Article

KMT2D Regulates thymic Egress by Modulating Maturation and integrin Expression

2022-10-07

Abstract excerpt

<h4>Objective</h4> There is a clinical need to understand how dysregulated thymocyte development, caused by pathogenic variants in the gene encoding the histone-modifying enzyme, lysine methyltransferase 2D ( KMT2D ), contributes to immune dysfunction, including immune deficiency, autoimmunity, and lymphoproliferative sequela, and immune-driven mortality in individuals with Kabuki syndrome type 1 (KS1). <h4>Met...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 6830f636-184e-547e-b8dc-c9d8ad3be98f
DOI: 10.1101/2022.10.04.510662

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

KMT2D Regulates thymic Egress by Modulating Maturation and integrin ExpressionDOI 10.1101/2022.10.04.510662Read

KMT2D regulates activation, localization, and integrin expression by T-cellsSemantic proximity Read

Molecular insights of KMT2D and clinical aspects of Kabuki syndrome type 1.Semantic proximity Read

Abnormal Peyer patch development and B-cell gut homing drive IgA deficiency in Kabuki syndrome.Semantic proximity Read

Characterizing the molecular impact of KMT2D variants on the epigenetic and transcriptional landscapes in Kabuki syndrome.Semantic proximity Read

Characterizing the molecular impact of<i>KMT2D</i>variants on the epigenetic and transcriptional landscapes in Kabuki SyndromeSemantic proximity Read

The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development.Semantic proximity Read

Epigenetic control of the immune system: a lesson from Kabuki syndrome.Semantic proximity Read

Defects of B-cell terminal differentiation in patients with type-1 Kabuki syndrome.Semantic proximity Read

Cooperative super-enhancer inactivation caused by heterozygous loss of CREBBP and KMT2D skews B cell fate decisions and yields T cell-depleted lymphomasSemantic proximity Read

Loss of KMT2C reprograms the epigenomic landscape in hPSCs resulting in NODAL overexpression and a failure of hemogenic endothelium specification.Semantic proximity Read

Myasthenia gravis-specific aberrant neuromuscular gene expression by medullary thymic epithelial cells in thymomaSemantic proximity Read

Genome-wide Screens Identify Lineage- and Tumor Specific-Genes Modulating MHC-I and MHC-II Immunosurveillance in Human LymphomasSemantic proximity Read