Severe liver degeneration and lack of NF-κ B activation in NEMO/IKKγ-deficient mice
Open accessAbstract
Phosphorylation of IκB, an inhibitor of NF-κB, is an important step in the activation of the transcription factor NF-κB. Phosphorylation is mediated by the IκB kinase (IKK) complex, known to contain two catalytic subunits: IKKα and IKKβ. A novel, noncatalytic component of this kinase complex called NEMO(NF-κBe ssential mo dulator)/IKKγ was identified recently. We have generated NEMO/IKKγ-deficient mice by gene targeting. Mutant embryos die at E12.5–E13.0 from severe liver damage due to apoptosis.NEMO/IKKγ-deficient primary murine embryonic fibroblasts (MEFs) lack detectable NF-κB DNA-binding activity in response to TNFα, IL-1, LPS, and Poly(IC) and do not show stimulus-dependent IκB kinase activity, which correlates with a lack of phosphorylation and degradation of IκBα. Consistent with these data, mutant MEFs show increased sensitivity to TNFα-induced apoptosis. Our data provide in vivo evidence that NEMO/IKKγ is the first essential, noncatalytic component of the IKK complex.
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Cellular senescence is involved in the progression of liver disease.
“Cellular senescence is implicated in the progression of liver disease.”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [63]
The “Liver degeneration in NEMO/IKKγ-deficient embryos” section attributes liver damage in mutant embryos to apoptosis, but does not address cellular senescence or the progression of liver disease. Searches for “cellular senescence liver disease progression” and “senescence senescent cells” found no passage addressing that link. (LLM, conf=0.76)
Experimental — accuracy not yet measuredTelomere dysfunction, a major driver of hepatocyte senescence, impairs liver regeneration and causes liver cirrhosis in mice.
“Telomere dysfunction, a major driver of hepatocyte senescence, impairs liver regeneration and induces liver cirrhosis in mice (63).”
From Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span (2021) · cites this paper as [63]
The Abstract and “Liver degeneration in NEMO/IKKγ-deficient embryos” section describe embryonic liver apoptosis following NEMO/IKKγ deficiency. Searches for telomere dysfunction, hepatocyte senescence, liver regeneration, and cirrhosis found no passage in our copy addressing the attributed claim. (LLM, conf=0.76)
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References 27 · Cited by 479
- Authors
- Rudolph, D., Yeh, W.-C., Wakeham, A., Rudolph, B., Nallainathan, D., Potter, J., Elia, A. J., & Mak, T. W.
- Affiliations
- University of Toronto (CA)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2000-04-01
- Volume
- 14
- Issue
- 7
- Pages
- 854-862
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W4297063097
- Cited by
- 479
- References
- 27
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 6 · 2023: 3 · 2022: 8 · 2021: 11 · 2020: 9 · 2019: 12 · 2018: 5 · 2017: 9 · 2016: 14 · 2015: 10 · 2014: 19 · 2013: 17 · 2012: 15
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- NEMO/IKKγ, NF-κB activation, IκB kinase complex, IκBα phosphorylation, liver degeneration, embryonic lethality, apoptosis, TNFα-induced apoptosis, embryonic fibroblasts, gene targeting
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