ArticleCancer cell2011
ATMIN is required for maintenance of genomic stability and suppression of B cell lymphoma.
Article in Cancer cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Osteosarcoma patient with Li-Fraumeni syndrome: the first case report in Vietnam.Frontiers in oncology · 2024Article
- ATMIN enhances invasion by altering PARP1 in MSS colorectal cancer.American journal of cancer research · 2022Article
- Comprehensive Analysis of a Zinc Finger Protein Gene-Based Signature with Regard to Prognosis and Tumor Immune Microenvironment in Osteosarcoma.Frontiers in genetics · 2022Article
- ATMIN Suppresses Metastasis by Altering the WNT-Signaling Pathway via PARP1 in MSI-High Colorectal Cancer.Annals of surgical oncology · 2021Article
- Review
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- An emerging regulatory network of NHEJ via DYNLL1-mediated 53BP1 redistribution.Annals of translational medicine · 2019Article
- Combined Genetic and Chromosomal Characterization of Wilms Tumors Identifies Chromosome 12 Gain as a Potential New Marker Predicting a Favorable Outcome.Neoplasia (New York, N.Y.) · 2019Article
- The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity.Nature communications · 2018Article
- Dynein light chain regulates adaptive and innate B cell development by distinctive genetic mechanisms.PLoS genetics · 2017Article
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- Perturbed hematopoiesis in mice lacking ATMIN.Blood · 2016Article
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- Mechanisms and consequences of ATMIN repression in hypoxic conditions: roles for p53 and HIF-1.Scientific reports · 2016Article
- DNA Repair Cofactors ATMIN and NBS1 Are Required to Suppress T Cell Activation.PLoS genetics · 2015Article
- Elucidation of IgH 3' region regulatory role during class switch recombination via germline deletion.Nature communications · 2015Article
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- ATMIN is required for the ATM-mediated signaling and recruitment of 53BP1 to DNA damage sites upon replication stress.DNA repair · 2014Article
- ATMIN is a transcriptional regulator of both lung morphogenesis and ciliogenesis.Development (Cambridge, England) · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Defective V(D)J rearrangement of immunoglobulin heavy or light chain (IgH or IgL) or class switch recombination (CSR) can initiate chromosomal translocations. The DNA-damage kinase ATM is required for the suppression of chromosomal translocations but ATM regulation is incompletely understood. Here, we show that mice lacking the ATM cofactor ATMIN in B cells (ATMIN(ΔB/ΔB)) have impaired ATM signaling and develop B cell lymphomas. Notably, ATMIN(ΔB/ΔB) cells exhibited defective peripheral V(D)J rearrangement and CSR, resulting in translocations involving the Igh and Igl loci, indicating that ATMIN is required for efficient repair of DNA breaks generated during somatic recombination. Thus, our results identify a role for ATMIN in regulating the maintenance of genomic stability and tumor suppression in B cells.
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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.