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362280

Sigma-Aldrich

Glycoprotein Deglycosylation Kit

Synonyme(s) :

Deglycosylation kit

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About This Item

Code UNSPSC :
41116133
Nomenclature NACRES :
NA.84

Fabricant/nom de marque

Calbiochem®

Niveau de qualité

100

Conditions de stockage

do not freeze

Température de stockage

2-8°C

Description générale

Kit contains all enzymes and reagents needed to remove all N-linked, all simple O-linked, and virtually all-complex O-linked oligosaccharides from glycoproteins in a single reaction at neutral pH. Suitable for use with native or denaturation protocols, with no degradation of protein. This kit has been assembled to contain sequencing grade enzymes without azide, BSA, or glycerol. Each kit can be used to deglycosylate up to 2 mg glycoprotein.

Composants

Bovine Fetuin Control, Denaturation Solution, Endo-α-N-Acetylgalactosaminidase, β1,4-Galactosidase, Glucosaminidase, N-Glycosidase F, Neuraminidase, Reaction Buffer, TRITON™ X-100 Detergent, and a user protocol.

Avertissement

Toxicity: Multiple Toxicity Values, refer to MSDS (O)

Caractéristiques

Assay Time: 3 h-5 days

Autres remarques

Chiba, A., et al. 1997. J. Biol. Chem.272, 2156.
Jiang, M.S., and Hart, G.W. 1997. J. Biol. Chem.272, 2421.
Wilkins, P.P., et al. 1996. J. Biol. Chem.271, 18732.
Altmann, F., et al. 1995. Glycoconj. J.12, 84.
Szkudlinski, M.W., et al. 1995.
Endocrinology136, 3325.
Pahlsson, P., et al. 1994. Glycoconj. J.11, 43.
Saito, S., et al. 1994. J. Biol. Chem.269, 5644.
Tarentino, A.L., and Plummer, T.H. 1994. Methods Enzymol.230, 44.
Iwase, H., Hotta, K. 1993. Methods. Mol. Biol.14, 151.
Stults, N.L., and Cummings, R.D. 1993. Glycobiology3, 589.
Hard, K., et al. 1992. Eur. J. Biochem.205, 785.
Kuraya, N., and Hase, S. 1992. J. Biochem. (Tokyo)112, 122.
Trimble, R.B., and Tarentino, A.L. 1991. J. Biol. Chem.266, 1646.
Fukuda, M., et al. 1987. J. Biol. Chem.262, 11952.
Sojar, H.T., and Bahl, O.P. 1987. Arch. Biochem. Biophys.259, 52.
Taga, E.M., et al. 1984. Biochemistry23, 815.
Kobata, A. 1979. Anal. Biochem.100, 1.
Uchida, Y., et al. 1979. J. Biochem (Tokyo)86, 1573.
Glasgow, L.R., et al. 1977. J. Biol. Chem.252, 8615.
Spiro, R.G., and Bhoyroo, V.D. 1974. J. Biol. Chem.249, 5704.
Due to the nature of the Hazardous Materials in this shipment, additional shipping charges may be applied to your order. Certain sizes may be exempt from the additional hazardous materials shipping charges. Please contact your local sales office for more information regarding these charges.

Informations légales

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Triton is a trademark of The Dow Chemical Company or an affiliated company of Dow

Mention d'avertissement

Danger

Classification des risques

Acute Tox. 3 Dermal - Aquatic Acute 1 - Aquatic Chronic 2 - Eye Dam. 1 - Repr. 2 - Skin Irrit. 2 - Skin Sens. 1

Code de la classe de stockage

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

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A Merkx-Jacques et al.
Journal of bacteriology, 186(8), 2253-2265 (2004-04-03)
flaA1 and wbpB are conserved genes with unknown biological function in Helicobacter pylori. Since both genes are predicted to be involved in lipopolysaccharide (LPS) biosynthesis, flagellum assembly, or protein glycosylation, they could play an important role in the pathogenesis of
Christoph Mück et al.
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Tumor necrosis factor-like cytokine 1A (TL1A) is expressed in endothelial cells and contributes to T-cell activation, via an extracellular fragment TL1A(L72-L251), generated by ectodomain shedding. Fragments of TL1A, referred to as vascular endothelial growth inhibitor, were found to induce growth
Jason A Wall et al.
American journal of physiology. Heart and circulatory physiology, 291(5), H2462-H2472 (2006-06-13)
Ischemia-reperfusion (I/R) has critical consequences in the heart. Recent studies on the functions of I/R-activated kinases, such as p38 mitogen-activated protein kinase (MAPK), showed that I/R injury is reduced in the hearts of transgenic mice that overexpress the p38 MAPK
Laura E Brown et al.
The Journal of biological chemistry, 291(27), 13926-13942 (2016-04-30)
The establishment of cell-cell contacts between presynaptic GABAergic neurons and their postsynaptic targets initiates the process of GABAergic synapse formation. GABAA receptors (GABAARs), the main postsynaptic receptors for GABA, have been recently demonstrated to act as synaptogenic proteins that can
Xiaoke Yin 殷晓科 et al.
Arteriosclerosis, thrombosis, and vascular biology, 39(9), 1859-1873 (2019-07-19)
Marfan syndrome (MFS) is caused by mutations in FBN1 (fibrillin-1), an extracellular matrix (ECM) component, which is modified post-translationally by glycosylation. This study aimed to characterize the glycoproteome of the aortic ECM from patients with MFS and relate it to

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