ArticleGenes and immunity2015
KMT1E-mediated chromatin modifications at the FcγRIIb promoter regulate thymocyte development.
Article in Genes and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Cytoplasmic localization of SETDB1‑induced Warburg effect via c‑MYC‑LDHA axis enhances migration and invasion in breast carcinoma.International journal of molecular medicine · 2024Article
- The Role of Protein Methyltransferases in Immunity.Molecules (Basel, Switzerland) · 2024Review
- Role of histone methyltransferase SETDB1 in regulation of tumourigenesis and immune response.Frontiers in pharmacology · 2022Review
- Article
- Review
- Control of Intra-Thymic αβ T Cell Selection and Maturation by H3K27 Methylation and Demethylation.Frontiers in immunology · 2019Review
- Immune responses to endogenous retroelements: taking the bad with the good.Nature reviews. Immunology · 2016Review
- SETDB1 mediated FosB expression increases the cell proliferation rate during anticancer drug therapy.BMB reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
This work examines the role the lysine methyltransferase KMT1E (Setdb1) in thymocyte development. We have developed and described a T cell-specific conditional knockout of Setdb1. A partial block was seen at the double-positive to single-positive transition, causing reduced numbers of single-positive T cells in the thymus and periphery. Knockout thymocytes had reduced numbers of CD69(+) and T-cell receptor TCRβ(+) cells and increased numbers of apoptotic cells in the double-positive compartment, suggesting an alteration in the selection process. Transcriptional profiling of thymocytes revealed that Setdb1 deletion derepresses expression of FcγRIIb, the inhibitory Fc receptor. We demonstrate that a KMT1E-containing complex directly interacts with the FcγRIIb promoter and that histone H3 at lysine 9 tri-methylation at this promoter is dependent on Setdb1 expression. Derepression of FcγRIIb causes exacerbated signaling through the TCR complex, with specifically increased phosphorylation of ZAP70, affecting selection. This work identifies KMT1E as a novel repressor of FcγRIIb and identifies an underappreciated role of FcγRIIb in fine tuning thymocyte development.
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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.