Description
Neurotensin, a hypotensive peptide first isolated from the bovine hypothalamus, neurotensin acts as a neurotransmitter and neurotransmodulator in the central nervous system, and also as a
local hormone in the small intestine. Neurotensin (NT) is a tridecapeptide that was originally isolated from extracts of the bovine hypothalamus
in 1973, based on its ability to cause a visible vasodilation
in the exposed cutaneous regions of anesthetized rats.
Uses
Neurotensin is a selective, non-competitive NMDA receptor antagonist.
Definition
ChEBI: Neurotensin is a 13 amino acid peptide hormone which is found in the central nervous system and the gastrointestinal tract. It behaves as a neurotransmitter in the brain, as a hormone in the gut, and also as a neuromodulator. It is implicated in the pathophysiology of several CNS disorders (including schizophrenia, Parkinson's disease, drug abuse, pain, cancer, inflammation, eating disorders and central control of blood pressure) due to its association with a wide variety of neurotransmitter systems such as dopaminergic, sertonergic, glutamatergic, GABAergic, and cholinergic systems. It has a role as a human metabolite, a mitogen, a neurotransmitter and a vulnerary. It is a conjugate base of a neurotensin(1+).
in vitro
due to nt/ntr1 signaling potentiates expression of mir-133α, the mechanism of nt-regulated mir-133α expression and examining the role of mir-133α in intracellular ntr1 trafficking in human ncm460 colonocytes are very important. the negative transcription regulator (zinc finger e-box binding homeobox 1) is involved in nt-induced mir-133α upregulation. a binding target of mir-133α (silencing of mir-133α or overexpression of aftiphilin (aftph)) lowered ntr1 trafficking to plasma membrane in human colonocytes without affecting ntr1 internalization. aftph to early endosomes and the trans-golgi network (tgn) were localized in unstimulated human colonic epithelial cells. ntr1 localization was reduced by aftph overexpression in early endosomes. at the same time, it also increased expression of proteins related to endosomes and the tgn trafficking pathway. ntr1 expression was increased by aftph overexpression and de-acidification of intracellular vesicles. these results suggest a novel mechanism of gpcr trafficking in human colonic epithelial cells accounts for why a microrna, mir-133α regulates ntr1 trafficking through its downstream target aftph.
storage
Desiccate at -20°C
References
[1]. law ik, jensen d, bunnett nw, pothoulakis c. neurotensin-induced mir-133α expression regulates neurotensin receptor 1 recycling through its downstream target aftiphilin. sci rep. 2016 feb 23;6:22195.
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