ArticleMolecular and cellular biology2007
The Bloom's syndrome helicase is critical for development and function of the alphabeta T-cell lineage.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 37 citations in OpenAlex.
- A dual role for cGAS in shaping cellular and organismal responses to genomic instability.Genes & development · 2026Article
- BLM regulates MALT1-driven NF-κB signalling and is targetable in B-cell malignancies.Cell death & disease · 2026Article
- Multi-dimensional immunoprotection of Ganoderma lucidum spore oil in immunosuppressed mice via microbiome-proteome-metabolome network analysis.Scientific reports · 2026Article
- Inborn errors of immunity with DNA repair disorders: at the interface of immune deficiency, immune dysregulation, and malignancy.Frontiers in immunology · 2026Review
- Review
- T-cell receptor signaling in Schimke immuno-osseous dysplasia is SMARCAL1-independent.Frontiers in immunology · 2022Article
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- Review
- Bloom syndrome protein restrains innate immune sensing of micronuclei by cGAS.The Journal of experimental medicine · 2019Article
- Bloom syndrome: research and data priorities for the development of precision medicine as identified by some affected families.Cold Spring Harbor molecular case studies · 2018Review
- Immunodeficiency in Bloom's Syndrome.Journal of clinical immunology · 2018Article
- Bloom's Syndrome: Clinical Spectrum, Molecular Pathogenesis, and Cancer Predisposition.Molecular syndromology · 2017Review
- Manipulation of DNA Repair Proficiency in Mouse Models of Colorectal Cancer.BioMed research international · 2016Review
- The Rothmund-Thomson syndrome helicase RECQL4 is essential for hematopoiesis.The Journal of clinical investigation · 2014Article
- Article
- Requirement for dicer in survival of proliferating thymocytes experiencing DNA double-strand breaks.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- A conditional mouse model for measuring the frequency of homologous recombination events in vivo in the absence of essential genes.Molecular and cellular biology · 2011Article
- Global transcriptional response to carbonic anhydrase IX deficiency in the mouse stomach.BMC genomics · 2010Article
- Irradiated Blm-deficient mice are a highly tumor prone model for analysis of a broad spectrum of hematologic malignancies.Leukemia research · 2010Article
- Disruption of Supv3L1 damages the skin and causes sarcopenia, loss of fat, and death.Mammalian genome : official journal of the International Mammalian Genome Society · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bloom's syndrome is a genetic disorder characterized by increased incidence of cancer and an immunodeficiency of unknown origin. The BLM gene mutated in Bloom's syndrome encodes a DNA helicase involved in the maintenance of genomic integrity. To explore the role of BLM in the immune system, we ablated murine Blm in the T-cell lineage. In the absence of Blm, thymocytes were severely reduced in numbers and displayed a developmental block at the beta-selection checkpoint that was partially p53 dependent. Blm-deficient thymocytes rearranged their T-cell receptor (TCR) beta genes normally yet failed to survive and proliferate in response to pre-TCR signaling. Furthermore, peripheral T cells were reduced in numbers, manifested defective homeostatic and TCR-induced proliferation, and produced extensive chromosomal damage. Finally, CD4(+) and CD8(+) T-cell responses were impaired upon antigen challenge. Thus, by ensuring genomic stability, Blm serves a vital role for development, maintenance, and function of T lymphocytes, suggesting a basis for the immune deficiency in Bloom's syndrome.
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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.