Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Alle Spezies anzeigen
Weitere Synonyme anzeigen
Wählen Sie die Spezies und Applikation aus
anti-Mouse (Murine) G6PC Antikörper:
anti-Human G6PC Antikörper:
anti-Rat (Rattus) G6PC Antikörper:
Sie gelangen zu unserer vorgefilterten Suche.
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
Show all 2 Pubmed References
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
Show all 2 Pubmed References
Cow (Bovine) 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
Hepatic mitochondrial dysfunction is a feature of glycogen (zeige GYS1 Antikörper) 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 (zeige GYS1 Antikörper) 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 s (zeige NOTCH1 Antikörper)how that glucose-6-phosphatase and perilipin-5 (G6PC/PLIN5) are (zeige PLIN5 Antikörper)upregulated (zeige PLIN5 Antikörper)in notch1 knockout (KO) mice.
We conclude that G6PD (zeige G6PD Antikörper) 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 Antikörper) levels could account for the induction of G6pc expression in the kidneys and intestine of L-G6pc-/- mice.
PPARalpha (zeige PPARA Antikörper) 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 Antikörper) are defective in G6pt-/- neutrophils.
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 (zeige UTS2R Antikörper) SNP rs2229611 in G6PC1 affects mRNA stability, expression and Glycogen (zeige GYS1 Antikörper) Storage Disease type-Ia risk
crystal structures of the FoxO1 (zeige FOXO1 Antikörper) DNA binding domain in complex with the G6PC1 promoter
Notch1 (zeige NOTCH1 Antikörper) expression is reduced and glucose-6-phosphatase and perilipin-5 (zeige PLIN5 Antikörper) (G6PC/PLIN5 (zeige PLIN5 Antikörper)) are upregulated in liver biopsies from nonalcoholic steatohepatitis (NASH (zeige SAMSN1 Antikörper)) and nonalcoholic fatty liver disease (NAFLD (zeige TSC2 Antikörper)) 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 Antikörper) is a crucial determinant of endogenous glucose production and is controlled by the glucose-6-phosphate transporter (zeige SLC37A4 Antikörper).
ApoA-IV (zeige APOA4 Antikörper) colocalizes with NR4A1 (zeige NR4A1 Antikörper), which suppresses G6Pase and PEPCK (zeige PEPCK Antikörper) 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