These Gck knock-out mice exhibit a decreased insulin secretory response to glucose. They are suitable for use in applications related to the study of maturity-onset diabetes.
Dr. Shimon Efrat, Sackler School of Medicine
Genetic Background | Generation |
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|
Allele Type | Gene Symbol | Gene Name |
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Targeted (Null/Knockout) | Gck | glucokinase |
Glucokinase catalyzes a rate-limiting step in glucose metabolism in hepatocytes and pancreatic beta cells and is considered the "glucose sensor" for regulation of insulin secretion. Patients with maturity-onset diabetes of the young (MODY) have heterozygous point mutations in the glucokinase gene that result in reduced enzymatic activity and decreased insulin secretion. Disruption of the glucokinase gene results in a phenotype similar to MODY in heterozygous mice. These mice manifest a decreased insulin secretory response to glucose.
Allele Name | targeted mutation 1, Shimon Efrat |
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Allele Type | Targeted (Null/Knockout) |
Allele Synonym(s) | GK- |
Gene Symbol and Name | Gck, glucokinase |
Gene Synonym(s) | |
Strain of Origin | 129P2/OlaHsd |
Chromosome | 11 |
Molecular Note | A fragment of the gene spanning exon 2 was replaced by a neomycin resistance cassette, resulting in a deletion and a frame shift of the transcript. Mice heterozygous for the targeted mutation had a 37% reduction in glucose phosphorylation activity in islet homogenates and a 28% reduction of activity in liver compared with wild-type littermates. |
Mutations Made By | Dr. Shimon Efrat, Sackler School of Medicine |
When using the GK- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003316 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Heterozygous or Wild-type for Gck<tm1Efr> |
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