ArticleMediators of inflammation2018
The Kat in the HAT: The Histone Acetyl Transferase Kat6b (MYST4) Is Downregulated in Murine Macrophages in Response to LPS.
Article in Mediators of inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Lysine Acetyltransferase 6A Drives M1 Macrophage Polarization Through Metabolic Reprogramming in Sepsis-Induced Acute Lung Injury.Biomolecules · 2026Article
- Clinical immunology in chromatinopathies: a scoping review.Frontiers in immunology · 2026Article
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Review
- BRPF1-KAT6A/KAT6B Complex: Molecular Structure, Biological Function and Human Disease.Cancers · 2022Review
- Lysine Acetyltransferase 2B predicts favorable prognosis and functions as anti-oncogene in cervical carcinoma.Bioengineered · 2021Article
- Cross-Species Insights Into Genomic Adaptations to Hypoxia.Frontiers in genetics · 2020Review
- Histone H3K23-specific acetylation by MORF is coupled to H3K14 acylation.Nature communications · 2019Article
- Metabolic immunomodulation of macrophage functional plasticity in nonhealing wounds.Current opinion in infectious diseases · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Epigenetic modulators, including histone methylases, demethylases, and deacetylases, have been implicated previously in the regulation of classical and alternative macrophage activation pathways. In this study, we show that the histone acetyl transferase (HAT) Kat6B (MYST4) is strongly suppressed (>80%) in macrophages by lipopolysaccharide (LPS) (M1 activation), while Kat6A, its partner in the MOZ/MORF complex, is reciprocally upregulated. This pattern of expression is not altered by LPS together with the adenosine receptor agonist NECA (M2d activation). This is despite the observation that miR-487b, a putative regulator of Kat6B expression, is mildly stimulated by LPS, but strongly suppressed by LPS/NECA. Other members of the MYST family of HATs (Kat5, Kat7, and Kat8) are unaffected by LPS treatment. Using the pLightswitch 3'UTR reporter plasmid, the miR-487b binding site in the Kat6b 3'UTR was found to play a role in the LPS-mediated suppression of Kat6B expression, but other as-yet unidentified factors are also involved. As Kat6B is a HAT that has the potential to modulate gene expression by its effects on chromatin accessibility, we are continuing our studies into the potential roles of this epigenetic modulator in macrophage activation pathways.
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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.