ArticleThe Journal of biological chemistry2016
Kruppel-like Factor 6 Promotes Macrophage-mediated Inflammation by Suppressing B Cell Leukemia/Lymphoma 6 Expression.
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 31 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Identification and validation of MicroRNA-mRNA Networks in Dorsal Root Ganglia after Peripheral Nerve Injury.International journal of medical sciences · 2022Pooled it
- An epigenome-wide analysis of DNA methylation, racialized and economic inequities, and air pollution.Clinical epigenetics · 2025Article
- Macrophage-Kruppel-Like Transcription Factor 6 Signaling Promotes Experimental Atherogenesis.The American journal of pathology · 2025Article
- The multi-organ landscape of B cells highlights dysregulated memory B cell responses in Crohn's disease.National science review · 2025Article
- KLF feedback loops in innate immunity.Frontiers in immunology · 2025Review
- Article
- Monocytes in allo-HSCT with aged donors secrete IL-1/IL-6/TNF to increase the risk of GVHD and damage the aged HSCs.iScience · 2024Article
- The evaluation of six genes combined value in glioma diagnosis and prognosis.Journal of cancer research and clinical oncology · 2023Article
- Analysis of the microglia transcriptome across the human lifespan using single cell RNA sequencing.Journal of neuroinflammation · 2023Article
- Participation of Krüppel-like Factors in Atherogenesis.Metabolites · 2023Review
- Regulation of macrophage IFNγ-stimulated gene expression by the transcriptional coregulator CITED1.Journal of cell science · 2023Article
- Blockade of innate inflammatory cytokines TNFImmunotherapy advances · 2023Article
- Single cell analysis of M. tuberculosis phenotype and macrophage lineages in the infected lung.The Journal of experimental medicine · 2021Article
- Review
- MIREyA: a computational approach to detect miRNA-directed gene activation.F1000Research · 2021Article
- Role of promoting inflammation of Krüppel-like factor 6 in acute kidney injury.Renal failure · 2020Article
- Review
- Krüppel-like factor 3 (KLF3) suppresses NF-κB-driven inflammation in mice.The Journal of biological chemistry · 2020Article
- Kruppel-like factor 6 promotes macrophage inflammatory and hypoxia response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- KLF6 Acetylation Promotes Sublytic C5b-9-Induced Production of MCP-1 and RANTES in Experimental Mesangial Proliferative Glomerulonephritis.International journal of biological sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Macrophages are the predominant innate immune cells recruited to tissues following injury or infection. These early-responding, pro-inflammatory macrophages play an essential role in the amplification of inflammation. However, macrophage pro-inflammatory gene expression should be tightly regulated to avert host tissue damage. In this study, we identify the Kruppel-like transcription factor 6 (KLF6)-B cell leukemia/lymphoma 6 (BCL6) signaling axis as a novel regulator of macrophage inflammatory gene expression and function. Utilizing complementary gain- and loss-of-function studies, we observed that KLF6 is essential for macrophage motility under ex vivo and in vivo conditions. Concordant with these observations, myeloid-specific deficiency of KLF6 significantly attenuates macrophage pro-inflammatory gene expression, recruitment, and progression of inflammation. At the molecular level, KLF6 suppresses BCL6 mRNA and protein expression by elevating PR domain-containing 1 with ZNF domain (PRDM1) levels in macrophages. Interestingly, pharmacological or genetic inhibition of BCL6 in KLF6-deficient macrophages completely abrogated the attenuation of pro-inflammatory cytokine/chemokine expression and cellular motility. Collectively, our observations reveal that KLF6 repress BCL6 to enhance macrophage inflammatory gene expression and function.
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What OpenQuestion holds
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.