17-beta Estradiol antibody
ELISA
Host: Sheep
unconjugated
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- Target See all 17-beta Estradiol products
- 17-beta Estradiol
- Reactivity
- Please inquire
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Host
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Sheep
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Conjugate
- This 17-beta Estradiol antibody is un-conjugated
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Application
- ELISA
- Specificity
- It recognizes 17 beta estradiol, a mammalian estrogenic hormone, produced in the ovaries, placenta and testis that has a role in normal sexual development and the regulation of the menstrual cycle. The following cross reactivites have been observed17-beta Oestradiol 100% Oestrone 14% Oestriol 5% Aldosterone, Cortisol, Corticosterone, DHEA, Deoxycorticosterone, Pregnenolone, Progesterone, 17OH-P and Testosterone all <0.01%
- Characteristics
- Sheep Anti-17-beta-Estradiol
- Purification
- Purified
- Isotype
- IgG
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- Restrictions
- For Research Use only
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- Format
- Liquid
- Reconstitution
- Supplied as 250ul of purified antibody. It is reconstituted with 50µl of sterile PBS. Its final concentration is 5.0 mg/ml. Please avoid freeze-thaw cycles.
- Storage
- -20 °C
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- Target
- 17-beta Estradiol
- Alternative Name
- 17-beta-Estradiol (17-beta Estradiol Products)
- Target Type
- Hormone
- Background
- 17 beta Estradiol is a potent mammalian estrogenic hormone that is produced in the ovaries (by the granulosa cells), in the placenta, testis and possibly the adrenal cortex. The hormone is synthesized enzymatically from acetate, cholesterol, progesterone and testosterone. In addition to anatomic and physiological regulation of reproduction and secondary sex characteristics, it also influences activities such as bone growth, brain development and maturation and the intracellular concentrations of calcium and certain second messenger molecules. Research demonstrates salutary effects of 17 beta estradiol following trauma-hemorrhage on different cell types. 17 beta estradiol also induces improved circulation through relaxation of the aorta and has an anti-apoptotic effect on endothelial cells. 17 beta estradiol is also implicated in the attenuation of H2O2-induced apoptosis via ER-dependent activation of caspase-9 and -3 in rat endothelial cells through mitochondria.
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