ArticleMolecular and cellular biology2002
The zinc finger domain of NEMO is selectively required for NF-kappa B activation by UV radiation and topoisomerase inhibitors.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 107 citations in OpenAlex.
- NEMO is essential for directing the kinases IKKα and ATM to the sites of DNA damage.Science signaling · 2025Article
- Upregulation of PD-L1 via HMGB1-Activated IRF3 and NF-κB Contributes to UV Radiation-Induced Immune Suppression.Cancer research · 2019Article
- All-atom molecular dynamics comparison of disease-associated zinc fingers.Journal of biomolecular structure & dynamics · 2018Article
- DNA damage-induced nuclear factor-kappa B activation and its roles in cancer progression.Journal of cancer metastasis and treatment · 2017Article
- IPO3-mediated Nonclassical Nuclear Import of NF-κB Essential Modulator (NEMO) Drives DNA Damage-dependent NF-κB Activation.The Journal of biological chemistry · 2015Article
- IKKβ in postnatal perichondrium remotely controls endochondral ossification of the growth plate through downregulation of MCP-5.Cell death and differentiation · 2015Article
- Withaferin A disrupts ubiquitin-based NEMO reorganization induced by canonical NF-κB signaling.Experimental cell research · 2015Article
- Quantification of cellular NEMO content and its impact on NF-κB activation by genotoxic stress.PloS one · 2015Article
- Covalent modification of the NF-κB essential modulator (NEMO) by a chemical compound can regulate its ubiquitin binding properties in vitro.The Journal of biological chemistry · 2014Article
- The role of constitutive nitric-oxide synthase in ultraviolet B light-induced nuclear factor κB activity.The Journal of biological chemistry · 2014Article
- Two-sided ubiquitin binding of NF-κB essential modulator (NEMO) zinc finger unveiled by a mutation associated with anhidrotic ectodermal dysplasia with immunodeficiency syndrome.The Journal of biological chemistry · 2013Article
- Identifying post-translational modifications of NEMO by tandem mass spectrometry after high affinity purification.Protein expression and purification · 2013Article
- Quantitative profiling of DNA damage and apoptotic pathways in UV damaged cells using PTMScan Direct.International journal of molecular sciences · 2012Article
- NF-κB-dependent microRNA-125b up-regulation promotes cell survival by targeting p38α upon ultraviolet radiation.The Journal of biological chemistry · 2012Article
- NEMO ensures signaling specificity of the pleiotropic IKKβ by directing its kinase activity toward IκBα.Molecular cell · 2012Article
- DNA damage-dependent NF-κB activation: NEMO turns nuclear signaling inside out.Immunological reviews · 2012Review
- Evidence that the kinase-truncated c-Src regulates NF-κB signaling by targeting NEMO.Journal of cellular biochemistry · 2011Article
- A cytosolic ATM/NEMO/RIP1 complex recruits TAK1 to mediate the NF-kappaB and p38 mitogen-activated protein kinase (MAPK)/MAPK-activated protein 2 responses to DNA damage.Molecular and cellular biology · 2011Article
- Dendritic cells from humans with hypomorphic mutations in IKBKG/NEMO have impaired mitogen-activated protein kinase activity.Human mutation · 2011Article
- Phosphorylation and polyubiquitination of transforming growth factor beta-activated kinase 1 are necessary for activation of NF-kappaB by the Kaposi's sarcoma-associated herpesvirus G protein-coupled receptor.Journal of virology · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Exposure of mammalian cells to UV radiation was proposed to stimulate the transcription factor NF-kappa B by a unique mechanism. Typically, rapid and strong inducers of NF-kappa B, such as tumor necrosis factor alpha (TNF-alpha) and bacterial lipopolysaccharide (LPS), lead to rapid phosphorylation and proteasomal degradation of its inhibitory protein, I kappa B alpha. In contrast, UV, a relatively slower and weaker inducer of NF-kappa B, was suggested not to require phosphorylation of I kappa B alpha for its targeted degradation by the proteasome. We now provide evidence to account for this peculiar degradation process of I kappa B alpha. The phospho-I kappa B alpha generated by UV is only detectable by expressing a Delta F-box mutant of the ubiquitin ligase beta-TrCP, which serves as a specific substrate trap for serine 32 and 36 phosphorylated I kappa B alpha. In agreement with this finding, we also find that the I kappa B kinase (IKK) phospho-acceptor sites on I kappa B alpha, core components of the IKK signalsome, and IKK catalytic activity are all required for UV signaling. Furthermore, deletion and point mutation analyses reveal that both the amino-terminal IKK-binding and the carboxy-terminal putative zinc finger domains of NEMO (IKK gamma) are critical for UV-induced NF-kappa B activation. Interestingly, the zinc finger domain is also required for NF-kappa B activation by two other slow and weak inducers, camptothecin and etoposide. In contrast, the zinc finger module is largely dispensable for NF-kappa B activation by the rapid and strong inducers LPS and TNF-alpha. Thus, we suggest that the zinc finger domain of NEMO likely represents a point of convergence for signaling pathways initiated by slow and weak NF-kappa B-activating conditions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.