567704
Sphingolipid Ceramide N-Deacylase, Pseudomonas sp.
Synonym(s):
SCDase
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About This Item
biological source
bacterial (Pseudomonas spp.)
Quality Level
form
liquid
specific activity
≥1 units/mL
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
avoid repeated freeze/thaw cycles
foreign activity
α- and β-N-acetylgalactosaminidase, α-fucosidase, α- and β-galactosidase, neuraminidases, none detected
shipped in
wet ice
storage temp.
−20°C
General description
Sphingolipid ceramide N-deacylase (SCDase) is a native sphingolipid ceramide N-deacylase from Pseudomonas species. It hydrolyzes the N-acyl linkage between fatty acids and the sphingosine base of ceramide in several sphingolipids and gangliosides. This enzyme catalyzes the condensation reaction between fatty acids and sphingosine bases and forms sphingolipids. It is also involved in transacylation reactions. SCDase is not recommended for hydrolysis of ceramide. It is also used to prepare lysoglycosphingolipids (lysoGSLs) effortlessly.
Application
Sphingolipid ceramide N-Deacylase, Pseudomonas sp. has been used as a PP2A enhancer to study its effects on phosphatase and tensin homolog (PTEN) in forkhead box O3 (FOXO3a) phosphorylation in primary CD4+ T cells.
Warning
Toxicity: Standard Handling (A)
Unit Definition
One unit is defined as the amount of enzyme that will hydrolyze 1 µmol of asialo-GM₁ per min at 37°C, pH 6.0.
Physical form
In 50 mM sodium acetate buffer, 0.1% LUBROL PX Detergent, pH 6.0.
Reconstitution
Following initial thaw, aliquot and freeze (-20°C).
Other Notes
Mitsutake, S., et al. 1997. Anal. Biochem. 247, 52.
Sueyoshi, N., et al. 1997. J. Lipid Res. 38, 1923.
Ito, M., et al. 1995. J. Biol. Chem. 270, 24370.
Sueyoshi, N., et al. 1997. J. Lipid Res. 38, 1923.
Ito, M., et al. 1995. J. Biol. Chem. 270, 24370.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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PLoS pathogens, 6(9), e1001103-e1001103 (2010-09-24)
Apoptosis in HIV-1-infected CD4+ primary T cells is triggered by the alteration of the PI3K and p53 pathways, which converge on the FOXO3a transcriptional activator. Tat alone can cause activation of FOXO3a and of its proapoptotic target genes. To understand
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