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Cited by 963

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Severe Liver Degeneration in Mice Lacking the IκB Kinase 2 Gene

Li, Qiutang, Antwerp, Daniel Van, Mercurio, Frank, Lee, Kuo-Fen, Verma, Inder M.·1999·Science

Abstract

Phosphorylation of inhibitor of kappa B (IκB) proteins is an important step in the activation of the transcription nuclear factor kappa B (NF-κB) and requires two IκB kinases, IKK1 (IKKα) and IKK2 (IKKβ). Mice that are devoid of the IKK2 gene had extensive liver damage from apoptosis and died as embryos, but these mice could be rescued by the inactivation of the gene encoding tumor necrosis factor receptor 1. Mouse embryonic fibroblast cells that were isolated from IKK2 –/– embryos showed a marked reduction in tumor necrosis factor–α (TNF-α)– and interleukin-1α–induced NF-κB activity and an enhanced apoptosis in response to TNF-α. IKK1 associated with NF-κB essential modulator (IKKγ/IKKAP1), another component of the IKK complex. These results show that IKK2 is essential for mouse development and cannot be substituted with IKK1.

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Metadata

Authors
Li, Q., Antwerp, D. V., Mercurio, F., Lee, K.-F., & Verma, I. M.
Venue
Science
Published
1999-04-09
Volume
284
Issue
5412
Pages
321-325
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2053372168
Cited by
963
References
3
FWCI
33.55
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Severe Liver Degeneration in Mice Lacking the IκB Kinase 2 Gene. https://app.cochat.ai/papers/10.1126/science.284.5412.321
The paper
Li, Q., Antwerp, D. V., Mercurio, F., Lee, K.-F., & Verma, I. M. (1999). Severe Liver Degeneration in Mice Lacking the IκB Kinase 2 Gene. Science. https://doi.org/10.1126/science.284.5412.321

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.