ATM prevents the persistence and propagation of chromosome breaks in lymphocytes.

No abstract is available for this paper.

• Publication year

  2007

• Venue

  Cell

• Publication date

  2007-07-13

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.CELL.2007.06.016PMID 17599403
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Enhanced intra‐switch region recombination during immunoglobulin class switch recombination in 53BP1–/– B cells

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• ATM deficiency impairs thymocyte maturation because of defective resolution of T cell receptor α locus coding end breaks

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• Defects in coding joint formation in vivo in developing ATM-deficient B and T lymphocytes

  2007influential reference
• ATM deficiency disrupts Tcra locus integrity and the maturation of CD4+CD8+ thymocytes.

  2007influential reference
• H2AX prevents DNA breaks from progressing to chromosome breaks and translocations.

  2006influential reference
• ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks

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• Switching on chromosomal translocations.

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• Common fragile sites as targets for chromosome rearrangements.

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• Regulation of hypermutation by activation-induced cytidine deaminase phosphorylation.

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• Role of genomic instability and p53 in AID-induced c-myc–Igh translocations

  2006influential reference
• Mechanism and control of V(D)J recombination at the immunoglobulin heavy chain locus.

  2006cited by this paper
• Rapid Activation of ATR by Ionizing Radiation Requires ATM and Mre11*

  2006cited by this paper
• 53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis.

  2006cited by this paper
• ATM stabilizes DNA double-strand-break complexes during V(D)J recombination

  2006cited by this paper
• Visualization of looping involving the immunoglobulin heavy-chain locus in developing B cells.

  2005cited by this paper
• Nibrin functions in Ig class-switch recombination.

  2005cited by this paper
• 53BP1 Cooperates with p53 and Functions as a Haploinsufficient Tumor Suppressor in Mice

  2005cited by this paper
• Genomic instability, endoreduplication, and diminished Ig class-switch recombination in B cells lacking Nbs1.

  2005cited by this paper
• Immunoglobulin Class Switch Recombination Is Impaired in Atm-deficient Mice

  2004influential reference
• 53BP1, an activator of ATM in response to DNA damage.

  2004cited by this paper
• Dynamics of DNA Double-Strand Breaks Revealed by Clustering of Damaged Chromosome Domains

  2004cited by this paper
• 53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination

  2004cited by this paper
• Continued maturation of thymic emigrants in the periphery

  2004cited by this paper
• ATM Is Required for Efficient Recombination between Immunoglobulin Switch Regions

  2004influential reference
• 53BP1 is required for class switch recombination

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• The proliferation gene expression signature is a quantitative integrator of oncogenic events that predicts survival in mantle cell lymphoma.

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• H2AX haploinsufficiency modifies genomic stability and tumor susceptibility.

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• The RAG-1/2 endonuclease causes genomic instability and controls CNS complications of lymphoblastic leukemia in p53/Prkdc-deficient mice.

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• Histone H2AX: a dosage-dependent suppressor of oncogenic translocations and tumors.

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• Evidence for Replicative Repair of DNA Double-Strand Breaks Leading to Oncogenic Translocation and Gene Amplification

  2002influential reference
• RAG-Mediated V(D)J Recombination Is Not Essential for Tumorigenesis in Atm-Deficient Mice

  2002cited by this paper
• Genomic Instability in Mice Lacking Histone H2AX

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• Unrepaired DNA breaks in p53-deficient cells lead to oncogenic gene amplification subsequent to translocations.

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• Sensing of intermediates in V(D)J recombination by ATM.

  2002cited by this paper
• AID is required to initiate Nbs1/γ-H2AX focus formation and mutations at sites of class switching

  2001influential reference
• Response to RAG-mediated V(D)J cleavage by NBS1 and γ-H2AX

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• Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX.

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• Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2).

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• Precursor B Cell Receptor–Dependent B Cell Proliferation and Differentiation Does Not Require the Bone Marrow or Fetal Liver Environment

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• Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme.

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• Antibody regulation of B cell development

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• Continued RAG expression in late stages of B cell development and no apparent re-induction after immunizion

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• Disruption of ATM in p53-null cells causes multiple functional abnormalities in cellular response to ionizing radiation

  1999cited by this paper
• RAG2:GFP knockin mice reveal novel aspects of RAG2 expression in primary and peripheral lymphoid tissues.

  1999influential reference
• Specific Expression of Activation-induced Cytidine Deaminase (AID), a Novel Member of the RNA-editing Deaminase Family in Germinal Center B Cells*

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• Lymphocyte life-span and memory.

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• Double-strand signal sequence breaks in V(D)J recombination are blunt, 5'-phosphorylated, RAG-dependent, and cell cycle regulated.

  1993cited by this paper
• Selective development of CD4+ T cells in transgenic mice expressing a class II MHC-restricted antigen receptor

  1989influential reference
• Altered immunoglobulin expression and functional silencing of self-reactive B lymphocytes in transgenic mice

  1988cited by this paper

• ATM in immunobiology: From lymphocyte development to cancer immunotherapy

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• Germline variants of DNA repair and immune genes in lymphoma from lymphoma‐cancer families

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• Ataxia Telangiectasia Mutated and MSH2 Control Blunt DNA End Joining in Ig Class Switch Recombination.

  2023cites this paper
• V(D)J Recombination: Orchestrating Diversity Without Damage

  2022cites this paper
• ATM and MSH2 control blunt DNA end joining in immunoglobulin class switch recombination

  2022cites this paper
• Mechanisms Underlying the Suppression of Chromosome Rearrangements by Ataxia-Telangiectasia Mutated

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• Nemo-Dependent, ATM-Mediated Signals from RAG DNA Breaks at Igk Feedback Inhibit Vκ Recombination to Enforce Igκ Allelic Exclusion

  2021cites this paper
• Distribution of copy number variations and rearrangement endpoints in human cancers with a review of literature.

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• DNA End Joining: G0-ing to the Core

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• Senataxin and RNase H2 act redundantly to suppress genome instability during class switch recombination

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• Mechanisms driving chromosomal translocations: lost in time and space

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• Elongation factor ELOF1 drives transcription-coupled repair and prevents genome instability

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• Targeting DNA Repair, Cell Cycle, and Tumor Microenvironment in B Cell Lymphoma

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• Suppressing proteasome mediated processing of topoisomerase II DNA-protein complexes preserves genome integrity

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• Endogenous topoisomerase II-mediated DNA breaks drive thymic cancer predisposition linked to ATM deficiency

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• The recent advances in non-homologous end-joining through the lens of lymphocyte development.

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• A robust CRISPR–Cas9-based fluorescent reporter assay for the detection and quantification of DNA double-strand break repair

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