.}",
year = "2005",
month = "2",
day = "1",
doi = "10.1080/15216540500078715",
language = "English (US)",
volume = "57",
pages = "83--91",
journal = "IUBMB Life",
issn = "1521-6543",
publisher = "Wiley-Blackwell",
number = "2",

}

Mechanisms of persistent NF-κB activation by HTLV-I tax. / Harhaj, Edward; Harhaj, Nicole S.

In: IUBMB Life, Vol. 57, No. 2, 01.02.2005, p. 83-91.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Mechanisms of persistent NF-κB activation by HTLV-I tax

AU - Harhaj, Edward

AU - Harhaj, Nicole S.

PY - 2005/2/1

Y1 - 2005/2/1

N2 - Human T cell leukemia virus type I (HTLV-I) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL). The HTLV-I Tax protein is thought to play a significant role in the initiation and pathogenesis of HTLV-I-mediated disease. Tax is a potent oncogene that deregulates cellular gene expression by persistently activating signaling pathways such as NF-κB. Tax activation of NF-κB is critical for the immortalization and survival of HTLV-I-infected T cells. In this review, we describe recent insights into the mechanisms employed by Tax to activate the canonical and noncanonical NF-κB signaling pathways. The adaptor function of Tax appears to be a common and important mechanism for the pathological activation of both NF-κB pathways.

AB - Human T cell leukemia virus type I (HTLV-I) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL). The HTLV-I Tax protein is thought to play a significant role in the initiation and pathogenesis of HTLV-I-mediated disease. Tax is a potent oncogene that deregulates cellular gene expression by persistently activating signaling pathways such as NF-κB. Tax activation of NF-κB is critical for the immortalization and survival of HTLV-I-infected T cells. In this review, we describe recent insights into the mechanisms employed by Tax to activate the canonical and noncanonical NF-κB signaling pathways. The adaptor function of Tax appears to be a common and important mechanism for the pathological activation of both NF-κB pathways.

UR - http://www.scopus.com/inward/record.url?scp=18244375016&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=18244375016&partnerID=8YFLogxK

U2 - 10.1080/15216540500078715

DO - 10.1080/15216540500078715

M3 - Review article

C2 - 16036567

AN - SCOPUS:18244375016

VL - 57

SP - 83

EP - 91

JO - IUBMB Life

JF - IUBMB Life

SN - 1521-6543

IS - 2

ER -