Phospho-ESR1 (S118) Antibody

Datasheet

Code CSB-RA007830A118phHU
Size US$350
Uniprot No. P03372
Image
  • IHC image of CSB-RA007830A118phHU diluted at 1:100 and staining in paraffin-embedded human breast cancer performed on a Leica BondTM system. After dewaxing and hydration, antigen retrieval was mediated by high pressure in a citrate buffer (pH 6.0). Section was blocked with 10% normal goat serum 30min at RT. Then primary antibody (1% BSA) was incubated at 4°C overnight. The primary is detected by a biotinylated secondary antibody and visualized using an HRP conjugated SP system.

Immunogen A synthesized peptide derived from Human Phospho-ESR1 (S118)
Species Reactivity Human
Tested Applications ELISA, IHC; Recommended dilution: IHC:1:50-1:200
Relevance Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Isoform 3 is involved in activation of NOS3 and endothelial nitric oxide production. Isoforms lacking one or several functional domains are thought to modulate transcriptional activity by competitive ligand or DNA binding and/or heterodimerization with the full-length receptor. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3. Isoform 3 can bind to ERE and inhibit isoform 1.
Form Liquid
Conjugate Non-conjugated
Storage Buffer Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Purification Method Affinity-chromatography
Isotype Rabbit IgG
Clonality Monoclonal
Alias Estrogen receptor, ER, ER-alpha, Estradiol receptor, Nuclear receptor subfamily 3 group A member 1, ESR1, ESR, NR3A1
Immunogen Species Homo sapiens (Human)
Protocols ELISA Protocol
Immunohistochemistry (IHC) Protocol
Research Area Signal Transduction
Gene Names ESR1
Storage Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
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Function Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Isoform 3 is involved in activation of NOS3 and endothelial nitric oxide production. Isoforms lacking one or several functional domains are thought to modulate transcriptional activity by competitive ligand or DNA binding and/or heterodimerization with the full-length receptor. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3. Isoform 3 can bind to ERE and inhibit isoform 1.
Involvement in disease Estrogen resistance (ESTRR)
Subcellular Location Isoform 1: Nucleus, Cytoplasm, Cell membrane, Peripheral membrane protein, Cytoplasmic side, Note=A minor fraction is associated with the inner membrane, SUBCELLULAR LOCATION: Isoform 3: Nucleus, Cytoplasm, Cell membrane, Peripheral membrane protein, Cytoplasmic side, Cell membrane, Single-pass type I membrane protein, Note=Associated with the inner membrane via palmitoylation (Probable), At least a subset exists as a transmembrane protein with a N-terminal extracellular domain, SUBCELLULAR LOCATION: Nucleus, Golgi apparatus, Cell membrane
Protein Families Nuclear hormone receptor family, NR3 subfamily
Tissue Specificity Widely expressed. Isoform 3 is not expressed in the pituitary gland.
Database Links

HGNC: 3467

OMIM: 133430

KEGG: hsa:2099

STRING: 9606.ENSP00000206249

UniGene: Hs.208124

Pathway Estrogen signaling pathway

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