ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Functional analysis of histone methyltransferase g9a in B and T lymphocytes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
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Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- G9a controls plasma cell differentiation through FOXO1 and ETS1 binding site regulatory networks.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Maturation and persistence of CAR T cells derived from human pluripotent stem cells via chemical inhibition of G9a/GLP.Cell stem cell · 2025Article
- The Role of Protein Methyltransferases in Immunity.Molecules (Basel, Switzerland) · 2024Review
- Establishment of H3K9-methylated heterochromatin and its functions in tissue differentiation and maintenance.Nature reviews. Molecular cell biology · 2022Review
- Metabolic control of epigenetic rearrangements in B cell pathophysiology.Open biology · 2022Review
- G9a: An Emerging Epigenetic Target for Melanoma Therapy.Epigenomes · 2021Article
- Frequent upregulation of G9a promotes RelB-dependent proliferation and survival in multiple myeloma.Experimental hematology & oncology · 2020Article
- Discovery of a Novel Chemotype of Histone Lysine Methyltransferase EHMT1/2 (GLP/G9a) Inhibitors: Rational Design, Synthesis, Biological Evaluation, and Co-crystal Structure.Journal of medicinal chemistry · 2019Article
- Cutting Edge: The Histone Methyltransferase G9a Is Required for Silencing of Helper T Lineage-Associated Genes in Proliferating CD8 T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Increased expression of G9A contributes to carcinogenesis and indicates poor prognosis in hepatocellular carcinoma.Oncology letters · 2018Article
- Clinicopathological significance of G9A expression in colorectal carcinoma.Oncology letters · 2018Article
- 53BP1 Contributes toJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Discovery of Potent and Selective Inhibitors for G9a-Like Protein (GLP) Lysine Methyltransferase.Journal of medicinal chemistry · 2017Article
- The H3K9 dimethyltransferases EHMT1/2 protect against pathological cardiac hypertrophy.The Journal of clinical investigation · 2017Article
- The Lysine Methyltransferase G9a in Immune Cell Differentiation and Function.Frontiers in immunology · 2017Review
- Pathological Ace2-to-Ace enzyme switch in the stressed heart is transcriptionally controlled by the endothelial Brg1-FoxM1 complex.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The lysine methyltransferase Ehmt2/G9a is dispensable for skeletal muscle development and regeneration.Skeletal muscle · 2016Article
- The histone methyltransferase SETDB1 represses endogenous and exogenous retroviruses in B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- KMT1E-mediated chromatin modifications at the FcγRIIb promoter regulate thymocyte development.Genes and immunity · 2015Article
- Functional Role of G9a Histone Methyltransferase in Cancer.Frontiers in immunology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Lymphocyte development is controlled by dynamic repression and activation of gene expression. These developmental programs include the ordered, tissue-specific assembly of Ag receptor genes by V(D)J recombination. Changes in gene expression and the targeting of V(D)J recombination are largely controlled by patterns of epigenetic modifications imprinted on histones and DNA, which alter chromatin accessibility to nuclear factors. An important component of this epigenetic code is methylation of histone H3 at lysine 9 (H3K9me), which is catalyzed by histone methyltransferases and generally leads to gene repression. However, the function and genetic targets of H3K9 methyltransferases during lymphocyte development remain unknown. To elucidate the in vivo function of H3K9me, we generated mice lacking G9a, a major H3K9 histone methyltransferase, in lymphocytes. Surprisingly, lymphocyte development is unperturbed in G9a-deficient mice despite a significant loss of H3K9me2 in precursor B cells. G9a deficiency is manifest as modest defects in the proliferative capacity of mature B cells and their differentiation into plasma cells following stimulation with LPS and IL-4. Precursor lymphocytes from the mutant mice retain tissue- and stage-specific control over V(D)J recombination. However, G9a deficiency results in reduced usage of Iglambda L chains and a corresponding inhibition of Iglambda gene assembly in bone marrow precursors. These findings indicate that the H3K9me2 epigenetic mark affects a highly restricted set of processes during lymphocyte development and activation.
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Registered trials
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