Overview
- Peptide KKTVYDEMDKNRC, corresponding to amino acid residues 329 - 341 of rat EDNRA (Accession P26684). Extracellular, 3rd loop.
Endothelin Receptor A (extracellular) Blocking Peptide (#BLP-ER004)
Western blot analysis of mouse brain lysate (lanes 1 and 3) and rat brain lysate (lanes 2 and 4):1-2. Anti-Endothelin Receptor A (extracellular) Antibody (#AER-004), (1:200).
3-4. Anti-Endothelin Receptor A (extracellular) Antibody (#AER-004), preincubated with Endothelin Receptor A (extracellular) Blocking Peptide (BLP-ER004).
Western blot analysis of mouse lung lysate:1. Anti-Endothelin Receptor A (extracellular) Antibody (#AER-004), (1:200).
2. Anti-Endothelin Receptor A (extracellular) Antibody (#AER-004), preincubated with Endothelin Receptor A (extracellular) Blocking Peptide (BLP-ER004).
Western blot analysis of human HUVEC endothelial cell line lysate (lanes 1 and 4), human SH-SY5Y neuroblastoma cell line lysate (lanes 2 and 5) and human U-87 MG glioblastoma cell line lysate (lanes 3 and 6):1-3. Anti-Endothelin Receptor A (extracellular) Antibody (#AER-004), (1:400).
4-6. Anti-Endothelin Receptor A (extracellular) Antibody (#AER-004), preincubated with Endothelin Receptor A (extracellular) Blocking Peptide (BLP-ER004).
The endothelin system is comprised of three active peptides, ET-1, 2, and 3, which are considered to be very powerful vasoconstrictive substances. In humans, endothelins mediate their actions via two specific G-Protein Coupled Receptors, ETAR and ETBR. Both ETAR and ETBR are present in heart and in human myocardium at similar levels.1,2
The endothelin receptors differ in their ligand specificity. While ETAR has varying affinities for the endothelin isoforms (ET-1 >ET-2>ET-3), ETBR shows no selective affinity.2,3 Subsequent studies have demonstrated the presence of endothelins in vascular as well as in non-vascular cells and tissues, having multiple biological activities.
Currently, there is increasing evidence that ET-1 may modulate mitogenesis, apoptosis, angiogenesis tumor invasion and the development of metastases.3
Overexpression of ET-1 and ETAR was reported in different malignancies including prostate cancer human Kaposi’s sarcoma, ovarian and breast carcinomas.4
In breast carcinomas overexpression of ET-1 and ETA receptors correlated with parameters that characterize aggressive types of breast cancer suggesting that analysis of ETAR expression might be used as a diagnostic marker for evaluating the progression of the disease and effectiveness of treatment. These and other findings have made ET receptors, and especially ETAR, promising therapeutic targets for pharmacological intervention.5-9
