ArticlePloS one2012
ER stress activates NF-κB by integrating functions of basal IKK activity, IRE1 and PERK.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers.
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Who cites it
216 citing papers in PubMed, 337 citations in OpenAlex.
- Transcriptomics-driven antiviral drug screening identifies ATF6 as a homeostatic regulator of ER stress and innate immunity.Journal of advanced research · 2026Article
- Anti-myeloma mechanisms of the selective NF-κB inhibitor QNZ.Molecular therapy. Oncology · 2026Article
- Epigallocatechin-3-gallate as a hepatoprotective agent against ochratoxin a: modulating ER stress and NF-κB/TNF-α/IL-6 responses.Mycotoxin research · 2026Article
- Evaluation of triumeq treatment on a TDP-43 mouse model of amyotrophic Lateral sclerosis.Scientific reports · 2026Article
- RANKL inhibits macrophage proinflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria.ImmunoHorizons · 2026Article
- Sequential transcriptional waves and NF-κB-driven chromatin remodeling direct drug-induced dedifferentiation in cancer.Nature communications · 2026Article
- Article
- The Role of ER Stress in Bilirubin Neurotoxicity: A Complex Molecular Network.Antioxidants (Basel, Switzerland) · 2026Review
- Iron deficiency aggravates hepatic inflammation in suckling piglets via endoplasmic reticulum stress-driven NF-κB pathway activation.Journal of animal science and biotechnology · 2026Article
- Endothelial IRE1 signaling maintains blood-brain barrier integrity and limits neuroinflammation after traumatic brain injury.Cell death & disease · 2026Article
- Insulin resistance induced by obesity: Mechanisms, metabolic implications and therapeutic approaches.Molecular biology reports · 2026Review
- Modulation of the unfolded protein response with a C-terminal fragment of MANF facilitates recovery in models of multiple sclerosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Spatial transcriptomic profiling identifies lacrimal-gland-epithelial cell-driven mechanisms underlying autoimmunity in Sjögren's disease.Frontiers in immunology · 2026Article
- The IRE1α Pathway Links Endoplasmic Reticulum Stress to Atherosclerosis-Related Inflammation and Lipid Accumulation.Mediators of inflammation · 2026Article
- Defining the role of β-cell IRE1α/XBP1 pathway and its gene regulatory network components in non-obese diabetic mice.Nature communications · 2025Article
- Spatial transcriptomic profiling identifies lacrimal gland epithelial cell-driven mechanisms underlying autoimmunity in Sjögren's disease.bioRxiv : the preprint server for biology · 2025Article
- Ferulic Acid Ameliorates Chromium-Induced Nephrotoxicity: Modulation of PERK/eIF2α/ATF4/CHOP, Nrf2, and Inflammatory Signaling.Biological trace element research · 2025Article
- Article
- Pimobendan alleviates myocyte apoptosis and fibrosis associated with mitral regurgitation by targeting endoplasmic reticulum stress.Animal models and experimental medicine · 2025Article
- Targeting the Unfolded Protein Response with Natural Products: Therapeutic Potential in ER Stress-Related Diseases.International journal of molecular sciences · 2025Review
156 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
NF-κB, a transcription factor, becomes activated during the Unfolded Protein Response (UPR), an endoplasmic reticulum (ER) stress response pathway. NF-κB is normally held inactive by its inhibitor, IκBα. Multiple cellular pathways activate IKK (IκBα Kinase) which phosphorylate IκBα leading to its degradation and NF-κB activation. Here, we find that IKK is required for maximum activation of NF-κB in response to ER stress. However, unlike canonical NFκB activation, IKK activity does not increase during ER stress, but rather the level of basal IKK activity is critical for determining the extent of NF-κB activation. Furthermore, a key UPR initiator, IRE1, acts to maintain IKK basal activity through IRE1's kinase, but not RNase, activity. Inputs from IRE1 and IKK, in combination with translation repression by PERK, another UPR initiator, lead to maximal NF-κB activation during the UPR. These interdependencies have a significant impact in cancer cells with elevated IKK/NF-κB activity such as renal cell carcinoma cells (786-0). Inhibition of IKK by an IKK inhibitor, which significantly decreases NF-κB activity, is overridden by UPR induction, arguing for the importance of considering UPR activation in cancer treatment.
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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.