Estrogen Receptor Alpha ELISA Kit (ER Alpha)

Full Name: Estrogen Receptor Alpha ELISA Kit (ER Alpha)
Reactivity: Human
Sample Type: Plasma, Tissue Homogenates, Serum, Biological Fluids
Sensitivity: 0.375 ng/ml


Estrogen receptor alpha (ER alpha) is a ligand-activated transcription factor that mediates physiological estrogenic signals to modulate diverse developmental and homeostatic processes ranging from reproductive tissue growth to bone density and cholesterol regulation. Upon estrogen binding, ERα dissociates from inhibitory heat shock proteins, dimerizes, and translocates to the nucleus where it engages estrogen response elements along DNA to activate or repress myriad target genes.

Encoded by ESR1, two isoforms of the receptor arise from alternative promoter usage and splicing to yield functionally distinct but homologous 66 kDa (full length) and 46 kDa (truncated) protein variants. ER alpha is expressed across reproductive tissues as well as bone, kidney, heart, brain, and other sites. Differential expression of ERα versus the related ERβ receptor allows tailored tissue responses to systemic estrogen fluctuations. Beyond endocrine regulation, ERα carries additional ligand-independent functions dictated by cell context.

Aberrant ER alpha signaling underlies estrogen-linked illnesses like infertility, endometriosis, and hormone-responsive cancers of the breast, uterus, and ovaries. Antiestrogen therapies to directly compete with endogenous estrogens for the ligand binding domain or indirectly decrease estrogen biosynthesis remain central to managing ERα-positive breast malignancies—which constitute the majority of cases. However, resistance frequently emerges over time. Elucidating the basis for tissue-specific ER alpha modulation promises more nuanced therapeutic opportunities. Developing selective estrogen receptor degraders and inhibitors of key cooperative transcription factor complexes also represent active areas of investigation to overcomedependence on traditional antagonists and deprivation approaches.


Human estrogen receptor alpha ELISA kit can measure concentrations of ER alpha (estrogen receptor alpha, Erα, ER-alpha, ESRESRA, estradiol receptor, nuclear receptor subfamily 3 group A member 1) present is plasma, serum, biological fluids or tissue homogenate samples.


All reagents supplied need to be stored at 2 °C – 8 °C, unopened reagents will retain reactivity until expiration date. Do not use reagents beyond this date.

  • One 96-Well Plate: Pre-coated with anti-ER Alpha antibody.
  • Standards: Lyophilized recombinant.
  • Sample/Standard Dilution Buffer.
  • Biotinylated-labelled Antibody.
  • Antibody Dilution Buffer.
  • HRP-Streptavidin Conjugate (SABC).
  • SABC Dilution Buffer.
  • TMB Substrate.
  • Wash Buffer (25x).
  • Plate Sealer.
  • Product Instructions.


For this estrogen receptor alpha ELISA kit, it is recommended that a standard curve is generated for each assay carried out.

Standard Curve: 0, 0.625, 1.25, 2.5, 5, 10, 20, 40 pg/ml.
Reactivity: Human
Sensitivity: 0.375 ng/ml
Range: 0.625 – 40 pg/ml
Principle: Sandwich, Double Antibody
Application: Research Use Only.


– Specificity: Highly specific for ER Alpha, no cross reactivity or interference between ER Alpha and analogues was detected.
– Recovery: Serum (92 – 105%), EDTA Plasma (86 – 102%), Heparin Plasma (86 – 105%).
– Linearity: Serum (91 – 103%), EDTA Plasma (83 – 91%), Heparin Plasma (83 – 99%).
– Precison Intra-Assay: CV < 8%
– Precison Inter-Assay: CV < 10%


  1. The physiological role of estrogen receptor functional domains. Essays Biochem. (2021) 65 (6): 867-875. Arao Y. and Korach K.S.
  2. 17β-Estradiol and estrogen receptor α protect right ventricular function in pulmonary hypertension via BMPR2 and apelin. J Clin Invest. (2021) 131 (6): e129433. Frump A.L., et al.
  3. Estrogen Receptors and Endometriosis. Int J Mol Sci. (2020) 21 (8): 2815. Chantalat E., et al.
  4. Roles of estrogen receptor-alpha in mediating life span: the hypothalamic deregulation hypothesis. Physiol Genomics. (2017) 49 (2): 88-95. Gouw A.M., et al.


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