ArticleFrontiers in immunology2022
ZC3H11A loss of function enhances NF-κB signaling through defective IκBα protein expression.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- Single-Cell Transcriptomic Landscape of Cervical Cancer Cell Lines Before and After Chemoradiotherapy.Cells · 2026Article
- Pulsed radiofrequency attenuates mechanical hypersensitivity in neuropathic pain rats by activating the Nrf2-regulated CaMKII/NF-κB signaling pathway.The Korean journal of pain · 2026Article
- Article
- Reduction reactions dominate the interactions between Mg alloys and cells: Understanding the mechanisms.Bioactive materials · 2025Article
- Targeting ZC3H11A elicits immunogenic cancer cell death through augmentation of antigen presentation and interferon response.Molecular therapy. Nucleic acids · 2024Article
- Analysis of the mRNA export protein ZC3H11A in HCMV infection and pan-cancer.Frontiers in microbiology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ZC3H11A is a cellular protein associated with the transcription export (TREX) complex that is induced during heat-shock. Several nuclear-replicating viruses exploit the mRNA export mechanism of ZC3H11A protein for their efficient replication. Here we show that ZC3H11A protein plays a role in regulation of NF-κB signal transduction. Depletion of ZC3H11A resulted in enhanced NF-κB mediated signaling, with upregulation of numerous innate immune related mRNAs, including IL-6 and a large group of interferon-stimulated genes. IL-6 upregulation in the absence of the ZC3H11A protein correlated with an increased NF-κB transcription factor binding to the IL-6 promoter and decreased IL-6 mRNA decay. The enhanced NF-κB signaling pathway in ZC3H11A deficient cells correlated with a defect in IκBα inhibitory mRNA and protein accumulation. Upon ZC3H11A depletion The IκBα mRNA was retained in the cell nucleus resulting in failure to maintain normal levels of the cytoplasmic IκBα mRNA and protein that is essential for its inhibitory feedback loop on NF-κB activity. These findings indicate towards a previously unknown mechanism of ZC3H11A in regulating the NF-κB pathway at the level of IkBα mRNA export.
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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.