ArticleMolecular and cellular biology2005
Snm1-deficient mice exhibit accelerated tumorigenesis and susceptibility to infection.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 34 citations in OpenAlex.
- SNM1A is crucial for efficient repair of complex DNA breaks in human cells.Nature communications · 2024Article
- Structure and Function of SNM1 Family Nucleases.Advances in experimental medicine and biology · 2023Review
- Dual targeting of Saccharomyces cerevisiae Pso2 to mitochondria and the nucleus, and its functional relevance in the repair of DNA interstrand crosslinks.G3 (Bethesda, Md.) · 2022Article
- The SNM1A DNA repair nuclease.DNA repair · 2020Review
- Genetically modified laboratory mice with sebaceous glands abnormalities.Cellular and molecular life sciences : CMLS · 2016Review
- A network-pathway based module identification for predicting the prognosis of ovarian cancer patients.Journal of ovarian research · 2016Article
- Fan1 deficiency results in DNA interstrand cross-link repair defects, enhanced tissue karyomegaly, and organ dysfunction.Genes & development · 2016Article
- FANCI is a negative regulator of Akt activation.Cell cycle (Georgetown, Tex.) · 2016Article
- Orchestrating the nucleases involved in DNA interstrand cross-link (ICL) repair.Cell cycle (Georgetown, Tex.) · 2011Review
- Human SNM1A and XPF-ERCC1 collaborate to initiate DNA interstrand cross-link repair.Genes & development · 2011Article
- The telomeric protein SNM1B/Apollo is required for normal cell proliferation and embryonic development.Aging cell · 2010Article
- DNA repair and recombination in higher plants: insights from comparative genomics of Arabidopsis and rice.BMC genomics · 2010Article
- SNMIB/Apollo protects leading-strand telomeres against NHEJ-mediated repair.The EMBO journal · 2010Article
- The multifunctional SNM1 gene family: not just nucleases.Future oncology (London, England) · 2010Review
- Ribozyme-mediated targeting of IkappaBgamma inhibits melanoma invasion and metastasis.The American journal of pathology · 2009Article
- SNM1A acts downstream of ATM to promote the G1 cell cycle checkpoint.Biochemical and biophysical research communications · 2008Article
- The protein hSnm1B is stabilized when bound to the telomere-binding protein TRF2.The Journal of biological chemistry · 2008Article
- Snm1B/Apollo mediates replication fork collapse and S Phase checkpoint activation in response to DNA interstrand cross-links.Oncogene · 2008Article
- Endogenous hSNM1B/Apollo interacts with TRF2 and stimulates ATM in response to ionizing radiation.DNA repair · 2008Article
- A limited role for p53 in modulating the immediate phenotype of Apc loss in the intestine.BMC cancer · 2008Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The eukaryotic SNM1 gene family has been implicated in a number of cellular pathways, including repair of DNA interstrand cross-links, involvement in VDJ recombination, repair of DNA double-strand breaks, and participation in cell cycle checkpoint pathways. In particular, mammalian SNM1 has been shown to be required in a mitotic checkpoint that causes arrest of cells in prophase prior to chromosome condensation in response to spindle poisons. Here, we report on the phenotype of a knockout of Snm1 in the mouse. Snm1-/- mice are viable and fertile but exhibit a complex phenotype. Both homozygous and heterozygous mice show a decline in survival compared to wild-type littermates. In homozygous mutant males, this reduction in survival is principally due to bacterial infections in the preputial and mandibular glands and to a lesser extent to tumorigenesis, while in homozygous and heterozygous females, it is due almost solely to tumorigenesis. The high incidence of bacterial infections in the homozygous mutant males suggests an immune dysfunction; however, examinations of T- and B-cell development and immunoglobulin class switching did not reveal a defect in these pathways. Crossing of Snm1 mutant mice with a Trp53 null mutant resulted in an increase in mortality and a restriction of the tumor type to lymphomas, particularly those of the thymus. Taken together, these findings demonstrate that Snm1 is a tumor suppressor in mice that in addition has a role in immunity.
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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.