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COS-7 cells transiently overexpressing human ERα (left panel) or ERβ1 (right panel) were both labeled with the anti-ERα antibody followed by biotinylated secondary antibody and peroxidase-labeled avidin. The monoclonal antibody directed against ERα (clone: mAN1, Cat. no. 49-1002) is used at 15 µg⁄ml. The antibody is clearly recognizing the ERα isoform and not ERβ
|Tested species reactivity||Human|
|Published species reactivity||Human|
|Host / Isotype||Mouse / IgG3|
|Immunogen||NH2 terminus of the human estrogen receptor alpha using a peptide antigen (Q19-K32) conjugated to KLH|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|ChIP assay (ChIP)||5 ug|
|Immunohistochemistry (IHC)||Assay Dependent|
|Western Blot (WB)||7 ug/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Immunohistochemistry (IHC)||See 1 publications below|
Estrogen Receptors (ER) are members of the steroid family of nuclear receptors. There are two different forms of the estrogen receptor, alpha and beta, encoded by separate genes (ESR1 and ESR2, respectively). Each protein contains distinct functional domains required for transcriptional activation, binding to estrogen response elements (ERE) in DNA, constitutive dimerization, binding to heat shock proteins, and ligand recognition. ER is a ligand-activated transcription factor, that when bound to estrogen hormone, induces a conformational change that allows dimerization and binding to EREs. When bound to DNA, ER can positively or negatively regulate gene transcription through the recruitment of coactivator or corepressor proteins. There are several different isoforms of both ER alpha and ER beta. ER is an important regulator of growth and differentiation in the mammary gland. The presence of ER in breast tumors indicates an increased likelihood of response to anti-estrogen (e.g. tamoxifen) therapy.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Neonatal overexpression of estrogen receptor-α alters midbrain dopamine neuron development and reverses the effects of low maternal care in female offspring.
49-1002 was used in immunohistochemistry to assess the impact on maternal behavior of neonatal manipulation of ERα in females that had experienced low versus high levels of postnatal maternal licking and grooming.
|Peña CJ,Champagne FA||Developmental neurobiology (75:1114)||2015|
ER-alpha; ESR; ESR1; estradiol receptor; estrogen nuclear receptor alpha; estrogen receptor alpha E1-E2-1-2; estrogen receptor alpha E1-N2-E2-1-2; estrogen receptor alpha splice variant, CTERP-1; estrogen receptor alpha splice variant, ERalphaDup5; estrogen receptor alpha splice variant, ERalphai45a; estrogen receptor alpha splice variant, ERalphai45bL; estrogen receptor alpha splice variant, ERalphai45bS; estrogen receptor alpha splice variant, ERalphai45c; estrogen receptor alpha splice variant, ERalphai56; estrogen receptor alpha splice variant, ERalphai67; NR3A1; nuclear receptor subfamily 3 group A member 1
ER; Era; ESR; ESR1; ESRA; ESTRR; NR3A1