ArticleThe Journal of biological chemistry2016
Krüppel-like Factor 3 (KLF3/BKLF) Is Required for Widespread Repression of the Inflammatory Modulator Galectin-3 (Lgals3).
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Wnt/β-catenin signaling regulates fibrotic atrophy of intra-articular adipose tissue in post-traumatic osteoarthritis.bioRxiv : the preprint server for biology · 2026Article
- KLF family of proteins in gastrointestinal tumors (Review).Oncology letters · 2026Review
- Role of vascular smooth muscle phenotypic transformation induced by histone modifications in the development of abdominal aortic aneurysms.Clinical epigenetics · 2025Review
- Galectin-3 in Cardiovascular Health: A Narrative Review Based on Life's Essential 8 and Life's Simple 7 Frameworks.Current issues in molecular biology · 2025Review
- KLF feedback loops in innate immunity.Frontiers in immunology · 2025Review
- Endothelial Cell Dysfunction and Hypoxia as Potential Mediators of Pain in Fabry Disease: A Human-Murine Translational Approach.International journal of molecular sciences · 2023Article
- The Role of Galectin-3 in Heart Failure-The Diagnostic, Prognostic and Therapeutic Potential-Where Do We Stand?International journal of molecular sciences · 2023Review
- SREBP1 regulatesMolecular therapy. Nucleic acids · 2022Article
- Acetylcholine-synthesizing macrophages in subcutaneous fat are regulated by βThe EMBO journal · 2021Article
- Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease.Cell & bioscience · 2021Review
- Eosinophil function in adipose tissue is regulated by Krüppel-like factor 3 (KLF3).Nature communications · 2020Article
- The evolution of the 9aaTAD domain in Sp2 proteins: inactivation with valines and intron reservoirs.Cellular and molecular life sciences : CMLS · 2020Article
- Krüppel-like factor 3 (KLF3) suppresses NF-κB-driven inflammation in mice.The Journal of biological chemistry · 2020Article
- Galectin-3 exacerbates ox-LDL-mediated endothelial injury by inducing inflammation via integrin β1-RhoA-JNK signaling activation.Journal of cellular physiology · 2019Article
- NEAT1/miR-23a-3p/KLF3: a novel regulatory axis in melanoma cancer progression.Cancer cell international · 2019Article
- Krüppel-like factors: Crippling and un-crippling metabolic pathways.JACC. Basic to translational science · 2018Article
- Galectin-3 Activation and Inhibition in Heart Failure and Cardiovascular Disease: An Update.Theranostics · 2018Review
- CD103Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Lgals3 gene encodes a multifunctional β-galactoside-binding protein, galectin-3. Galectin-3 has been implicated in a broad range of biological processes from chemotaxis and inflammation to fibrosis and apoptosis. The role of galectin-3 as a modulator of inflammation has been studied intensively, and recent evidence suggests that it may serve as a protective factor in obesity and other metabolic disorders. Despite considerable interest in galectin-3, little is known about its physiological regulation at the transcriptional level. Here, using knockout mice, chromatin immunoprecipitations, and cellular and molecular analyses, we show that the zinc finger transcription factor Krüppel-like factor 3 (KLF3) directly represses galectin-3 transcription. We find that galectin-3 is broadly up-regulated in KLF3-deficient mouse tissues, that KLF3 occupies regulatory regions of the Lgals3 gene, and that KLF3 directly binds its cognate elements (CACCC boxes) in the galectin-3 promoter and represses its activation in cellular assays. We also provide mechanistic insights into the regulation of Lgals3, demonstrating that C-terminal binding protein (CtBP) is required to drive optimal KLF3-mediated silencing. These findings help to enhance our understanding of how expression of the inflammatory modulator galectin-3 is controlled, opening up avenues for potential therapeutic interventions in the future.
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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.