Glucokinase
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Glucokinase is a glucose-phosphorylating enzyme that has an important role in glucose homeostasis. Glucokinase acts as a glucose sensot of pancreatic β-cells. Glucokinase regulates the conversion of glucose to glucogen as well as gluconeogenesis. Glucokinase in mammals can phosphorylate hexoses like mannose or fructose in addition to glucose. Glucokinase can be studied in research on diabetes.
For research use only. We do not sell to patients.
- CAS No.: 9001-36-9
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
EC Number
2.7.1.2
Enzyme Activity
≥10 U/mg soild
Unit Definition
One unit is defined as the amount of enzyme that will cause the phosphorolysis of one micromole of inosine to hypoxanthine and ribose 1-phosphate per min at pH 7.7 at 37°C.
Chemical Information
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CAS No. 9001-36-9
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Appearance Solid
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Color White to off-white
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SMILES
[Glucokinase]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent & Solubility
In Vitro:
H2O : ≥ 50 mg/mL
* "≥" means soluble, but saturation unknown.
Protocols
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Human Islet Cell Culture
The method of preserving islets in vitro, with purified reduced immunogenicity. The steps are islet isolation, islet cell purification, in vitro determination of islet function and islet cell culture.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
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Data Sheet (266 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. Matschinsky F. M. (2009). Assessing the potential of glucokinase activators in diabetes therapy. Nature reviews. Drug discovery, 8(5), 399-416. [Content Brief]
[2]. Iynedjian P. B. (2009). Molecular physiology of mammalian glucokinase. Cellular and molecular life sciences : CMLS, 66(1), 27-42. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)