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Merck
CN

N5521

α(2→3,6) Neuraminidase from Clostridium perfringens (C. welchii)

recombinant, expressed in E. coli, buffered aqueous solution, ≥250 units/mg protein

Synonym(s):

Acyl-Neuraminyl Hydrolase, Sialidase

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About This Item

UNSPSC Code:
12352204
NACRES:
NA.32
EC Number:
3.2.1.18 (BRENDA, IUBMB)
MDL number:
MFCD01092201
Specific activity:
≥250 units/mg protein
Recombinant:
expressed in E. coli

Key Documents

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Product Name

α(2→3,6) Neuraminidase from Clostridium perfringens (C. welchii), recombinant, expressed in E. coli, buffered aqueous solution, ≥250 units/mg protein

recombinant

expressed in E. coli

form

buffered aqueous solution

specific activity

≥250 units/mg protein

mol wt

~41 kDa

foreign activity

proteases, none detected

shipped in

wet ice

storage temp.

2-8°C

Quality Level

200

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Related Categories

Biochem/physiol Actions

Releases α(2→3)- and α(2→6)-linked N-acetylneuraminic acid from complex oligosaccharides.

Other Notes

One unit will hydrolyze 1 μmole of 4-methylumbelliferyl α-D-N-acetylneuraminide per min at pH 5.0 at 37 °C

Packaging

Provided with 5× reaction buffer (250 mM sodium phosphate, pH 6.0).

Physical form

Solution in 20 mM Tris-HCl, pH 7.5, and 25 mM NaCl.

Preparation Note

Expressed in glycosidase-free hosts.

pictograms

Health hazard
GHS08

signalword

Danger

hcodes

H334

Hazard Classifications

Resp. Sens. 1

Storage Class

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

Regulatory Information

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Certificates of Analysis (COA)

Lot/Batch Number
SLCP9548
SLBR7969V
SLBP5239V
SLBP0133V
SLBM4467V

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Charles R Beck et al.
Influenza and other respiratory viruses, 7 Suppl 1, 14-24 (2013-02-12)
The objectives of this study were to: (1) reflect on key stages in the discovery, development and pre-pandemic use of neuraminidase inhibitors (NAIs), (2) summarise the evidence of NAI effectiveness for treatment and prophylaxis of seasonal influenza prior to the
Rodolfo Ocadiz-Delgado et al.
BMC infectious diseases, 13, 20-20 (2013-01-19)
In April 2009, public health surveillance detected an increased number of influenza-like illnesses in Mexico City's hospitals. The etiological agent was subsequently determined to be a spread of a worldwide novel influenza A (H1N1) triple reassortant. The purpose of the
Weijia Wang et al.
Journal of virology, 87(8), 4642-4649 (2013-02-15)
In 2009, we successfully produced a high-yield live attenuated H1N1pdm A/California/7/2009 vaccine (CA/09 LAIV) by substitution of three residues (K119E, A186D, and D222G) in the hemagglutinin (HA) protein. Since then, we have generated and evaluated additional H1N1pdm vaccine candidates from
S Bhatt et al.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 368(1614), 20120382-20120382 (2013-02-06)
Few questions on infectious disease are more important than understanding how and why avian influenza A viruses successfully emerge in mammalian populations, yet little is known about the rate and nature of the virus' genetic adaptation in new hosts. Here
Ramaiah Arunachalam et al.
Interdisciplinary sciences, computational life sciences, 4(4), 282-290 (2013-01-29)
The aim of the present investigation was to discover the genetic relationships of 2009 pandemic novel influenza A/H1N1 virus (NIV) external antigens Hemagglutinin (HA) and Neuraminidase (NA) with other influenza viruses by performing phylogenetic, comparative and statistical analyses. Phylogenetic trees
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