ArticleTransgenic research2011
Disruption of the Survival Motor Neuron (SMN) gene in pigs using ssDNA.
Article in Transgenic research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 52 citations in OpenAlex.
- Growth Hormone Strongly Induces hJournal of clinical research in pediatric endocrinology · 2026Article
- Proteasome localization and activity in pig brain andFrontiers in cellular neuroscience · 2024Article
- Testing spatial working memory in pigs using an automated T-maze.Oxford open neuroscience · 2023Article
- Future of biomedical, agricultural, and biological systems research using domesticated animals.Biology of reproduction · 2022Article
- Intravenous AAV9 administration results in safe and widespread distribution of transgene in the brain of mini-pig.Frontiers in cell and developmental biology · 2022Article
- Nearly 30 Years of Animal Models to Study Amyotrophic Lateral Sclerosis: A Historical Overview and Future Perspectives.International journal of molecular sciences · 2021Review
- Comparative anatomy of the mammalian neuromuscular junction.Journal of anatomy · 2020Article
- Genome-editing technologies to improve research, reproduction, and production in pigs.Molecular reproduction and development · 2017Review
- Molecular characterization and analysis of the porcineBiochimie open · 2016Article
- Enhanced genome editing in mammalian cells with a modified dual-fluorescent surrogate system.Cellular and molecular life sciences : CMLS · 2016Article
- Genetically engineered livestock for biomedical models.Transgenic research · 2016Review
- Cloning and characterization of the porcine DBC1 gene encoding deleted in bladder cancer.Molecular biology reports · 2015Article
- Genetically modified pigs to model human diseases.Journal of applied genetics · 2014Review
- Transgenic pig carrying green fluorescent proteasomes.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Use of single stranded targeting DNA or negative selection does not further increase the efficiency of a GGTA1 promoter trap.Journal of molecular cloning & genetic recombination · 2013Article
- Genetically engineered pig models for human diseases.Annual review of animal biosciences · 2013Review
- Completion of the swine genome will simplify the production of swine as a large animal biomedical model.BMC medical genomics · 2012Article
- SMN-inducing compounds for the treatment of spinal muscular atrophy.Future medicinal chemistry · 2012Review
- Bifunctional RNAs targeting the intronic splicing silencer N1 increase SMN levels and reduce disease severity in an animal model of spinal muscular atrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Utility of survival motor neuron ELISA for spinal muscular atrophy clinical and preclinical analyses.PloS one · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Spinal Muscular Atrophy (SMA) is an autosomal recessive neurodegenerative disease that is a result of a deletion or mutation of the SMN1 (Survival Motor Neuron) gene. A duplicated and nearly identical copy, SMN2, serves as a disease modifier as increasing SMN2 copy number decreases the severity of the disease. Currently many therapeutic approaches for SMA are being developed. Therapeutic strategies aim to modulate splicing of SMN2-derived transcripts, increase SMN2 gene expression, increase neuro-protection of motor neurons, stabilize the SMN protein, replace the SMN1 gene and reconstitute the motor neuron population. It is our goal to develop a pig animal model of SMA for the development and testing of therapeutics and evaluation of toxicology. In the development of a SMA pig model, it was important to demonstrate that the human SMN2 gene would splice appropriately as the model would be based on the presence of the human SMN2 transgene. In this manuscript, we show splicing of the human SMN1 and SMN2 mini-genes in porcine cells is consistent with splicing in human cells, and we report the first genetic knockout of a gene responsible for a neurodegenerative disease in a large animal model using gene targeting with single-stranded DNA and somatic cell nuclear transfer.
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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.