ArticleThe Journal of experimental medicine2009
Histone H2AX stabilizes broken DNA strands to suppress chromosome breaks and translocations during V(D)J recombination.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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Who cites it
40 citing papers in PubMed, 53 citations in OpenAlex.
- IL-7 promotes the formation of DNA double strand breaks and DNA repair in murine pro-B cells.Frontiers in immunology · 2025Article
- Locus folding mechanisms determine modes of antigen receptor gene assembly.The Journal of experimental medicine · 2024Article
- FLASH-RT does not affect chromosome translocations and junction structures beyond that of CONV-RT dose-rates.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023Article
- FLASH-RT does not affect chromosome translocations and junction structures beyond that of CONV-RT dose-rates.bioRxiv : the preprint server for biology · 2023Article
- DNA Damage Response and Repair in Adaptive Immunity.Frontiers in cell and developmental biology · 2022Review
- V(D)J Recombination: Recent Insights in Formation of the Recombinase Complex and Recruitment of DNA Repair Machinery.Frontiers in cell and developmental biology · 2022Review
- Mechanisms Underlying the Suppression of Chromosome Rearrangements by Ataxia-Telangiectasia Mutated.Genes · 2021Review
- DNA double-strand breaks induce H2Ax phosphorylation domains in a contact-dependent manner.Nature communications · 2020Article
- Loss of H3K36 Methyltransferase SETD2 Impairs V(D)J Recombination during Lymphoid Development.iScience · 2020Article
- Generation and CRISPR/Cas9 editing of transformed progenitor B cells as a pseudo-physiological system to study DNA repair gene function in V(D)J recombination.Journal of immunological methods · 2017Article
- H2AX facilitates classical non-homologous end joining at the expense of limited nucleotide loss at repair junctions.Nucleic acids research · 2017Article
- Genome Instability and γH2AX.International journal of molecular sciences · 2017Review
- Immature Lymphocytes InhibitJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Contribution of canonical nonhomologous end joining to chromosomal rearrangements is enhanced by ATM kinase deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The RNA-Binding Proteins Zfp36l1 and Zfp36l2 Enforce the Thymic β-Selection Checkpoint by Limiting DNA Damage Response Signaling and Cell Cycle Progression.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- DNA Repair and Cytokines: TGF-β, IL-6, and Thrombopoietin as Different Biomarkers of Radioresistance.Frontiers in oncology · 2016Review
- Somatic inactivation of ATM in hematopoietic cells predisposes mice to cyclin D3 dependent T cell acute lymphoblastic leukemia.Cell cycle (Georgetown, Tex.) · 2015Article
- Histone deacetylation critically determines T cell subset radiosensitivity.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- RAG2's acidic hinge restricts repair-pathway choice and promotes genomic stability.Cell reports · 2013Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The H2AX core histone variant is phosphorylated in chromatin around DNA double strand breaks (DSBs) and functions through unknown mechanisms to suppress antigen receptor locus translocations during V(D)J recombination. Formation of chromosomal coding joins and suppression of translocations involves the ataxia telangiectasia mutated and DNA-dependent protein kinase catalytic subunit serine/threonine kinases, each of which phosphorylates H2AX along cleaved antigen receptor loci. Using Abelson transformed pre-B cell lines, we find that H2AX is not required for coding join formation within chromosomal V(D)J recombination substrates. Yet we show that H2AX is phosphorylated along cleaved Igkappa DNA strands and prevents their separation in G1 phase cells and their progression into chromosome breaks and translocations after cellular proliferation. We also show that H2AX prevents chromosome breaks emanating from unrepaired RAG endonuclease-generated TCR-alpha/delta locus coding ends in primary thymocytes. Our data indicate that histone H2AX suppresses translocations during V(D)J recombination by creating chromatin modifications that stabilize disrupted antigen receptor locus DNA strands to prevent their irreversible dissociation. We propose that such H2AX-dependent mechanisms could function at additional chromosomal locations to facilitate the joining of DNA ends generated by other types of DSBs.
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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.