The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Epstein–Barr virus-transforming protein latent infection membrane protein 1 activates transcription factor NF-κB through a pathway that includes the NF-κB-inducing kinase and the IκB kinases IKKα and IKKβ
Abstract
The Epstein–Barr virus oncoprotein latent infection membrane protein 1 (LMP1) is a constitutively aggregated pseudo-tumor necrosis factor receptor (TNFR) that activates transcription factor NF-κB through two sites in its C-terminal cytoplasmic domain. One site is similar to activated TNFRII in associating with TNFR-associated factors TRAF1 and TRAF2, and the second site is similar to TNFRI in associating with the TNFRI death domain interacting protein TRADD. TNFRI has been recently shown to activate NF-κB through association with TRADD, RIP, and TRAF2; activation of the NF-κB-inducing kinase (NIK); activation of the IκBα kinases (IKKα and IKKβ); and phosphorylation of IκBα. IκBα phosphorylation on Ser-32 and Ser-36 is followed by its degradation and NF-κB activation. In this report, we show that NF-κB activation by LMP1 or by each of its effector sites is mediated by a pathway that includes NIK, IKKα, and IKKβ. Dominant negative mutants of NIK, IKKα, or IKKβ substantially inhibited NF-κB activation by LMP1 or by each of its effector sites.
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“Overexpression of a pcDNA3-IKK 𝛃 vector in transfected cells has been shown to induce robust activation of NF𝛋 B (56).”
From The Hematopoiesis-Specific GTP-Binding Protein RhoH Is GTPase Deficient and Modulates Activities of Other Rho GTPases by an Inhibitory Function (2002) · cites this paper as [56]
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Cites
A cytokine-responsive IκB kinase that activates the transcription factor NF-κB
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The TNF receptor 1-associated protein TRADD signals cell death and NF-κB activation
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IKK-1 and IKK-2: Cytokine-Activated IκB Kinases Essential for NF-κB Activation
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Zandi, E., Rothwarf, D. M., Delhase, M., Hayakawa, M., & Karin, M. (1997) · Cell · doi:10.1016/s0092-8674(00)80406-7 · Cited by 1,816
MAP3K-related kinase involved in NF-KB induction by TNF, CD95 and IL-1
Malinin, N. L., Boldin, M. P., Kovalenko, A. V., & Wallach, D. (1997) · Nature · doi:10.1038/385540a0 · Cited by 1,280
Self-citationAn EBV membrane protein expressed in immortalized lymphocytes transforms established rodent cells
Wang, D., Liebowitz, D., & Kieff, E. (1985) · Cell · doi:10.1016/0092-8674(85)90256-9 · Cited by 1,225
Self-citationTNF-Dependent Recruitment of the Protein Kinase RIP to the TNF Receptor-1 Signaling Complex
Hsu, H., Huang, J., Shu, H.-B., Baichwal, V., & Goeddel, D. V. (1996) · Immunity · doi:10.1016/s1074-7613(00)80252-6 · Cited by 1,182
IκB Kinase-β: NF-κB Activation and Complex Formation with IκB Kinase-α and NIK
Woronicz, J. D., Gao, X., Cao, Z., Rothe, M., & Goeddel, D. V. (1997) · Science · doi:10.1126/science.278.5339.866 · Cited by 1,181
Identification and Characterization of an IκB Kinase
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Targeted disruption of the p50 subunit of NF-κB leads to multifocal defects in immune responses
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Research works printed but not linked: 3
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Cited by
IKKβ/NF-κB Activation Causes Severe Muscle Wasting in Mice
Cai, D., Frantz, J. D., Tawa, N. E., Melendez, P. A., Oh, B.-C., Lidov, H. G. W., Hasselgren, P.-O., Frontera, W. R., Lee, J., Glass, D. J., et al. (2004) · Cell · doi:10.1016/j.cell.2004.09.027 · Cited by 1,367
Li, X., Bu, X., Lu, B., Avraham, H., Flavell, R. A., & Lim, B. (2002) · Molecular and Cellular Biology · doi:10.1128/mcb.22.4.1158-1171.2002 · Cited by 153
Metadata
- Authors
- Sylla, B. S., Hung, S. C., Davidson, D. M., Hatzivassiliou, E., Malinin, N. L., Wallach, D., Gilmore, T. D., Kieff, E., & Mosialos, G.
- Affiliations
- Departments of Microbiology and Molecular Genetics and Medicine, Harvard Medical School and Brigham and Women’s Hospital, 181 Longwood Avenue, Boston, MA, 02115; Department of Membrane Research and Biophysics, The Weizmann Institute of Science, 76100 Rehovot, Israel; and Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1998-08-18
- Volume
- 95
- Issue
- 17
- Pages
- 10106-10111
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 137
- References
- 41
- Language
- en
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