Format

Send to

Choose Destination
See comment in PubMed Commons below
J Biol Chem. 1999 Aug 13;274(33):22911-4.

IKKgamma serves as a docking subunit of the IkappaB kinase (IKK) and mediates interaction of IKK with the human T-cell leukemia virus Tax protein.

Author information

1
Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.

Abstract

The tax gene product of human T-cell leukemia virus type I induces activation of transcription factor NF-kappaB, which contributes to deregulated expression of various cellular genes. Tax expression triggers persistent phosphorylation and degradation of the NF-kappaB inhibitory proteins IkappaBalpha and IkappaBbeta, resulting in constitutive nuclear expression of NF-kappaB. Recent studies demonstrate that Tax activates the IkappaB kinase (IKK), although the underlying mechanism remains unclear. In this report, we show that Tax physically interacts with a regulatory component of the IKK complex, the NF-kappaB essential modulator or IKKgamma (NEMO/IKKgamma). This molecular interaction appears to be important for recruiting Tax to the IKK catalytic subunits, IKKalpha and IKKbeta. Expression of NEMO/IKKgamma greatly promotes binding of Tax to IKKalpha and IKKbeta and stimulates Tax-mediated IKK activation. Interestingly, a mutant form of Tax defective in IKK activation exhibited a markedly diminished level of NEMO/IKKgamma association. These findings suggest that the physical interaction of Tax with NEMO/IKKgamma may play an important role in Tax-mediated IKK activation.

PMID:
10438454
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center