SAB4500812
Anti-Estrogen Receptor-α antibody produced in rabbit
affinity isolated antibody
Synonym(s):
ER, ESR, ESR1, ESTR, ESTRA
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 66 kDa
species reactivity
mouse, human
concentration
~1 mg/mL
technique(s)
ELISA: 1:20000
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ESR1(2099)
General description
Anti-Estrogen Receptor-α Antibody detects endogenous levels of total Estrogen Receptor-α protein.
Immunogen
The antiserum was produced against synthesized peptide derived from human Estrogen Receptor-alpha.
Immunogen Range: 91-140
Immunogen Range: 91-140
Features and Benefits
Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.
Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
nwg
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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Qiaoying Lv et al.
Cancer letters, 442, 137-147 (2018-11-14)
Continuous estrogen signaling is thought to be the main mechanism causing endometrial cancer (EC). Studies have demonstrated that CD163+ macrophages could promote the development of estrogen-dependent EC, but the mechanisms involved remain unclear. We found that CD163+ macrophages were the
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