ArticleAmerican journal of clinical and experimental immunology2012
Regulation and function of nuclear IκBα in inflammation and cancer.
Article in American journal of clinical and experimental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
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- NF-ĸβ upregulates ADAMTS5 expression by direct binding after TNF-α treatment in OUMS-27 chondrosarcoma cell line.Molecular biology reports · 2020Article
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- Role of Resveratrol in Regulating Cutaneous Functions.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- CRM1, a novel independent prognostic factor overexpressed in invasive breast carcinoma of poor prognosis.Oncology letters · 2018Article
- Atomic basis of CRM1-cargo recognition, release and inhibition.Seminars in cancer biology · 2014Review
- Co-treatment of Naringenin and Ketoprofen-RGD Suppresses Cell Proliferation via Calmodulin/PDE/cAMP/PKA Axis Pathway in Leukemia and Ovarian Cancer Cells.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The nuclear translocation and accumulation of IκBα represents an important mechanism regulating transcription of NFκB-dependent pro-inflammatory and anti-apoptotic genes. The nuclear accumulation of IκBα can be induced by post-induction repression in stimulated cells, inhibition of the CRM1-dependent nuclear IκBα export by leptomycin B, and by the inhibition of the 26S proteasome. In addition, IκBα is constitutively localized in the nucleus of human neutrophils, likely contributing to the high rate of spontaneous apoptosis in these cells. In the nucleus, IκBα suppresses transcription of NFκB-dependent pro-inflammatory and anti-apoptotic genes, representing an attractive therapeutic target. However, the inhibition of NFκB-dependent genes by nuclear IκBα is promoter specific, and depends on the subunit composition of NFκB dimers and post-translational modifications of the recruited NFκB proteins. In addition, several recent studies have demonstrated an NFκB-independent role of the nuclear IκBα. In this review, we discuss the mechanisms leading to the nuclear accumulation of IκBα and its nuclear functions as potential targets for anti-inflammatory and anti-cancer therapies.
Indexed as
Identifiers
23885315PMC3714182W1853720043What OpenQuestion holds
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.