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Key Documents

RAB1027

Sigma-Aldrich

Human CD59 ELISA Kit

for cell culture supernatants, plasma, and serum samples

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About This Item

UNSPSC Code:
41116158
NACRES:
NA.32

species reactivity

human

packaging

kit of 96 wells (12 strips x 8 wells)

technique(s)

ELISA: suitable

input

sample type cell culture supernatant(s)
sample type serum sample(s)
sample type plasma

assay range

inter-assay cv: <12%
intra-assay cv: <10%
sensitivity: 40 pg/ml

detection method

colorimetric

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... CD59(966)

General description

This ELISA antibody pair detects human CD59. Other species are not determined.

Application

For research use only. Not for use in diagnostic procedures.
Please refer to the attached Protocolfor details.

Other Notes

A sample Certificate of Analysis is available for this product. Please type the word sample in the text box provided for lot number.

pictograms

Corrosion

signalword

Warning

hcodes

Hazard Classifications

Met. Corr. 1

Storage Class

8A - Combustible corrosive hazardous materials

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Sheng-Wei Luo et al.
Fish & shellfish immunology, 89, 486-497 (2019-04-14)
CD59, a multifunctional glycoprotein, not only plays a regulatory role in complement cascades, but also participates in modulation of teleostean immunity. In this study, full length sequence of EcCD59 was obtained, comprising a 5'UTR of 163 bp, an ORF of
Yang Yie Sio et al.
Scientific reports, 10(1), 715-715 (2020-01-22)
Post-glycosylphosphatidylinositol (GPI) attachment to proteins 3, also known as PGAP3 or PERLD1 (PER1-like domain-containing protein 1), participates in the lipid remodeling process of glycosylphosphatidylinositol (GPI) anchor proteins during post-translational modification. Functional defect in PERLD1 was previously hypothesized to influence this
Diego Martínez-López et al.
Journal of the American College of Cardiology, 75(16), 1926-1941 (2020-04-25)
The mechanisms underlying early atherosclerotic plaque formation are not completely understood. Moreover, plasma biomarkers of subclinical atherosclerosis are lacking. The purpose of this study was to analyze the temporal and topologically resolved protein changes taking place in human aortas with

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