HTLV-I Tax protein binds to MEKK1 to stimulate IkappaB kinase activity and NF-kappaB activation.

Abstract:

:NF-kappaB, a key regulator of the cellular inflammatory and immune response, is activated by the HTLV-I transforming and transactivating protein Tax. We show that Tax binds to the amino terminus of the protein kinase MEKK1, a component of an IkappaB kinase complex, and stimulates MEKK1 kinase activity. Tax expression increases the activity of IkappaB kinase beta (IKKbeta) to enhance phosphorylation of serine residues in IkappaB alpha that lead to its degradation. Dominant negative mutants of both IKKbeta and MEKK1 prevent Tax activation of the NF-kappaB pathway. Furthermore, recombinant MEKK1 stimulates IKKbeta phosphorylation of IkappaB alpha. Thus, Tax-mediated increases in NF-kappaB nuclear translocation result from direct interactions of Tax and MEKK1 leading to enhanced IKKbeta phosphorylation of IkappaB alpha.

journal_name

Cell

journal_title

Cell

authors

Yin MJ,Christerson LB,Yamamoto Y,Kwak YT,Xu S,Mercurio F,Barbosa M,Cobb MH,Gaynor RB

doi

10.1016/s0092-8674(00)81447-6

subject

Has Abstract

pub_date

1998-05-29 00:00:00

pages

875-84

issue

5

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(00)81447-6

journal_volume

93

pub_type

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