ArticleMolecular and cellular biology2008
Homologous recombination is necessary for normal lymphocyte development.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Continuous multi-omics pathway enrichment analysis resolves hidden functional heterogeneity.Briefings in bioinformatics · 2026Article
- Genetic Risk Variants for Class Switching Recombination Defects in Ataxia-Telangiectasia Patients.Journal of clinical immunology · 2022Article
- Are Pathogenic Germline Variants in Metastatic Melanoma Associated with Resistance to Combined Immunotherapy?Cancers · 2020Article
- Enhancing the efficacy of glycolytic blockade in cancer cellsCancer biology & therapy · 2019Article
- XRCC2 (X-ray repair cross complementing 2).Atlas of genetics and cytogenetics in oncology and haematology · 2019Article
- Destabilized SMC5/6 complex leads to chromosome breakage syndrome with severe lung disease.The Journal of clinical investigation · 2016Article
- The GIY-YIG Type Endonuclease Ankyrin Repeat and LEM Domain-Containing Protein 1 (ANKLE1) Is Dispensable for Mouse Hematopoiesis.PloS one · 2016Article
- RECQ helicases are deregulated in hematological malignancies in association with a prognostic value.Biomarker research · 2016Article
- Attenuating homologous recombination stimulates an AID-induced antileukemic effect.The Journal of experimental medicine · 2013Article
- Activation-induced cytidine deaminase-initiated off-target DNA breaks are detected and resolved during S phase.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Widespread genomic breaks generated by activation-induced cytidine deaminase are prevented by homologous recombination.Nature immunology · 2010Article
- Chromosomal translocations caused by either pol32-dependent or pol32-independent triparental break-induced replication.Molecular and cellular biology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Primary immunodeficiencies are rare but serious diseases with diverse genetic causes. Accumulating evidence suggests that defects in DNA double-strand break (DSB) repair can underlie many of these syndromes. In this context, the nonhomologous end joining pathway of DSB repair is absolutely required for lymphoid development, but possible roles for the homologous recombination (HR) pathway have remained more controversial. While recent evidence suggests that HR may indeed be important to suppress lymphoid transformation, the specific relationship of HR to normal lymphocyte development remains unclear. We have investigated roles of the X-ray cross-complementing 2 (Xrcc2) HR gene in lymphocyte development. We show that HR is critical for normal B-cell development, with Xrcc2 nullizygosity leading to p53-dependent early S-phase arrest. In the absence of p53 (encoded by Trp53), Xrcc2-null B cells can fully develop but show high rates of chromosome and chromatid fragmentation. We present a molecular model wherein Xrcc2 is important to preserve or restore replication forks during rapid clonal expansion of developing lymphocytes. Our findings demonstrate a key role for HR in lymphoid development and suggest that Xrcc2 defects could underlie some human primary immunodeficiencies.
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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.