ArticleCirculation2009
Disruption of striated preferentially expressed gene locus leads to dilated cardiomyopathy in mice.
Article in Circulation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Human Transcriptomic Meta-Analysis Identifies Immune-Redox Remodeling and Impaired Vascular Wall Homeostasis in Abdominal Aortic Aneurysm.International journal of molecular sciences · 2026Pooled it
- Phosphorylation of RYR1 at SerScience signaling · 2025Article
- Potential compensatory mechanisms preserving cardiac function in myotubular myopathy.Cellular and molecular life sciences : CMLS · 2024Article
- Striated preferentially expressed gene deficiency leads to mitochondrial dysfunction in developing cardiomyocytes.Basic research in cardiology · 2024Article
- Dynamin-2 reduction rescues the skeletal myopathy of a SPEG-deficient mouse model.JCI insight · 2022Article
- Dilated-Left Ventricular Non-Compaction Cardiomyopathy in a Pediatric Case withInternational journal of molecular sciences · 2022Article
- Characterization of a novel zebrafish model of SPEG-related centronuclear myopathy.Disease models & mechanisms · 2022Article
- SPEG: a key regulator of cardiac calcium homeostasis.Cardiovascular research · 2021Review
- Striated Preferentially Expressed Protein Kinase (SPEG) in Muscle Development, Function, and Disease.International journal of molecular sciences · 2021Review
- Exploring Obscurin and SPEG Kinase Biology.Journal of clinical medicine · 2021Article
- Genetic variants are identified to increase risk of COVID-19 related mortality from UK Biobank data.Human genomics · 2021Article
- Striated Preferentially Expressed Protein Kinase (SPEG)-Deficient Skeletal Muscles Display Fewer Satellite Cells with Reduced Proliferation and Delayed Differentiation.The American journal of pathology · 2020Article
- Genetic variants are identified to increase risk of COVID-19 related mortality from UK Biobank data.medRxiv : the preprint server for health sciences · 2020Article
- A Novel Recessive Mutation in SPEG Causes Early Onset Dilated Cardiomyopathy.PLoS genetics · 2020Article
- Double the trouble: giant proteins with dual kinase activity in the heart.Biophysical reviews · 2020Review
- The expanding spectrum of neurological disorders of phosphoinositide metabolism.Disease models & mechanisms · 2019Review
- SPEG, an Indispensable Kinase of SERCA2a for Calcium Homeostasis.Circulation research · 2019Article
- Murine obscurin and Obsl1 have functionally redundant roles in sarcolemmal integrity, sarcoplasmic reticulum organization, and muscle metabolism.Communications biology · 2019Article
- Deciphering the evolutionary signatures of pinnipeds using novel genome sequences: The first genomes of Phoca largha, Callorhinus ursinus, and Eumetopias jubatus.Scientific reports · 2018Article
- A novel SPEG mutation causes non-compaction cardiomyopathy and neuropathy in a floppy infant with centronuclear myopathy.Acta neuropathologica communications · 2018Article
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundThe striated preferentially expressed gene (Speg) generates 4 different isoforms through alternative promoter use and tissue-specific splicing. Depending on the cell type, Speg isoforms may serve as markers of striated or smooth muscle differentiation. METHODS AND
resultsTo elucidate function of Speg gene isoforms, we disrupted the Speg gene locus in mice by replacing common exons 8, 9, and 10 with a lacZ gene. beta-Galactosidase activity was detected in cardiomyocytes of the developing heart starting at day 11.5 days post coitum (dpc). beta-Galactosidase activity in other cell types, including vascular smooth muscle cells, did not begin until 18.5 dpc. In the developing heart, protein expression of only Spegalpha and Spegbeta isoforms was present in cardiomyocytes. Homozygous Speg mutant hearts began to enlarge by 16.5 dpc, and by 18.5 dpc, they demonstrated dilation of right and left atria and ventricles. These cardiac abnormalities in the absence of Speg were associated with a cellular hypertrophic response, myofibril degeneration, and a marked decrease in cardiac function. Moreover, Speg mutant mice exhibited significant neonatal mortality, with increased death occurring by 2 days after birth.
conclusionsThese findings demonstrate that mutation of the Speg locus leads to cardiac dysfunction and a phenotype consistent with a dilated cardiomyopathy.
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