| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print August 13, 2004
Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, Piscataway, NJ 08854-8082
Corresponding Author: xiao{at}biology.rutgers.edu
Processing of the nf-kappab2 gene product p100 to generate p52 is a tightly regulated event, consistent with the fact that the processing product, p52 is hardly detected in most cell types including T cells, although the precursor p100 is expressed abundantly in these cells. However, in T cells transformed by the human T-cell leukemia virus type I (HTLV-I), p100 processing is very active, resulting in high level expression of p52. Since overproduction of p52 is associated with lymphoid hyperplasia and transformation, deregulation of p100 processing may be part of the oncogenic mechanism of HTLV-I. We previously demonstrated that HTLV-I Tax oncoprotein is a potent inducer of p100 processing, through specifically targeting IKKalpha via IKKgamma to p100 to trigger p100 phosphorylation and ubiquitination. Here, we further show that Tax-mediated recruitment of IKKalpha to p100 requires serines 866 and 870 of p100, shown to be essential for inducible processing of p100. Upon interaction with p100, activated IKKalpha phosphorylates both N- and C-terminal serines of p100 (serines 99, 108, 115, 123 and 872), serving as a critical step in Tax-induced p100 processing. Using a genetic approach, we find that beta-transducin repeat-containing protein (beta-TrCP), a component of the SCF ubiquitin ligase complex, previously shown to be required for physiological p100 processing mediated by NF-B-inducing kinase (NIK), is only partially involved in Tax-induced processing of p100. These results indicate that both beta-TrCP-dependent and independent mechanisms contribute to Tax-deregulated p100 processing, further suggesting the involvement of different mechanisms in cellular and viral pathways of p100 processing.
J. Biol. Chem, 10.1074/jbc.M403689200
Submitted on April 2, 2004
Revised on July 1, 2004
Accepted on August 13, 2004
Tax deregulation of NF-kappaB2 p100 processing involves both beta-TrCP-dependent and independent mechanisms
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  G. Qing, Z. Qu, and G. Xiao Endoproteolytic processing of C-terminally truncated NF-{kappa}B2 precursors at {kappa}B-containing promoters PNAS, March 27, 2007; 104(13): 5324 - 5329. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Barry and K. Fruh Viral Modulators of Cullin RING Ubiquitin Ligases: Culling the Host Defense Sci. Signal., May 16, 2006; 2006(335): pe21 - pe21. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Qing, Z. Qu, and G. Xiao Stabilization of Basally Translated NF-{kappa}B-inducing Kinase (NIK) Protein Functions as a Molecular Switch of Processing of NF-{kappa}B2 p100 J. Biol. Chem., December 9, 2005; 280(49): 40578 - 40582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Qing and G. Xiao Essential Role of I{kappa}B Kinase {alpha} in the Constitutive Processing of NF-{kappa}B2 p100 J. Biol. Chem., March 18, 2005; 280(11): 9765 - 9768. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Qing, Z. Qu, and G. Xiao Regulation of NF-{kappa}B2 p100 Processing by Its cis-Acting Domain J. Biol. Chem., January 7, 2005; 280(1): 18 - 27. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
