ArticleProceedings of the National Academy of Sciences of the United States of America2017
Functional importance of stripping in NFκB signaling revealed by a stripping-impaired IκBα mutant.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Frustration in physiology and molecular medicine.Molecular aspects of medicine · 2025Review
- Article
- NF-κB: master regulator of cellular responses in health and disease.Immunity & inflammation · 2025Review
- Herbal Remedies for Hepatic Inflammation: Unravelling Pathways and Mechanisms for Therapeutic Intervention.Current pharmaceutical design · 2025Review
- Fuzzy protein-DNA interactions and beyond: A common theme in transcription?Current opinion in structural biology · 2024Review
- The multifunctional role of intrinsic disorder in NF-κB signaling.Biochemical Society transactions · 2023Review
- Processing stimulus dynamics by the NF-κB network in single cells.Experimental & molecular medicine · 2023Review
- In-Cell Chemical Crosslinking Identifies Hotspots for SQSTM-1/p62-IκBα Interaction That Underscore a Critical Role of p62 in Limiting NF-κB Activation Through IκBα Stabilization.Molecular & cellular proteomics : MCP · 2023Article
- Overexpression of IκB⍺ modulates NF-κB activation of inflammatory target gene expression.Frontiers in molecular biosciences · 2023Article
- Advances in Hydrogen/Deuterium Exchange Mass Spectrometry and the Pursuit of Challenging Biological Systems.Chemical reviews · 2022Review
- Tumor-promoting mechanisms of macrophage-derived extracellular vesicles-enclosed microRNA-660 in breast cancer progression.Breast cancer research and treatment · 2022Article
- IκBα is required for full transcriptional induction of some NFκB-regulated genes in response to TNF in MCF-7 cells.NPJ systems biology and applications · 2021Article
- Single-molecule conformational dynamics of a transcription factor reveals a continuum of binding modes controlling association and dissociation.Nucleic acids research · 2021Article
- Origin of the Functional Distinctiveness of NF-κB/p52.Frontiers in cell and developmental biology · 2021Review
- First Responders Shape a Prompt and Sharp NF-κB-Mediated Transcriptional Response to TNF-α.iScience · 2020Article
- Structure and dynamics of the ASB9 CUL-RING E3 Ligase.Nature communications · 2020Article
- Pretreatment withDrug design, development and therapy · 2020Article
- Article
- Genome reading by the NF-κB transcription factors.Nucleic acids research · 2019Review
- Exclusivity and Compensation in NFκB Dimer Distributions and IκB Inhibition.Biochemistry · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Stress-response transcription factors such as NFκB turn on hundreds of genes and must have a mechanism for rapid cessation of transcriptional activation. We recently showed that the inhibitor of NFκB signaling, IκBα, dramatically accelerates the dissociation of NFκB from transcription sites, a process we have called "stripping." To test the role of the IκBα C-terminal PEST (rich in proline, glutamic acid, serine, and threonine residues) sequence in NFκB stripping, a mutant IκBα was generated in which five acidic PEST residues were mutated to their neutral analogs. This IκBα(5xPEST) mutant was impaired in stripping NFκB from DNA and formed a more stable intermediate ternary complex than that formed from IκBα(WT) because DNA dissociated more slowly. NMR and amide hydrogen-deuterium exchange mass spectrometry showed that the IκBα(5xPEST) appears to be "caught in the act of stripping" because it is not yet completely in the folded and NFκB-bound state. When the mutant was introduced into cells, the rate of postinduction IκBα-mediated export of NFκB from the nucleus decreased markedly.
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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.