ArticleProceedings of the National Academy of Sciences of the United States of America2011
Essential role of Mediator subunit Med1 in invariant natural killer T-cell development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Med1 deletion reprograms dental epithelium into a hair-forming epidermal architecture associated with Trp63 induction.Biochemistry and biophysics reports · 2026Article
- Amyloid Precursor Protein Processing Links Female Urgency Urinary Incontinence with Alzheimer's Disease: Implications for Treatment.International journal of molecular sciences · 2026Article
- Endothelium-Treg Communication Through Extracellular Vesicle Transfer Exacerbates Acute Respiratory Distress Syndrome.Journal of extracellular vesicles · 2026Article
- Vitamin D May Increase the Number of CD4-CD8+ NKT-like Cells in Humans-A Novel Insight into Potential Immunomodulatory Action.Nutrients · 2025Article
- Nuclear receptor-driven immunometabolic crosstalk: immune-centric pharmacology targeting the inflamed nexus.Frontiers in cell and developmental biology · 2025Review
- Mediator complex subunit 1 architects a tumorigenic Treg cell program independent of inflammation.Cell reports. Medicine · 2024Article
- Mediator 1 ablation induces enamel-to-hair lineage conversion in mice through enhancer dynamics.Communications biology · 2023Article
- MED1 Ablation Promotes Oral Mucosal Wound Healing via JNK Signaling Pathway.International journal of molecular sciences · 2022Article
- Med1 controls CD8 T cell maintenance through IL-7R-mediated cell survival signalling.Journal of cellular and molecular medicine · 2021Article
- Transcriptional Regulation of Dental Epithelial Cell Fate.International journal of molecular sciences · 2020Review
- USP22 controls iNKT immunity through MED1 suppression of histone H2A monoubiquitination.The Journal of experimental medicine · 2020Article
- PDCD5 regulates iNKT cell terminal maturation and iNKT1 fate decision.Cellular & molecular immunology · 2019Article
- Methylation of H3K27 and H3K4 in key gene promoter regions of thymus in RA mice is involved in the abnormal development and differentiation of iNKT cells.Immunogenetics · 2019Article
- Differential Control ofFrontiers in immunology · 2019Article
- The ins and outs of type I iNKT cell development.Molecular immunology · 2019Review
- Regulation of the terminal maturation of iNKT cells by mediator complex subunit 23.Nature communications · 2018Article
- Mediator 1 contributes to enamel mineralization as a coactivator for Notch1 signaling and stimulates transcription of the alkaline phosphatase gene.The Journal of biological chemistry · 2017Article
- Mediator facilitates transcriptional activation and dynamic long-range contacts at the IgH locus during class switch recombination.The Journal of experimental medicine · 2016Article
- iNKT cells require TSC1 for terminal maturation and effector lineage fate decisions.The Journal of clinical investigation · 2014Article
- CCAR1/CoCoA pair-mediated recruitment of the Mediator defines a novel pathway for GATA1 function.Genes to cells : devoted to molecular & cellular mechanisms · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD1d-restricted invariant NKT (iNKT) cells are a unique lineage of T lymphocytes that regulate both innate and adaptive immunity. The Mediator complex forms the bridge between transcriptional activators and the general transcription machinery. Med1/TRAP220 (also called DRIP205) is a key component of Mediator that interacts with ligand-bound hormone receptors, such as the vitamin D receptor. Here, we show that T-cell-specific Med1 deficiency results in a specific block in iNKT cell development but the development of conventional αβ T cells remains grossly normal. The defect is cell-intrinsic and depends neither on apoptosis, cell-cycle control, nor on CD1d expression of CD4(+)CD8(+) double-positive thymocytes. Surprisingly, ectopic expression of a Vα14-Jα18 T-cell receptor transgene completely rescues the defect caused by Med1 deficiency. At the molecular level, thymic iNKT cells in Med1(-/-) animals display reduced levels of IL-2Rβ and T-bet expression and could not complete terminal maturation. Thus, Med1 is essential for a complete intrathymic development of iNKT cells.
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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.