Endothelin-2 (1-31) ELISA Kit (DEIA6191)

Regulatory status: For research use only, not for use in diagnostic procedures.

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serum, EDTA-plasma, cell culture media supernatant, tissues extracts
Species Reactivity
Intended Use
The ET-2 (1-31) EIA Kit is a complete kit for the quantitative determination of ET-2 (1-31) in serum, EDTA-plasma, supernatant of cell culture media and extract from tissue.
Contents of Kit
1. Precoated plate: Anti-ET-225-31 Rabbit IgG Affinity Purify. 96 Wells x 1
2. Labeled antibody: HRP conjugated Anti- ET-2 Rabbit IgG Fab' Affinity Purify. 10.5 mL x 1
3. EIA buffer: 1% BSA, 0.05% Tween 20 in PBS. 30 mL x 1
4. Standard: ET-2 (1-31). 0.5 mL x 1
5. Stop solution: 1N H2SO4. 11 mL x 1
6. Chromogen: TMB solution. 15 mL x 1
7. Wash buffer Conc.: 0.05% Tween 20 in phosphate buffer (X40). 50 mL x 1
8. Solution for Labeled antibody: 1% BSA, 0.05% Tween 20 in PBS. 10.5 mL x 1
Storage Condition: 2-8°C. For more detailed information, please download the following document on our website.
Detection Range
3.91-500 pg/mL


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Granulosa cell endothelin-2 expression is fundamental for ovulatory follicle rupture


Authors: Cacioppo, Joseph A.; Lin, Po-Ching Patrick; Hannon, Patrick R.; McDougle, Daniel R.; Gal, Arnon; Ko, CheMyong

Ovulation is dependent upon numerous factors mediating follicular growth, vascularization, and ultimately oocyte release via follicle rupture. Endothelin-2 (EDN2) is a potent vasoconstrictor that is transiently produced prior to follicle rupture by granulosa cells of periovulatory follicles and induces ovarian contraction. To determine the role of Edn2 expression, surgical transplant and novel conditional knockout mice were super-ovulated and analyzed. Conditional knockout mice utilized a new iCre driven by the Esr2 promoter to selectively remove Edn2. Follicle rupture and fertility were significantly impaired in the absence of ovarian Edn2 expression. When ovaries of Edn2KO mice were transplanted in wild type recipients, significantly more corpora lutea containing un-ovulated oocytes were present after hormonal stimulation (1.0 vs. 5.4, p = 0.010). Following selective ablation of Edn2 in granulosa cells, Esr2-Edn2KO dams had reduced oocytes ovulated (3.8 vs. 16.4 oocytes/ovary) and smaller litters (4.29 +/- 1. 02 vs. 8.50 pups/dam). However, the number of pregnancies per pairing was not different and the reproductive axis remained intact. Esr2-Edn2KO ovaries had a higher percentage of antral follicles and fewer corpora lutea; follicles progressed to the antral stage but many were unable to rupture. Conditional loss of endothelin receptor A in granulosa cells also decreased ovulation but did not affect fecundity. These data demonstrate that EDN2-induced intraovarian contraction is a critical trigger of normal ovulation and subsequent fecundity.

A putative silencer variant in a spontaneous canine model of retinitis pigmentosa


Authors: Kaukonen, Maria; Quintero, Ileana B.; Mukarram, Abdul Kadir; Hytonen, Marjo K.; Holopainen, Saila; Wickstrom, Kaisa; Kyostila, Kaisa; Arumilli, Meharji; Jalomaki, Sari; Daub, Carsten O.; Kere, Juha; Lohi, Hannes

Author summary Retinitis pigmentosa (RP) is a blinding eye disease that affects nearly two million people worldwide. Several genes and variants have been associated with the disease, but still 30-80% of the patients lack genetic diagnosis. There is currently no standard treatment for RP, and much is expected from gene therapy. A similar disease, called progressive retinal atrophy (PRA), affects many dog breeds. We performed clinical, genetic and functional analyses to find the genetic cause for PRA in Miniature Schnauzers. We discovered two forms of PRA in the breed, named type 1 and 2, and show that they are genetically distinct as they map to different chromosomes, 15 and X, respectively. Further genetic, bioinformatic and functional analyses discovered a fully penetrant recessive variant in a putative silencer region for type 1 PRA. Silencer regions are important for gene regulation and we found that two of its predicted target genes, EDN2 and COL9A2, were overexpressed in the retina of the affected dog. Defects in both EDN2 and COL9A2 have been associated with retinal degeneration. This study provides new insights to retinal biology while the genetic test guides better breeding choices. Retinitis pigmentosa (RP) is the leading cause of blindness with nearly two million people affected worldwide. Many genes have been implicated in RP, yet in 30-80% of the RP patients the genetic cause remains unknown. A similar phenotype, progressive retinal atrophy (PRA), affects many dog breeds including the Miniature Schnauzer. We performed clinical, genetic and functional experiments to identify the genetic cause of PRA in the breed. The age of onset and pattern of disease progression suggested that at least two forms of PRA, types 1 and 2 respectively, affect the breed, which was confirmed by genome-wide association study that implicated two distinct genomic loci in chromosomes 15 and X, respectively. Whole-genome sequencing revealed a fully segregating recessive regulatory variant in type 1 PRA. The associated variant has a very recent origin based on haplotype analysis and lies within a regulatory site with the predicted binding site of HAND1::TCF3 transcription factor complex. Luciferase assays suggested that mutated regulatory sequence increases expression. Case-control retinal expression comparison of six best HAND1::TCF3 target genes were analyzed with quantitative reverse-transcriptase PCR assay and indicated overexpression of EDN2 and COL9A2 in the affected retina. Defects in both EDN2 and COL9A2 have been previously associated with retinal degeneration. In summary, our study describes two genetically different forms of PRA and identifies a fully penetrant variant in type 1 form with a possible regulatory effect. This would be among the first reports of a regulatory variant in retinal degeneration in any species, and establishes a new spontaneous dog model to improve our understanding of retinal biology and gene regulation while the affected breed will benefit from a reliable genetic testing.

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