Recombinant Human Glucose-6-phosphatase (G6PC), partial

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Code CSB-YP009118HU1
MSDS
Size $436
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Purity
Greater than 85% as determined by SDS-PAGE.
Target Names
G6PC1
Uniprot No.
Research Area
Cancer
Alternative Names
(Glucose-6-phosphatase)(G-6-Pase)(G6Pase)(Glucose-6-phosphatase alpha)(G6Pase-alpha)
Species
Homo sapiens (Human)
Source
Yeast
Expression Region
82-117aa
Target Protein Sequence
QRPYWWVLDTDYYSNTSVPLIKQFPVTCETGPGSPS
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
5.6 kDa
Protein Length
Partial
Tag Info
C-terminal 6xHis-tagged
Form
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.
Description

The production process of the recombinant human glucose-6-phosphatase (G6PC) involves fusing a gene fragment encoding amino acids 82 to 117 of the human G6PC protein with a C-terminal 6xHis-tag. This fusion construct is then inserted into a suitable expression vector. Subsequently, the recombinant vector is introduced into the yeast expression system to facilitate the expression of the desired recombinant human G6PC protein. Following successful expression, the recombinant G6PC protein is extracted and purified from the yeast cell lysate. Its purity, determined by SDS-PAGE analysis, is confirmed to be above 85%.

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Target Background

Function
Hydrolyzes glucose-6-phosphate to glucose in the endoplasmic reticulum. Forms with the glucose-6-phosphate transporter (SLC37A4/G6PT) the complex responsible for glucose production in the terminal step of glycogenolysis and gluconeogenesis. Hence, it is the key enzyme in homeostatic regulation of blood glucose levels.
Gene References into Functions
  1. 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 PMID: 28829278
  2. 3'-UTR SNP rs2229611 in G6PC1 affects mRNA stability, expression and Glycogen Storage Disease type-Ia risk PMID: 28502559
  3. crystal structures of the FoxO1 DNA binding domain in complex with the G6PC1 promoter PMID: 28223045
  4. 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. PMID: 27428080
  5. 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. PMID: 28360385
  6. 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. PMID: 26958868
  7. ApoA-IV colocalizes with NR4A1, which suppresses G6Pase and PEPCK gene expression at the transcriptional level, reducing hepatic glucose output and lowering blood glucose. PMID: 26556724
  8. 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. PMID: 24980439
  9. 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. PMID: 25001192
  10. The spectrum of mutations in the G6PC gene. PMID: 24355556
  11. Lipopolysaccharide and monophosphoryl lipid A also up-regulated G6PC and PCK1 transcript abundance in a TLR4-dependent manner. PMID: 23465595
  12. 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. PMID: 21983240
  13. 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 PMID: 21733854
  14. data mitigate against G6PD deficiency contributing to stroke risk in individuals with sickle cell anemia. PMID: 21328436
  15. description of G6PC mutations in Thailand patients with glycogen storage disease type Ia PMID: 19832742
  16. 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 PMID: 11739393
  17. active site of G6Pase: role of HIS176 as the nucleophile forming the phosphohistidine-enzyme intermediate during catalysis PMID: 12093795
  18. 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 PMID: 12373566
  19. The amino-terminal domain of G6PT is required for optimal glucose-6-phosphate uptake activity. PMID: 12444104
  20. maximum repression of basal glucose-6-phosphatase catalytic subunit (G6Pase) gene transcription by insulin requires two distinct promoter regions, designated that together form an insulin response unit. PMID: 12556524
  21. Five mutants lack microsomal G6P uptake activity and one retains residual activity, suggesting that in G6PT the signature motif is a functional element required for microsomal glucose-6-phosphate transport. PMID: 12560945
  22. a novel, widely expressed G6Pase-related protein, PAP2.8/UGRP, renamed here G6Pase-beta couples with the G6P transporter to form an active G6Pase complex that can hydrolyze G6P to glucose PMID: 13129915
  23. Glc-6-Pase-alpha and Glc-6-Pase-beta share a similar active site structure, topology, and mechanism of action PMID: 14718531
  24. G6pc expression was functionally silenced by adenovirus-mediated delivery of short hairpin RNA. PMID: 14759518
  25. Findings suggest that the screening for 727G-->T and R83H mutations of glucose-6-phosphatase gene in conjunction with the 1176 polymorphism linkage analysis is a good method for gene and prenatal diagnosis of glycogen storage disease Ia. PMID: 15696478
  26. HNF4alpha, CREM, HNF1alpha, and C/EBPalpha have roles in transcriptional regulation of the glucose-6-phosphatase gene by cAMP/vasoactive intestinal peptide in the intestine PMID: 16893891
  27. G6PC1 hepatic activity was abnormally low in 98 SIDS (preterm, n=13; term, n=85), and non-SIDS preterm infants (n=35) compared to term non-SIDS infants (n=29) and adults (n=9) PMID: 17354259
  28. analysis of mutation spectrum of glycogen storage disease type Ia in Tunisia PMID: 18008183
  29. summary of the reported G6PC mutations and review what mutagenesis studies have revealed about the structure and function of the G6PC catalytic unit [review] PMID: 18449899
  30. EGF also inhibits hepatic G6Pase gene expression in vivo PMID: 18847435
  31. Identification of a risk conferring single nucleotide polymorphism in G6PC for type 2 diabetes in a Chinese population. PMID: 19082990
  32. Increased transcriptional expression of PEPCK1 and G6Pc does not account for increased gluconeogenesis and fasting hyperglycemia in patients with type 2 diabetes mellitus. PMID: 19587243

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Involvement in disease
Glycogen storage disease 1A (GSD1A)
Subcellular Location
Endoplasmic reticulum membrane; Multi-pass membrane protein.
Protein Families
Glucose-6-phosphatase family
Database Links

HGNC: 4056

OMIM: 232200

KEGG: hsa:2538

STRING: 9606.ENSP00000253801

UniGene: Hs.212293

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