ArticleMolecular and cellular biochemistry2013
Alternative splicing of human insulin receptor gene (INSR) in type I and type II skeletal muscle fibers of patients with myotonic dystrophy type 1 and type 2.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Therapeutic advances in type 1 myotonic dystrophy complicated with type 2 diabetes mellitus.Frontiers in neurology · 2025Review
- Trends in insulin resistance: insights into mechanisms and therapeutic strategy.Signal transduction and targeted therapy · 2022Review
- Targeting Myotonic Dystrophy Type 1 with Metformin.International journal of molecular sciences · 2022Review
- Splice-switching of the insulin receptor pre-mRNA alleviates tumorigenic hallmarks in rhabdomyosarcoma.NPJ precision oncology · 2022Article
- Transcriptional signatures of synaptic vesicle genes define myotonic dystrophy type I neurodegeneration.Neuropathology and applied neurobiology · 2021Article
- Review
- Diabetes, metformin and cancer risk in myotonic dystrophy type I.International journal of cancer · 2020Article
- A CRISPR-Cas13a Based Strategy That Tracks and Degrades Toxic RNA in Myotonic Dystrophy Type 1.Frontiers in genetics · 2020Article
- High Prevalence and Gender-Related Differences of Gastrointestinal Manifestations in a Cohort of DM1 Patients: A Perspective, Cross-Sectional Study.Frontiers in neurology · 2020Article
- Endurance exercise leads to beneficial molecular and physiological effects in a mouse model of myotonic dystrophy type 1.Muscle & nerve · 2019Article
- RNA processing in skeletal muscle biology and disease.Transcription · 2019Review
- Insulin Signaling as a Key Moderator in Myotonic Dystrophy Type 1.Frontiers in neurology · 2019Review
- Article
- Integrative analysis reveals functional and regulatory roles of H3K79me2 in mediating alternative splicing.Genome medicine · 2018Article
- Myotonic Dystrophy and Developmental Regulation of RNA Processing.Comprehensive Physiology · 2018Review
- Insulin Receptor Isoforms in Physiology and Disease: An Updated View.Endocrine reviews · 2017Review
- (CCUG)Disease models & mechanisms · 2017Article
- Receptor and post-receptor abnormalities contribute to insulin resistance in myotonic dystrophy type 1 and type 2 skeletal muscle.PloS one · 2017Article
- Increased risk of tumor in DM1 is not related to exposure to common lifestyle risk factors.Journal of neurology · 2016Article
- miR-30-5p Regulates Muscle Differentiation and Alternative Splicing of Muscle-Related Genes by Targeting MBNL.International journal of molecular sciences · 2016Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
INSR, one of those genes aberrantly expressed in myotonic dystrophy type 1 (DM1) and type 2 (DM2) due to a toxic RNA effect, encodes for the insulin receptor (IR). Its expression is regulated by alternative splicing generating two isoforms: IR-A, which predominates in embryonic tissue, and IR-B, which is highly expressed in adult, insulin-responsive tissues (skeletal muscle, liver, and adipose tissue). The aberrant INSR expression detected in DM1 and DM2 muscles tissues, characterized by a relative increase of IR-A versus IR-B, was pathogenically related to the insulin resistance occurring in DM patients. To assess if differences in the aberrant splicing of INSR could underlie the distinct fiber type involvement observed in DM1 and DM2 muscle tissues, we have used laser capture microdissection (LCM) and RT-PCR, comparing the alternative splicing of INSR in type I and type II muscle fibers isolated from muscle biopsies of DM1, DM2 patients and controls. In the controls, the relative amounts of IR-A and IR-B showed no obvious differences between type I and type II fibers, as in the whole muscle tissue. In DM1 and DM2 patients, both fiber types showed a similar, relative increase of IR-A versus IR-B, as also evident in the whole muscle tissue. Our data suggest that the distinct fiber type involvement in DM1 and DM2 muscle tissues would not be related to qualitative differences in the expression of INSR. LCM can represent a powerful tool to give a better understanding of the pathogenesis of myotonic dystrophies, as well as other myopathies.
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