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GPR37L1 Receptor Antibodies

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GPR37L1 (non-phospho), G protein-coupled Receptor 37L1 Antibody
GPR37L1 (non-phospho), G protein-coupled...
The non-phospho-GPR37L1 receptor antibody is directed against the distal end of the carboxyl-terminal tail of human GPR37L1. It can be used to detect total GPR37L1 receptors in Western blots independent of phosphorylation. The GPR37L1...
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GPR37L1 is an orphan class A G protein-coupled receptor that is closely related to GPR37 and is predominantly expressed in the central nervous system. Its expression is particularly enriched in glial cells, including astrocytes, Bergmann glia of the cerebellum and oligodendrocyte-lineage cells, with additional expression reported in neural progenitor cells. GPR37L1 has also been detected at low levels in peripheral tissues, including the heart and gastrointestinal tract, although its physiological relevance outside the CNS remains uncertain. The receptor is still considered pharmacologically orphan, and no endogenous ligand has been conclusively established. Prosaposin and its peptide fragment prosaptide have been proposed as ligands for GPR37L1, but these interactions have not been sufficiently validated and are not currently accepted as definitive receptor pharmacology. More recently, maresin-1 (MaR1), a specialized pro-resolving lipid mediator, has been proposed as a functional GPR37L1 ligand involved in glioprotective and analgesic signaling, although this pharmacology also requires further independent validation. Functionally, GPR37L1 appears to regulate glial physiology, neuronal homeostasis and neuroprotection, and genetic studies indicate an important role in cerebellar development and central cardiovascular regulation. GPR37L1-deficient animals develop increased blood pressure and cardiac hypertrophy, suggesting that the receptor may represent a novel target for hypertension and cardiovascular disease. At present, no approved drug or selective clinical-stage small-molecule agonist or antagonist for GPR37L1 is available, making it an attractive but still poorly characterized target for CNS, inflammatory and cardiovascular drug discovery. For more information on GPR37L1 pharmacology please refer to the IUPHAR database. For further reading refer to:

Davenport AP, Alexander SP, Sharman JL, Pawson AJ, Benson HE, Monaghan AE, Liew WC, Mpamhanga CP, Bonner TI, Neubig RR, Pin JP, Spedding M, Harmar AJ. International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands. Pharmacol Rev. 2013 May 17;65(3):967-86. doi: 10.1124/pr.112.007179. PMID: 23686350; PMCID: PMC3698937.

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.

GPR37L1 is an orphan class A G protein-coupled receptor that is closely related to GPR37 and is predominantly expressed in the central nervous system. Its expression is particularly enriched in... read more »
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GPR37L1 Receptor Antibodies

GPR37L1 is an orphan class A G protein-coupled receptor that is closely related to GPR37 and is predominantly expressed in the central nervous system. Its expression is particularly enriched in glial cells, including astrocytes, Bergmann glia of the cerebellum and oligodendrocyte-lineage cells, with additional expression reported in neural progenitor cells. GPR37L1 has also been detected at low levels in peripheral tissues, including the heart and gastrointestinal tract, although its physiological relevance outside the CNS remains uncertain. The receptor is still considered pharmacologically orphan, and no endogenous ligand has been conclusively established. Prosaposin and its peptide fragment prosaptide have been proposed as ligands for GPR37L1, but these interactions have not been sufficiently validated and are not currently accepted as definitive receptor pharmacology. More recently, maresin-1 (MaR1), a specialized pro-resolving lipid mediator, has been proposed as a functional GPR37L1 ligand involved in glioprotective and analgesic signaling, although this pharmacology also requires further independent validation. Functionally, GPR37L1 appears to regulate glial physiology, neuronal homeostasis and neuroprotection, and genetic studies indicate an important role in cerebellar development and central cardiovascular regulation. GPR37L1-deficient animals develop increased blood pressure and cardiac hypertrophy, suggesting that the receptor may represent a novel target for hypertension and cardiovascular disease. At present, no approved drug or selective clinical-stage small-molecule agonist or antagonist for GPR37L1 is available, making it an attractive but still poorly characterized target for CNS, inflammatory and cardiovascular drug discovery. For more information on GPR37L1 pharmacology please refer to the IUPHAR database. For further reading refer to:

Davenport AP, Alexander SP, Sharman JL, Pawson AJ, Benson HE, Monaghan AE, Liew WC, Mpamhanga CP, Bonner TI, Neubig RR, Pin JP, Spedding M, Harmar AJ. International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands. Pharmacol Rev. 2013 May 17;65(3):967-86. doi: 10.1124/pr.112.007179. PMID: 23686350; PMCID: PMC3698937.

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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