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N5521

Sigma-Aldrich

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

Enzyme Commission number:
3.2.1.18 (BRENDA, IUBMB)
MDL number:
MFCD01092201
UNSPSC Code:
12352204
NACRES:
NA.32

recombinant

expressed in E. coli

Quality Level

200

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

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Related Categories

Biochem/physiol Actions

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

Packaging

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

Unit Definition

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

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

Signal Word

Danger

Hazard Statements

H334

Precautionary Statements

P261 - P284 - P501

Hazard Classifications

Resp. Sens. 1

Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

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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
Andrew T Pavia
Infectious disease clinics of North America, 27(1), 157-175 (2013-02-13)
Respiratory viruses have long been appreciated as a cause of community acquired pneumonia (CAP), particularly among children, people with serious medical comorbidities, and military recruits. They are increasingly recognized as a cause of CAP among adults. Polymerase chain reaction-based testing
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