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We envisage these data and models finding utility when investigating the muscle-specific functions of the 11beta-HSD1/G6PT/H6PDH triad.
Data s (Montrer NOTCH1 Kits ELISA)how that glucose-6-phosphatase and perilipin-5 (G6PC/PLIN5) are (Montrer PLIN5 Kits ELISA)upregulated (Montrer PLIN5 Kits ELISA)in notch1 knockout (KO) mice.
We conclude that G6PD (Montrer G6PD Kits ELISA) 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 (Montrer GCG Kits ELISA) levels could account for the induction of G6pc expression in the kidneys and intestine of L-G6pc-/- mice.
PPARalpha (Montrer PPARA Kits ELISA) 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 (Montrer HNF4A Kits ELISA) alpha's stimulatory effect of peroxisome proliferator-activated receptor gamma co-activator-1 (Montrer PPARGC1A Kits ELISA) 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 (Montrer CXCL2 Kits ELISA) are defective in G6pt-/- neutrophils.
G6pc expression was functionally silenced by adenovirus-mediated delivery of short hairpin RNA.
muscle expresses both Glc-6-Pase-beta and Glc-6-P transporter and that they can couple to form an active Glc-6-Pase complex
crystal structures of the FoxO1 (Montrer FOXO1 Kits ELISA) DNA binding domain in complex with the G6PC1 promoter
Notch1 (Montrer NOTCH1 Kits ELISA) expression is reduced and glucose-6-phosphatase and perilipin-5 (Montrer PLIN5 Kits ELISA) (G6PC/PLIN5 (Montrer PLIN5 Kits ELISA)) are upregulated in liver biopsies from nonalcoholic steatohepatitis (NASH (Montrer SAMSN1 Kits ELISA)) and nonalcoholic fatty liver disease (NAFLD (Montrer TSC2 Kits ELISA)) 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 (Montrer APRT Kits ELISA) is a crucial determinant of endogenous glucose production and is controlled by the glucose-6-phosphate transporter (Montrer SLC37A4 Kits ELISA).
ApoA-IV (Montrer APOA4 Kits ELISA) colocalizes with NR4A1 (Montrer NR4A1 Kits ELISA), which suppresses G6Pase and PEPCK (Montrer PEPCK Kits ELISA) 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.
Lipopolysaccharide and monophosphoryl lipid A also up-regulated G6PC and PCK1 (Montrer PCK1 Kits ELISA) transcript abundance in a TLR4 (Montrer TLR4 Kits ELISA)-dependent manner.
LSD1 (Montrer KDM1A Kits ELISA) regulates transcription activation of two gluconeogenic genes, FBP1 (Montrer FBP1 Kits ELISA) and G6Pase.
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