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hepatic G6Pase-alpha deficiency causes metabolic reprogramming, leading to enhanced glycolysis and elevated hexose monophosphate shunt that along with impaired autophagy can contribute to hepatocellular adenoma/carcinoma development in glycogen (zeige GYS1 Proteine) storage disease type Ia.
We envisage these data and models finding utility when investigating the muscle-specific functions of the 11beta-HSD1/G6PT/H6PDH triad.
Data show that glucose-6-phosphatase and perilipin-5 (G6PC/PLIN5) are upregulated in notch1 knockout (KO) mice.
We conclude that G6PD (zeige G6PD Proteine) deficiency at the level of the animals in the present study may not be a risk factor for developing CSN-OT, but this remains to be verified for human subjects
The results strongly suggested that the increase of glucagon (zeige GCG Proteine) levels could account for the induction of G6pc expression in the kidneys and intestine of L-G6pc-/- mice.
PPARalpha (zeige PPARA Proteine) is responsible for glucose production through the up-regulation of hepatic G6Pase gene expression during fasting or type 2 diabetes animal models
gene transcription in H4IIE cells mediated by hepatocyte nuclear factor-4 alpha's stimulatory effect of peroxisome proliferator-activated receptor gamma co-activator-1 alpha
Evidence for the expression of the catalytic domain of hepatic glucose-6-phosphatase in pancreatic islets.
Loss of G6pt activity causes neutropenia, and local production of the chemokines KC and macrophage inflammatory protein-2 (zeige CXCL2 Proteine) are defective in G6pt-/- neutrophils.
G6pc expression was functionally silenced by adenovirus-mediated delivery of short hairpin RNA.
Microarrays revealed that G6PC mRNA was upregulated following GDNF-mediated dopaminergic differentiation of SH-SY5Y cells. Array association analysis showed three downregulated microRNAs that could possibly influence G6PC translation. Although qRT-PCR results were not significant, they did support the microarray findings with regard to trend. Western blotting also confirmed increased G6PC protein expression following GDNF
3'-UTR SNP rs2229611 in G6PC1 affects mRNA stability, expression and Glycogen (zeige GYS1 Proteine) Storage Disease type-Ia risk
crystal structures of the FoxO1 (zeige FOXO1 Proteine) DNA binding domain in complex with the G6PC1 promoter
Notch1 expression is reduced and glucose-6-phosphatase and perilipin-5 (G6PC/PLIN5) are upregulated in liver biopsies from nonalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease (NAFLD) patients.
Mutation analysis of the G6PC gene revealed that GSD Ia accounted for 11% in GSD patients with involvement of liver. Three patients were homozygous for R83C mutation. In addition, a novel stop mutation, Y85X, was identified in a patient with the typical features of GSD Ia.
Post-translational regulation of the glucose-6-phosphatase complex by cyclic AMP (zeige APRT Proteine) is a crucial determinant of endogenous glucose production and is controlled by the glucose-6-phosphate transporter (zeige SLC37A4 Proteine).
ApoA-IV (zeige APOA4 Proteine) colocalizes with NR4A1 (zeige NR4A1 Proteine), which suppresses G6Pase and PEPCK (zeige PEPCK Proteine) gene expression at the transcriptional level, reducing hepatic glucose output and lowering blood glucose.
By direct DNA sequencing, three novel G6PC variations were identified which expanded the G6PC mutation spectrum, and provided conclusive genetic evidences for the definitive diagnosis of the Chinese patients.
This study is the first to demonstrate a functional relationship between the critical gluconeogenic and glycogenolytic enzyme G6PC with the metabolic adaptations during glioblastoma invasion.
The spectrum of mutations in the G6PC gene.
Glucose-6-phosphatase (G6Pase) is a multi-subunit integral membrane protein of the endoplasmic reticulum that is composed of a catalytic subunit and transporters for G6P, inorganic phosphate, and glucose. This gene (G6PC) is one of the three glucose-6-phosphatase catalytic-subunit-encoding genes in human: G6PC, G6PC2 and G6PC3. Glucose-6-phosphatase catalyzes the hydrolysis of D-glucose 6-phosphate to D-glucose and orthophosphate and is a key enzyme in glucose homeostasis, functioning in gluconeogenesis and glycogenolysis. Mutations in this gene cause glycogen storage disease type I (GSD1). This disease, also known as von Gierke disease, is a metabolic disorder characterized by severe hypoglycemia associated with the accumulation of glycogen and fat in the liver and kidneys.
, glucose-6-phosphatase alpha
, glucose-6-phosphatase, catalytic (glycogen storage disease type I, von Gierke disease)
, glucose-6-phosphatase catalytic subunit