ArticleThe Journal of biological chemistry2014
IκB kinase β (IKBKB) mutations in lymphomas that constitutively activate canonical nuclear factor κB (NFκB) signaling.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
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- Discriminating activating, deactivating and resistance variants in protein kinases.Genome medicine · 2025Article
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- Wnt/β-catenin activation by mutually exclusive FBXW11 and CTNNB1 hotspot mutations drives salivary basal cell adenoma.Nature communications · 2025Article
- Exploiting gene dependency to inform drug development for multiple myeloma.Scientific reports · 2022Article
- Mechanistic insights into the activation of the IKK kinase complex by the Kaposi's sarcoma herpes virus oncoprotein vFLIP.The Journal of biological chemistry · 2022Article
- Heterozygous IKKβ activation loop mutation results in a complex immunodeficiency syndrome.The Journal of allergy and clinical immunology · 2021Article
- Haplotype-resolved and integrated genome analysis of the cancer cell line HepG2.Nucleic acids research · 2019Article
- Context-Dependent Role of IKKβ in Cancer.Genes · 2017Review
- NF-κB in Hematological Malignancies.Biomedicines · 2017Review
- Gain-of-Function Mutations in the Toll-Like Receptor Pathway: TPL2-Mediated ERK1/ERK2 MAPK Activation, a Path to Tumorigenesis in Lymphoid Neoplasms?Frontiers in cell and developmental biology · 2016Article
- EcSTAT3ic about K63-Linked Ubiquitylation of IKKβ.Cell cycle (Georgetown, Tex.) · 2015Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Somatic mutations altering lysine 171 of the IKBKB gene that encodes (IKKβ), the critical activating kinase in canonical (NFκB) signaling, have been described in splenic marginal zone lymphomas and multiple myeloma. Lysine 171 forms part of a cationic pocket that interacts with the activation loop phosphate in the activated wild type kinase. We show here that K171E IKKβ and K171T IKKβ represent kinases that are constitutively active even in the absence of activation loop phosphorylation. Predictive modeling and biochemical studies establish why mutations in a positively charged residue in the cationic pocket of an activation loop phosphorylation-dependent kinase result in constitutive activation. Transcription activator-like effector nuclease-based knock-in mutagenesis provides evidence from a B lymphoid context that K171E IKKβ contributes to lymphomagenesis.
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Registered trials
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.