Cloning of a Human Insulin-Stimulated Protein Kinase (ISPK-1) Gene and Analysis of Coding Regions and mRNA Levels of the ISPK-1 and the Protein Phosphatase-1 Genes in Muscle From NIDDM Patients
Abstract
Complementary DNA encoding three catalytic subunits of protein phosphatase 1 (PP1α, PP1β, and PP1γ) and the insulin-stimulated protein kinase 1 (ISPK-1) was analyzed for variations in the coding regions related to insulin-resistant glycogen synthesis in skeletal muscle of 30 patients with non-insulin-dependent diabetes mellitus (NIDDM). The human ISPK-1 cDNA was cloned from T-cell leukemia and placental cDNA libraries and mapped to the short arm of the human × chromosome. Single-strand conformation polymorphism (SSCP) analysis identified a total of six variations in the coding regions of the PP1 genes: two in PP1α at codons 90 and 255; one in PP1γ at codon 67; and three in PP1γ at codons 11,269, and 273, respectively. All were, however, silent single nucleotide substitutions. SSCP analysis of the ISPK-1 gene identified one silent polymorphism at codon 266 and one amino acid variant at codon 38 (Ile→Ser). This variant was primarily found in one male NIDDM patient. This subject, however, did not exhibit an impairment of muscle insulin-stimulated glycogen synthase activation. No significant differences were found in mRNA levels in muscle of the four genes between 15 NIDDM patients and 14 healthy subjects. Our findings suggest that 1) genetic abnormalities in the coding regions of PP1α, PP1β, PP1γ, and ISPK-1 are unlikely to be frequently occurring causes of the reduced insulin-stimulated activation of the glycogen synthesis in muscle from the analyzed group of NIDDM patients; 2) the mRNA levels of PP1α, PP1β, PP1γ, and ISPK-1 are normal in muscle from the NIDDM patients; and 3) putative inherited defects in insulin-stimulated activation of muscle glycogen synthesis in patients with insulin-resistant NIDDM may be located further upstream of ISPK-1 in the insulin action cascade.
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No structural gene abnormalities in the catalytic subunit of PP1 were detected in Pima Indians with type 2 diabetes.
“No structural gene abnormalities in the catalytic subunit of PP1 were detected in Pima Indians.”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [226]
In Danish type 2 diabetic subjects, several silent nucleotide substitutions were found in the PP1 and ISPK-1 genes.
“Several silent nucleotide substitutions were found in the PP1 and ISPK-1 genes in the Danish population”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [226]
In Danish type 2 diabetic subjects, skeletal muscle mRNA levels of the PP1 and ISPK-1 genes were normal.
“the mRNA levels of both genes were normal in skeletal muscle.”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [226]
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- Authors
- Bjørbæk, C., Vik, T. A., Echwald, S. M., Yang, P.-Y., Vestergaard, H., Wang, J. P., Webb, G. C., Richmond, K., Hansen, T., Erikson, R. L., Gabor Miklos, G. L., Cohen, P. T. W., & Pedersen, O.
- Affiliations
- Novo Nordisk (Denmark) (DK)
- Indiana University School of Medicine (US)
- Harvard University (US)
- Queen Elizabeth Hospital (AU)
- The Australian National University Canberra, Australia
- University of Dundee (GB)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1995-01-01
- Volume
- 44
- Issue
- 1
- Pages
- 90-97
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2069100646
- Cited by
- 59
- References
- 0
- Citations by year
- 2023: 1 · 2018: 2 · 2017: 1 · 2015: 2 · 2014: 1 · 2013: 2
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- National Institutes of Health (5r35ca042580-14)
- National Cancer Institute (CA 42580)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-00874)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Glycogen Storage Diseases and Myoclonus
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- protein phosphatase 1, type 2 diabetes, skeletal muscle, insulin resistance, glycogen synthesis, glycogen synthase activation, silent polymorphism, X chromosome, mRNA levels, cDNA cloning
- MeSH terms
- Amino Acid Sequence, Base Sequence, Biopsy, Cloning, Molecular, Diabetes Mellitus, Type 2, Female, Gene Expression Regulation, Glycogen Synthase, Humans, Male, Middle Aged, Molecular Sequence Data, Phosphoprotein Phosphatases, Polymorphism, Genetic, RNA, Messenger, Blotting, Northern, Gene Expression Regulation, Enzymologic, Polymerase Chain Reaction, Protein Serine-Threonine Kinases, DNA, Complementary, Muscle, Skeletal, Ribosomal Protein S6 Kinases, Protein Phosphatase 1
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