Galactose 1-phosphate
Galactose 1-phosphate acts as a competitive substrate inhibitor of galactose-1-phosphate uridylyltransferase (GALT). Galactose 1-phosphate is a competitive inhibitor of Phosphoglucomutase, yet the rate at which this enzyme converts Galactose 1-phosphate to Galactose-6-phosphate is 400 times slower than the rate of converting Glucose-1-phosphate. Galactose 1-phosphate can be used in studies related to Saccharomyces cerevisiae infection and type I galactosemia.
For research use only. We do not sell to patients.
- CAS No.: 2255-14-3
- Formula: C6H13O9P
- Molecular Weight:260.14
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
IC50 & Target
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Human Endogenous Metabolite |
In Vitro
Galactose 1-phosphate acts as a competitive substrate inhibitor of Escherichia coli galactose-1-phosphate uridylyltransferase (GALT), which can displace UMP from the covalently bound UMP-GALT intermediate to form UDP-galactose[1].
Galactose 1-phosphate acts as a competitive inhibitor of Phosphoglucomutase, yet the reaction rate at which this enzyme converts Galactose 1-phosphate to galactose-6-phosphate is 400 times slower than that of glucose-1-phosphate conversion[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2255-14-3
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Molecular Weight 260.14
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Formula C6H13O9P
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SMILES
O=P(O)(O)O[C@H]1O[C@@H]([C@H](O)[C@H](O)[C@H]1O)CO
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Structure Classification
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Initial Source
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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.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. McCorvie TJ, et al. The structural and molecular biology of type I galactosemia: Enzymology of galactose 1-phosphate uridylyltransferase. IUBMB Life. 2011;63(9):694-700. [Content Brief]
[2]. de Jongh WA, et al. The roles of galactitol, galactose-1-phosphate, and phosphoglucomutase in galactose-induced toxicity in Saccharomyces cerevisiae. Biotechnol Bioeng. 2008;101(2):317-326. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)