ArticleThe Journal of allergy and clinical immunology2024
MYSM1 attenuates DNA damage signals triggered by physiologic and genotoxic DNA breaks.
Article in The Journal of allergy and clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Methodological Landscape of DNA Damage Response Detection: From Conventional Assays to Future Innovations.Current issues in molecular biology · 2026Review
- Altered phenotype and gene expression of regulatory T cells (Tregs) in children with Autism, and the relationship with comorbid gastrointestinal symptoms.Journal of neuroinflammation · 2026Article
- Altered Phenotype and Gene Expression of Regulatory T cells (Tregs) in Children with Autism, and the Relationship with Comorbid Gastrointestinal Symptoms.Research square · 2025Article
- E0703 targets ERβ to facilitate the upregulation of GLI3, thereby alleviating irradiation-induced DNA damage on lymphocytes.Cellular & molecular biology letters · 2025Article
- Genetic and Clinical Progression of MYSM1 Related Bone Marrow Failure into Myeloid Malignancies: Case Series and Review of Literature.Clinical hematology international · 2025Article
- Deubiquitinase MYSM1 promotes doxorubicin-induced cardiotoxicity by mediating TRIM21-ferroptosis axis in cardiomyocytes.Cell communication and signaling : CCS · 2024Article
- The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation.Cells · 2024Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPatients with deleterious variants in MYSM1 have an immune deficiency characterized by B-cell lymphopenia, hypogammaglobulinemia, and increased radiosensitivity. MYSM1 is a histone deubiquitinase with established activity in regulating gene expression. MYSM1 also localizes to sites of DNA injury but its function in cellular responses to DNA breaks has not been elucidated.
objectivesThis study sought to determine the activity of MYSM1 in regulating DNA damage responses (DDRs) to DNA double-stranded breaks (DSBs) generated during immunoglobulin receptor gene (Ig) recombination and by ionizing radiation.
methodsMYSM1-deficient pre- and non-B cells were used to determine the role of MYSM1 in DSB generation, DSB repair, and termination of DDRs.
resultsGenetic testing in a newborn with abnormal screen for severe combined immune deficiency, T-cell lymphopenia, and near absence of B cells identified a novel splice variant in MYSM1 that results in nearly absent protein expression. Radiosensitivity testing in patient's peripheral blood lymphocytes showed constitutive γH2AX, a marker of DNA damage, in B cells in the absence of irradiation, suggesting a role for MYSM1 in response to DSBs generated during Ig recombination. Suppression of MYSM1 in pre-B cells did not alter generation or repair of Ig DSBs. Rather, loss of MYSM1 resulted in persistent DNA damage foci and prolonged DDR signaling. Loss of MYSM1 also led to protracted DDRs in U2OS cells with irradiation induced DSBs.
conclusionsMYSM1 regulates termination of DNA damage responses but does not function in DNA break generation and repair.
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Registered trials
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