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anti-Mouse (Murine) G6PC Antikörper:
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Mouse (Murine) Polyclonal G6PC Primary Antibody für WB - ABIN4894612
Tao, Zhang, Zeng, Shulman, Jin: Niclosamide ethanolamine-induced mild mitochondrial uncoupling improves diabetic symptoms in mice. in Nature medicine 2014
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Cow (Bovine) Polyclonal G6PC Primary Antibody für WB - ABIN2781769
Wang, Zhang, Luo, Jiang, Zhang, Guo, Zhao, Zhu, Zhang, Yang, Li: Hepatocyte TRAF3 promotes liver steatosis and systemic insulin resistance through targeting TAK1-dependent signalling. in Nature communications 2016
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Human Polyclonal G6PC Primary Antibody für IHC, WB - ABIN2781770
Iwasa, Kobayashi, Mifuji-Moroka, Hara, Miyachi, Sugimoto, Tanaka, Fujita, Gabazza, Takei: Branched-chain amino acid supplementation reduces oxidative stress and prolongs survival in rats with advanced liver cirrhosis. in PLoS ONE 2013
The results reveal a previously unrecognized physiological function of NFYA in controlling glucose metabolism by up-regulating the gluconeogenic genes Pck1 and G6pc.
Hepatic mitochondrial dysfunction is a feature of glycogen storage disease type Ia with glucose-6-phosphatase deficiency.
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 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 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 levels could account for the induction of G6pc expression in the kidneys and intestine of L-G6pc-/- mice.
PPARalpha 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 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
Brain contains a functional glucose-6-phosphatase complex capable of endogenous glucose production.
Hippel Lindau tumor suppressor regulates hepatic glucose metabolism by controlling expression of glucose transporter 2 and glucose 6-phosphatase
HNF-4 and Foxo1 are required for reciprocal transcriptional regulation of glucokinase and glucose-6-phosphatase genes in response to fasting and feeding
EGF also inhibits hepatic G6Pase gene expression in vivo
study identified SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling expression of hepatic G6Pase; SRC-2 modulates G6Pase expression by acting as a coactivator with the orphan nuclear receptor RORalpha
The neutropenia in patients with G6PC3 or G6PT mutations is a metabolite-repair deficiency.
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 Storage Disease type-Ia risk
crystal structures of the FoxO1 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 is a crucial determinant of endogenous glucose production and is controlled by the glucose-6-phosphate transporter.
ApoA-IV colocalizes with NR4A1, which suppresses G6Pase and PEPCK 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 transcript abundance in a TLR4-dependent manner.
LSD1 regulates transcription activation of two gluconeogenic genes, FBP1 and G6Pase.
Both GSD-1a and G6PT strongly colocalised in perinuclear membranes. showed that GSD1 mutations did neither alter the G6PC or G6PT chimera localisation, nor the interaction between G6PT termini.
results reveal a novel link between glucose metabolism and the DNA damage signaling pathway and suggest a possible role for PEPCK and G6P in the DNA damage response
data mitigate against G6PD deficiency contributing to stroke risk in individuals with sickle cell anemia.
description of G6PC mutations in Thailand patients with glycogen storage disease type Ia
we report the results of structure and function studies of the 48 missense mutations and the DeltaF327 codon deletion mutation, grouped as active site, helical, and nonhelical mutations
active site of G6Pase: role of HIS176 as the nucleophile forming the phosphohistidine-enzyme intermediate during catalysis
homozygosity for one G6PC mutation, G188R, seems to be associated with a glycogen storage disease type I non-a phenotype and homozygosity for the 727G>T mutation may be associated with a milder phenotype but an increased risk for hepatocellular carcinoma
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