Uncoated Human SOST (Sclerostin) ELISA Kit (E-UNEL-H0364)

Name: Uncoated Human SOST (Sclerostin) ELISA Kit
Brand: Elabscience
SKU: E-UNEL-H0364
Price: 399.0 USD
Availability: InStock

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Uncoated Human SOST (Sclerostin) ELISA Kit - 1

All	Size	Price	Qty
	96T*5	$ 399.00	- +
	96T*15	$ 958.00	- +

Ancillary Products Available: Ancillary Reagent Kit

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Product Summary

The new series of Elabscience^® Uncoated ELISA kits contain the basic components required for the ELISA experiments. For customers who have rich experience and can establish their own ELISA system, uncoated kit is an ideal choice to save costs.

Detection Range	62.5-4000 pg/mL
Sample Volume	100 μL
Total Assay Time	24 h
Reactivity	Human
Specificity	This kit recognizes Human SOST in samples.No significant cross-reactivity or interference between Human SOST and analogues was observed
Recovery	80%-120%
Sample Type	Serum, plasma
Detection Method	Colorimetric method, ELISA, Sandwich
Assay Type	Sandwich-ELISA
Size	96T5 / 96T15
Storage	-20℃
Expiration Date	12 months

Performance

Typical data

The following data was generated by the Quality Control Department, under controlled laboratory conditions (ambient temperature: 18-25 °C, relative humidity: 35-75%) using standardized procedures (TMB reaction at 37 °C in the dark for 15 minutes, followed by termination and OD measurement). These values are provided for reference only. Actual results may vary due to differences in laboratory conditions, operator technique, and equipment. Users are required to generate a standard curve using their own experimental data.

pg/ml	OD1	OD2	Mean OD	Corrected OD
4000	2.297	2.269	2.283	2.208
2000	1.421	1.467	1.444	1.369
1000	0.763	0.791	0.777	0.702
500	0.488	0.486	0.487	0.412
250	0.260	0.272	0.266	0.191
125	0.169	0.165	0.167	0.092
62.5	0.126	0.118	0.122	0.047
0	0.073	0.077	0.075	-

Background

Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of this gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease.