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
Celljournal_title
Cellauthors
Yin MJ,Christerson LB,Yamamoto Y,Kwak YT,Xu S,Mercurio F,Barbosa M,Cobb MH,Gaynor RBdoi
10.1016/s0092-8674(00)81447-6subject
Has Abstractpub_date
1998-05-29 00:00:00pages
875-84issue
5eissn
0092-8674issn
1097-4172pii
S0092-8674(00)81447-6journal_volume
93pub_type
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