Jean-Pierre Vincent

TL;DR: Radioautographic studies of [125I-Tyr3]NT binding to rat brain tissue sections in the absence and presence of levocabastine revealed markedly different regional distributions of the two NT binding components.

TL;DR: A growing body of evidence suggests that neuropeptide binding to G protein-linked receptors may result in internalization of receptor-ligand complexes, followed by intracellular mobilization and degradation of the ligand into its target cells.

TL;DR: Investigation of the effects of neurotensin on calcium mobilization and protein kinase C (PKC) activation in HT29 cells and the role of GTP-binding proteins (G-proteins) in the neurotensIn response found that Na+ and GTP converted the high-affinity neurotens in-binding sites into lower affinity binding sites, characteristic of those receptors which interact with G- Proteins.

TL;DR: One of the primary inactivating cleavages of neurotensin by rat brain synaptic membranes occurs at the Arg8‐Arg9 peptide bond, leading to the formation of NT1‐8 and NT9‐13, and the role of a postproline dipeptidyl‐aminopeptidase is established in the secondary processing of NT 9‐13 formation.

TL;DR: Results suggest that neurotensin-induced internalization of the 50- and 60-kDa subunits initially present on the cell surface triggers insertion of the 100-k da subunit into the membrane from an intracellular compartment.