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Ni-NTA His•Bind® Resin

Synonym(s):

nickel affinity gel, nickel charged agarose

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About This Item

UNSPSC Code:
41106500
NACRES:
NA.56

form

slurry

Quality Level

400

manufacturer/tradename

Novagen®

storage condition

do not freeze

application(s)

life science and biopharma

shipped in

ambient

storage temp.

2-8°C

General description

Ni-NTA His•Bind Resin is a high-performance Ni2+-charged agarose used for rapid one-step purification of proteins containing a His•Tag sequence by metal chelation chromatography. NTA chemistry minimizes metal leaching during purification and is compatible with up to 10 mM β-mercaptoethanol or 1 mM Tris(hydroxypropyl)phosphine (THP) for reduction of disulfide bonds. Ni-NTA His•Bind Resin has a binding capacity of 5–10 mg His•Tag fusion protein per ml resin.

Supplied as a 50% slurry; the quantity/pack is based on the amount of the settled resin.

Warning

Toxicity: Flammable (J)

Other Notes

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.

Legal Information

HIS-BIND is a registered trademark of Merck KGaA, Darmstadt, Germany
NOVAGEN is a registered trademark of Merck KGaA, Darmstadt, Germany

pictograms

Flame
GHS02

signalword

Danger

hcodes

H225

Hazard Classifications

Flam. Liq. 2

Storage Class

3 - Flammable liquids

wgk_germany

WGK 1

Certificates of Analysis (COA)

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Deposition of H2A.Z in chromatin is known to be mediated by a conserved SWR1 chromatin-remodeling complex in eukaryotes. However, little is known about whether and how the SWR1 complex cooperates with other chromatin regulators. Using immunoprecipitation followed by mass spectrometry
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Rapid synthesis and release of active antimicrobial peptides (AMPs) is an important strategy in innate immune. Processing of the precursor into the active form is a common posttranslational modification of AMPs in mammals. However, in invertebrates, the mechanism of AMP

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