ArticleGenesis (New York, N.Y. : 2000)2009
Generation of mice with a conditional allele for G6pc.
Article in Genesis (New York, N.Y. : 2000), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Generation of a glycogen storage disease mouse model with fatty liver and its treatment by PPAR-α agonist bezafibrate.Frontiers in pharmacology · 2026Article
- The GCKR-P446L gene variant predisposes to raised blood cholesterol and lower blood glucose in the P446L mouse-a model for GCKR rs1260326.Molecular metabolism · 2023Article
- Gene therapy and genome editing for type I glycogen storage diseases.Frontiers in molecular medicine · 2023Review
- Yap signalling regulates ductular reactions in mice with CRISPR/Cas9-induced glycogen storage disease type Ia.Animal cells and systems · 2022Article
- Impaired Very-Low-Density Lipoprotein catabolism links hypoglycemia to hypertriglyceridemia in Glycogen Storage Disease type Ia.Journal of inherited metabolic disease · 2021Article
- Recent development and gene therapy for glycogen storage disease type Ia.Liver research (Beijing, China) · 2017Article
- Downregulation of SIRT1 signaling underlies hepatic autophagy impairment in glycogen storage disease type Ia.PLoS genetics · 2017Article
- Type I glycogen storage diseases: disorders of the glucose-6-phosphatase/glucose-6-phosphate transporter complexes.Journal of inherited metabolic disease · 2015Review
- Development of hepatocellular adenomas and carcinomas in mice with liver-specific G6Pase-α deficiency.Disease models & mechanisms · 2014Article
- Metabolic reprogramming by class I and II histone deacetylases.Trends in endocrinology and metabolism: TEM · 2013Review
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Glucose-6-phosphatase-alpha (G6Pase-alpha or G6PC) catalyzes the hydrolysis of glucose-6-phosphate to glucose and is a key enzyme in interprandial glucose homeostasis. Mutations in the human G6PC gene, expressed primarily in the liver, kidney, and intestine, cause glycogen storage disease Type Ia (GSD-Ia), an autosomal recessive disorder characterized by a disturbed glucose homeostasis. For better understanding of the roles of G6Pase-alpha in different tissues and in pathological conditions, we have generated mice harboring a conditional null allele for G6pc by flanking Exon 3 of the G6pc gene with loxP sites. We confirmed the null phenotype by using the EIIa-Cre transgenic approach to generate mice lacking Exon 3 of the G6pc gene. The resulting homozygous Cre-recombined null mice manifest a phenotype mimicking G6Pase-alpha-deficient mice and human GSD-Ia patients. This G6pc conditional null allele will be valuable to examine the consequence of tissue-specific G6Pase-alpha deficiency and the mechanisms of long-term complications in GSD-Ia.
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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.