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MAS1 Receptor Antibodies

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MAS1 (non-phospho), MAS1 Receptor Antibody
MAS1 (non-phospho), MAS1 Receptor Antibody
The non-phospho-MAS1 receptor antibody is directed against the distal end of the carboxyl-terminal tail of human MAS1. It can be used to detect total MAS1 receptors in Western blots independent of phosphorylation. The MAS1 antibody can...
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MAS1, also known as the Mas receptor, is a class A G protein-coupled receptor implicated in the protective arm of the renin–angiotensin system. Angiotensin-(1–7), a peptide generated mainly by ACE2-mediated cleavage of angiotensin II, is its proposed endogenous agonist, although direct receptor activation has not been consistently reproduced across experimental systems. The nonpeptide compound AVE 0991 and the peptide antagonist A-779 are commonly used to probe Mas-dependent responses. MAS1 expression has been reported in vascular endothelium, the heart, kidneys, and brain. In vascular models, Mas-dependent signaling can increase endothelial nitric oxide production and promote vasodilation. The angiotensin-(1–7)–Mas axis has also been linked to reduced inflammation and fibrosis in preclinical models. ACE2 activity regulates the local availability of angiotensin-(1–7), while crosstalk with the angiotensin II type 1 receptor can shape the net response. Synthetic angiotensin-(1–7), known as TXA-127, has been evaluated in clinical trials, including a randomized trial in hospitalized patients with COVID-19. No selective MAS1-targeted drug is currently approved for therapeutic use. For more information on MAS1 pharmacology please refer to the IUPHAR database. For further reading refer to:

Alexander SP, Battey J, Benson HE, Benya RV, Bonner TI, Davenport AP, Dhanachandra Singh K, Eguchi S, Harmar A, Holliday N, Jensen RT, Karnik S, Kostenis E, Liew WC, Monaghan AE, Mpamhanga C, Neubig R, Pawson AJ, Pin JP, Sharman JL, Spedding M, Spindel E, Stoddart L, Storjohann L, Thomas WG, Tirupula K, Vanderheyden P. Class A Orphans in GtoPdb v.2023.1. IUPHAR/BPS Guide to Pharmacology CITE. 2023; 2023(1). Available from: https://doi.org/10.2218/gtopdb/F16/2023.1.

MAS1, also known as the Mas receptor, is a class A G protein-coupled receptor implicated in the protective arm of the renin–angiotensin system. Angiotensin-(1–7), a peptide generated mainly by... read more »
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MAS1 Receptor Antibodies

MAS1, also known as the Mas receptor, is a class A G protein-coupled receptor implicated in the protective arm of the renin–angiotensin system. Angiotensin-(1–7), a peptide generated mainly by ACE2-mediated cleavage of angiotensin II, is its proposed endogenous agonist, although direct receptor activation has not been consistently reproduced across experimental systems. The nonpeptide compound AVE 0991 and the peptide antagonist A-779 are commonly used to probe Mas-dependent responses. MAS1 expression has been reported in vascular endothelium, the heart, kidneys, and brain. In vascular models, Mas-dependent signaling can increase endothelial nitric oxide production and promote vasodilation. The angiotensin-(1–7)–Mas axis has also been linked to reduced inflammation and fibrosis in preclinical models. ACE2 activity regulates the local availability of angiotensin-(1–7), while crosstalk with the angiotensin II type 1 receptor can shape the net response. Synthetic angiotensin-(1–7), known as TXA-127, has been evaluated in clinical trials, including a randomized trial in hospitalized patients with COVID-19. No selective MAS1-targeted drug is currently approved for therapeutic use. For more information on MAS1 pharmacology please refer to the IUPHAR database. For further reading refer to:

Alexander SP, Battey J, Benson HE, Benya RV, Bonner TI, Davenport AP, Dhanachandra Singh K, Eguchi S, Harmar A, Holliday N, Jensen RT, Karnik S, Kostenis E, Liew WC, Monaghan AE, Mpamhanga C, Neubig R, Pawson AJ, Pin JP, Sharman JL, Spedding M, Spindel E, Stoddart L, Storjohann L, Thomas WG, Tirupula K, Vanderheyden P. Class A Orphans in GtoPdb v.2023.1. IUPHAR/BPS Guide to Pharmacology CITE. 2023; 2023(1). Available from: https://doi.org/10.2218/gtopdb/F16/2023.1.

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