Overview
- Peptide CGEQHSLVPLPQEAPE, corresponding to amino acid residues 377-392 of rat NTSR2 (Accession Q63384). Intracellular, C-terminus.
- Rat and mouse brain and dorsal root ganglion lysates (1:200-1:400).
- Western blot analysis of rat dorsal root ganglion lysates:1. Anti-Neurotensin Receptor 2 Antibody (#ANT-016), (1:200).
2. Anti-Neurotensin Receptor 2 Antibody, preincubated with Neurotensin Receptor 2 Blocking Peptide (#BLP-NT016). - Western blot analysis of rat brain lysates:1. Anti-Neurotensin Receptor 2 Antibody (#ANT-016), (1:200).
2. Anti-Neurotensin Receptor 2 Antibody, preincubated with Neurotensin Receptor 2 Blocking Peptide (#BLP-NT016). - Western blot analysis of mouse brain lysates:1. Anti-Neurotensin Receptor 2 Antibody (#ANT-016), (1:400).
2. Anti-Neurotensin Receptor 2 Antibody, preincubated with Neurotensin Receptor 2 Blocking Peptide (#BLP-NT016).
- Rat dorsal root ganglion sections (frozen), (1:100) and stomach sections (paraffin embedded), (1:50).
- Paraformaldehyde-fixed rat C6 glioma cells (1:200).
Neurotensin receptor 2 (NTR2) is one of three receptors that mediate the effects of the tridecapeptide neurotensin. Neurotensin is synthesized and secreted from neurons in the central neural system (CNS) and from endocrine cells in the gastrointestinal tract.
NTR2 and NTR1 belong to the 7-transmembrane domain, G-protein coupled receptor (GPCR) superfamily while the third neurotensin receptor NTR3 (also called Sortilin) is a type I membrane protein with a large extracellular domain. Both NTR1 and NTR3 bind neurotensin with high affinity while NTR2 binds it with low affinity.1
NTR2 signals preferentially through Gaq, resulting in the activation phopholipase C and intracellular Ca2+mobilization. However, the exact signaling mechanisms subsequent to NTR2 activation appear to depend on the species and on the cellular system in which the receptor is studied.
NTR2 is expressed mainly in the central nervous system and dorsal root ganglion (DRG) neurons but has been also observed in peripheral tissues such as gastric parietal cells where it probably mediates the neurotensin-induced effects on gastric acid secretion.2
The most established physiological role of NTR2 is its role in pain transmission as NTR2-defficient mice showed that NTR2 is the likely mediator of the neurotensin-induced analgesic responses.3