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Neurotensin的可视化放大

Neurotensin

A neuropeptide with diverse biological activities

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  • 货号: ajci16956
  • CAS: 39379-15-2
  • 别名: 神经降压素
  • 分子式: C78H121N21O20
  • 分子量: 1672.94
  • 纯度: >98%
  • 溶解度: Soluble to 0.70 mg/ml in sterile water
  • 储存: Desiccate at -20°C
  • 库存: 现货

Background

IC50: N/A


Neurotensin (NT) can activate the G protein-coupled receptor, the neurotensin receptor 1 (NTR1). NT, a 13-amino acid neuropeptide, expressed in the central nervous system, and the intestine, including ileum3 and colon.


Neurotensin receptor 1 (NTR1) is a G protein-coupled receptor (neurotensin, NT) with high affinity.


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.


In vivo: So far, no study in vivo has been conducted.


Clinical trial: So far, no clinical study has been conducted.

Reference:
[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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