Dominant negative Tax double mutants as molecular inhibitors for w.t. Tax gene functions

Mahmoud Egbaria; Yulia Tabakin-Fix; Mahmoud Huleihel

doi:10.1016/j.leukres.2008.10.023

Dominant negative Tax double mutants as molecular inhibitors for w.t. Tax gene functions

Mahmoud Egbaria, Yulia Tabakin-Fix, Mahmoud Huleihel

Virology

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

Tax plays a key role in HTLV-1 pathogenicity, partly due to its capacity of constitutive NF-κB activation. Δ58Tax does not translocate to the nucleus and traps w.t. Tax molecules in the cytoplasm but still retains the cytoplasmic NF-κB activation ability. Therefore, it enhances the w.t. Tax activation of NF-κB when co-expressed at lower level than w.t. Tax. However, the double mutants Δ58Tax (M22) and Δ58Tax (148) are defective also in the cytoplasmic NF-κB activation. They were found as capable of blocking the w.t. Tax-induced NF-κB-dependent activation even when expressed at low levels. These double mutants may, therefore, be used as powerful tools for blocking w.t. Tax functions.

Original language	English
Pages (from-to)	974-979
Number of pages	6
Journal	Leukemia Research
Volume	33
Issue number	7
DOIs	https://doi.org/10.1016/j.leukres.2008.10.023
State	Published - 1 Jul 2009

Keywords

CBP
Cytoplasm Tax mutants
Double Tax mutants
HTLV-1
NF-κB
Tax

ASJC Scopus subject areas

Hematology
Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.leukres.2008.10.023

Cite this

@article{53a71912331f442e9ead70690b1387f9,

title = "Dominant negative Tax double mutants as molecular inhibitors for w.t. Tax gene functions",

abstract = "Tax plays a key role in HTLV-1 pathogenicity, partly due to its capacity of constitutive NF-κB activation. Δ58Tax does not translocate to the nucleus and traps w.t. Tax molecules in the cytoplasm but still retains the cytoplasmic NF-κB activation ability. Therefore, it enhances the w.t. Tax activation of NF-κB when co-expressed at lower level than w.t. Tax. However, the double mutants Δ58Tax (M22) and Δ58Tax (148) are defective also in the cytoplasmic NF-κB activation. They were found as capable of blocking the w.t. Tax-induced NF-κB-dependent activation even when expressed at low levels. These double mutants may, therefore, be used as powerful tools for blocking w.t. Tax functions.",

keywords = "CBP, Cytoplasm Tax mutants, Double Tax mutants, HTLV-1, NF-κB, Tax",

author = "Mahmoud Egbaria and Yulia Tabakin-Fix and Mahmoud Huleihel",

note = "Funding Information: This study on HTLV-1 is supported by grants from the Israel Science Foundation (ISF).",

year = "2009",

month = jul,

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doi = "10.1016/j.leukres.2008.10.023",

language = "English",

volume = "33",

pages = "974--979",

journal = "Leukemia Research",

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publisher = "Elsevier Ltd.",

number = "7",

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TY - JOUR

T1 - Dominant negative Tax double mutants as molecular inhibitors for w.t. Tax gene functions

AU - Egbaria, Mahmoud

AU - Tabakin-Fix, Yulia

AU - Huleihel, Mahmoud

N1 - Funding Information: This study on HTLV-1 is supported by grants from the Israel Science Foundation (ISF).

PY - 2009/7/1

Y1 - 2009/7/1

N2 - Tax plays a key role in HTLV-1 pathogenicity, partly due to its capacity of constitutive NF-κB activation. Δ58Tax does not translocate to the nucleus and traps w.t. Tax molecules in the cytoplasm but still retains the cytoplasmic NF-κB activation ability. Therefore, it enhances the w.t. Tax activation of NF-κB when co-expressed at lower level than w.t. Tax. However, the double mutants Δ58Tax (M22) and Δ58Tax (148) are defective also in the cytoplasmic NF-κB activation. They were found as capable of blocking the w.t. Tax-induced NF-κB-dependent activation even when expressed at low levels. These double mutants may, therefore, be used as powerful tools for blocking w.t. Tax functions.

AB - Tax plays a key role in HTLV-1 pathogenicity, partly due to its capacity of constitutive NF-κB activation. Δ58Tax does not translocate to the nucleus and traps w.t. Tax molecules in the cytoplasm but still retains the cytoplasmic NF-κB activation ability. Therefore, it enhances the w.t. Tax activation of NF-κB when co-expressed at lower level than w.t. Tax. However, the double mutants Δ58Tax (M22) and Δ58Tax (148) are defective also in the cytoplasmic NF-κB activation. They were found as capable of blocking the w.t. Tax-induced NF-κB-dependent activation even when expressed at low levels. These double mutants may, therefore, be used as powerful tools for blocking w.t. Tax functions.

KW - CBP

KW - Cytoplasm Tax mutants

KW - Double Tax mutants

KW - HTLV-1

KW - NF-κB

KW - Tax

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U2 - 10.1016/j.leukres.2008.10.023

DO - 10.1016/j.leukres.2008.10.023

M3 - Article

AN - SCOPUS:67349176642

SN - 0145-2126

VL - 33

SP - 974

EP - 979

JO - Leukemia Research

JF - Leukemia Research

IS - 7

ER -

Dominant negative Tax double mutants as molecular inhibitors for w.t. Tax gene functions

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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