ArticleThe Journal of biological chemistry2020
Krüppel-like factor 3 (KLF3) suppresses NF-κB-driven inflammation in mice.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
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- Metabolic dysfunction-associated steatotic liver disease alters brain function and behavior: Insights from liver-targeted siRNA therapy.Science advances · 2025Article
- Age is an intrinsic driver of inflammatory responses to malaria.Nature communications · 2025Article
- Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis.Cells · 2025Review
- Signaling through the nicotinic acetylcholine receptor in the liver protects against the development of metabolic dysfunction-associated steatohepatitis.PLoS biology · 2024Article
- Macrophages in immunoregulation and therapeutics.Signal transduction and targeted therapy · 2023Review
- DNA methyltransferase inhibition induces dynamic gene expression changes in lung CD4Scientific reports · 2023Article
- Pan-cancer analysis of Krüppel-like factor 3 and its carcinogenesis in pancreatic cancer.Frontiers in immunology · 2023Article
- Genomic heterozygosity is associated with parasite abundance, but the effects are not mediated by host condition.Evolutionary ecology · 2023Article
- Robust temporal map of human in vitro myelopoiesis using single-cell genomics.Nature communications · 2022Article
- Acetylcholine-synthesizing macrophages in subcutaneous fat are regulated by βThe EMBO journal · 2021Article
- Comprehensive Analysis of ceRNA Regulation Network Involved in the Development of Coronary Artery Disease.BioMed research international · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial products such as lipopolysaccharides (or endotoxin) cause systemic inflammation, resulting in a substantial global health burden. The onset, progression, and resolution of the inflammatory response to endotoxin are usually tightly controlled to avoid chronic inflammation. Members of the NF-κB family of transcription factors are key drivers of inflammation that activate sets of genes in response to inflammatory signals. Such responses are typically short-lived and can be suppressed by proteins that act post-translationally, such as the SOCS (suppressor of cytokine signaling) family. Less is known about direct transcriptional regulation of these responses, however. Here, using a combination of
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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.