ArticleBMC genomics2013
Exome sequencing of senescence-accelerated mice (SAM) reveals deleterious mutations in degenerative disease-causing genes.
Article in BMC genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Senescence accelerated mouse-prone 8: a model of neuroinflammation and aging with features of sporadic Alzheimer's disease.Stem cells (Dayton, Ohio) · 2025Review
- Shared genetic architecture between grip strength and cognitive function: insights from large-scale genome-wide cross-trait analysis.Frontiers in genetics · 2025Article
- Dopaminergic neuron loss in mice due to increased levels of wild-type human α-Synuclein only takes place under conditions of accelerated aging.Scientific reports · 2024Article
- DNA Mutagenicity of Hydroxyhydroquinone in Roasted Coffee Products and Its Suppression by Chlorogenic Acid, a Coffee Polyphenol, in Oxidative-Damage-Sensitive SAMP8 Mice.International journal of molecular sciences · 2024Article
- Review
- Senescence-accelerated mice prone 8 (SAMP8) in male as a spontaneous osteoarthritis model.Arthritis research & therapy · 2022Article
- Heart failure with preserved ejection fraction in humans and mice: embracing clinical complexity in mouse models.European heart journal · 2021Review
- Protection of MCC950 against Alzheimer's disease via inhibiting neuronal pyroptosis in SAMP8 mice.Experimental brain research · 2020Article
- Modulation of KDM1A with vafidemstat rescues memory deficit and behavioral alterations.PloS one · 2020Article
- Nonalcoholic Fatty Liver Disease Demonstrates a Pre-fibrotic and Premalignant Molecular Signature.Digestive diseases and sciences · 2019Article
- Wild-type and SAMP8 mice show age-dependent changes in distinct stem cell compartments of the interfollicular epidermis.PloS one · 2019Article
- Impact of Oxidative Stress on Age-Associated Decline in Oocyte Developmental Competence.Frontiers in endocrinology · 2019Review
- Distribution of endogenous gammaretroviruses and variants of the Fv1 restriction gene in individual mouse strains and strain subgroups.PloS one · 2019Article
- Senescent cells expose and secrete an oxidized form of membrane-bound vimentin as revealed by a natural polyreactive antibody.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Stereomicroscopic 3D-pattern profiling of murine and human intestinal inflammation reveals unique structural phenotypes.Nature communications · 2015Article
- Regulation of the p19(Arf)/p53 pathway by histone acetylation underlies neural stem cell behavior in senescence-prone SAMP8 mice.Aging cell · 2015Article
- Senescence-accelerated OXYS rats: a model of age-related cognitive decline with relevance to abnormalities in Alzheimer disease.Cell cycle (Georgetown, Tex.) · 2014Review
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Authors and funding
25 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSenescence-accelerated mice (SAM) are a series of mouse strains originally derived from unexpected crosses between AKR/J and unknown mice, from which phenotypically distinct senescence-prone (SAMP) and -resistant (SAMR) inbred strains were subsequently established. Although SAMP strains have been widely used for aging research focusing on their short life spans and various age-related phenotypes, such as immune dysfunction, osteoporosis, and brain atrophy, the responsible gene mutations have not yet been fully elucidated.
resultsTo identify mutations specific to SAMP strains, we performed whole exome sequencing of 6 SAMP and 3 SAMR strains. This analysis revealed 32,019 to 38,925 single-nucleotide variants in the coding region of each SAM strain. We detected Ogg1 p.R304W and Mbd4 p.D129N deleterious mutations in all 6 of the SAMP strains but not in the SAMR or AKR/J strains. Moreover, we extracted 31 SAMP-specific novel deleterious mutations. In all SAMP strains except SAMP8, we detected a p.R473W missense mutation in the Ldb3 gene, which has been associated with myofibrillar myopathy. In 3 SAMP strains (SAMP3, SAMP10, and SAMP11), we identified a p.R167C missense mutation in the Prx gene, in which mutations causing hereditary motor and sensory neuropathy (Dejerine-Sottas syndrome) have been identified. In SAMP6 we detected a p.S540fs frame-shift mutation in the Il4ra gene, a mutation potentially causative of ulcerative colitis and osteoporosis.
conclusionsOur data indicate that different combinations of mutations in disease-causing genes may be responsible for the various phenotypes of SAMP strains.
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