ReviewBritish journal of cancer2014
Novel functions of chromatin-bound IκBα in oncogenic transformation.
Review in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Inhibition of Jurkat T Cell Proliferation by Active Components ofJournal of microbiology and biotechnology · 2020Article
- Differential behavior of NF-κB, IκBα and EGFR during the renal carcinogenic process in an experimental modelOncology letters · 2020Article
- Role of the NFκB-signaling pathway in cancer.OncoTargets and therapy · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear factor-κB (NF-κB) signalling pathway participates in a multitude of biological processes, which imply the requirement of a complex and precise regulation. IκB (for Inhibitor of kappaB) proteins, which bind and retain NF-κB dimers in the cytoplasm, are the main contributors to negative regulation of NF-κB under non-stimulation conditions. Nevertheless, increasing evidences indicate that IκB proteins exert specific nuclear roles that directly contribute to the control of gene transcription. In particular, hypophosphorylated IκBβ can bind the promoter region of TNFα leading to persistent gene transcription in macrophages and contributing to the regulation of the inflammatory response. Recently, we demonstrated that phosphorylated and SUMOylated IκBα reside in the nucleus of the cells where it binds to chromatin leading to specific transcriptional repression. Mechanistically, IκBα associates and regulates Polycomb Repressor Complex activity, a function that is evolutionary conserved from flies to mammals, as indicate the homeotic phenotype of Drosophila mutants. Here we discuss the implications of chromatin-bound IκBα function in the context of tumorigenesis.
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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.