Ask about this productRelated genes to: NTSR1 Blocking Peptide
- Gene:
- NTSR1 NIH gene
- Name:
- neurotensin receptor 1
- Previous symbol:
- -
- Synonyms:
- NTR
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-30
- Date modifiied:
- 2016-10-05
Related products to: NTSR1 Blocking Peptide
Related articles to: NTSR1 Blocking Peptide
- We investigated neurotensin receptor 1 (NTSR1) as a potential mediator of the mechanical immune barrier that contributes to T-cell exclusion. - Source: PubMed
Publication date: 2026/06/22
Wu HaomingWang YangSong JunYan BaoxiangWang ChiLiu JinpengHe DahengWeiss Heidi LRychahou PiotrBanerjee MoumitaLi JingEvers B Mark - The intricate crosstalk between the immune and endocrine systems maintains physiological homeostasis of an organism by synchronizing immune, reproductive and neuroendocrine functions. The present study employed an integrative framework combining network pharmacology, molecular docking, and in-vivo approaches to investigate the role of neurotensin (NTS) in regulating inflammatory-steroidogenic interactions. Thirty six healthy female mice were randomly assigned to six groups (n = 6/group): control, LPS (1 mg/kg bw), LPS + PD149163 (NTSR agonist; 50 μg/kg bw), LPS + PD149163 (100 μg/kg bw, Only PD149163, Only PD149163. After 32 days, plasma and ovarian samples were collected for biochemical analyses. An in-silico approach was employed to assess the potential interaction of SR48692/NTSR antagonist with the key proteins of steroidogenic pathway (CYP19A1,17 ꞵ-HSD, Progesterone receptor). Our findings indicate that LPS markedly suppresses CYP19A1 and estrogen production. Furthermore, NTSR activation using PD149163 robustly reverses LPS-driven-CYP19A1 suppression in the brain, ovary, as well as in the plasma plausibly via its potent anti-inflammatory mechanisms. The network pharmacology analysis offers innovative framework that allows for a holistic and systematic analysis of interaction between NTS-associated genes and ovarian inflammation-related targets. Molecular docking analyses support the functional relevance of NTSR signaling in steroidogenic regulation. Our results delineate the NTSR-dependent mechanism that safeguards steroidogenic pathways against inflammatory insults. Altogether, network pharmacology, molecular docking analyses, and experimental validation deepen our insights into neuro-endocrine-immune crosstalk and exhibited NTS as a compelling therapeutic target in alleviating inflammation-driven endocrine disruption. PD149163 presumably protect against the endocrinological disorders arising from inflammation-driven disruption of the HPG axis. - Source: PubMed
Publication date: 2026/06/19
Srivastava SoniaMohanty Banalata - Disruption of cation homeostasis is increasingly recognized as a driver of breast cancer (BC) progression, yet a clinically actionable gene signature that quantifies this disturbance has been lacking. This study aims to systematically explore the value of cation homeostasis-related genes in the prognosis assessment of BC through bioinformatics analysis, construct and validate a prognostic model based on these genes, and integrate immune mechanism and drug sensitivity analyses to provide novel biomarkers and potential therapeutic targets for precise prognosis evaluation and individualized treatment of BC. - Source: PubMed
Publication date: 2026/04/29
Xu MingxingYe ZhihaoHong WeiminZhu LiquanHe ChaoqiYang ZhuotaoHu JunsiQian DaMeng XuliRen Zhuozhuo - Neurotensin receptor-1 (NTSR1) is a promising target for prostate cancer imaging. This study evaluates the first-in-human NTSR1-directed radiotracer [F]-AlF-NOTA-neurotensin and compares it with [Ga]Ga-PSMA-617. - Source: PubMed
Publication date: 2026/06/17
He JiaweiWang YinzhaoTang WeiGao XiaomeiCai YiTang YongxiangHu Shuo - Targeting neurotensin receptor 1 (NTSR1), which is overexpressed in several solid malignancies, remains a promising strategy for molecular imaging. Neurotensin (NT), the endogenous ligand for NTSR1, binds to NTSR1 with subnanomolar affinity but suffers from rapid degradation due to proteolytic cleavage at the Arg-Arg, Pro-Tyr, and Tyr-Ile peptide bonds. To address this limitation, we designed a series of NT(6-13) analogs by introducing noncanonical amino acids at the Tyr position to improve receptor binding and metabolic stability. The N-terminus of the strongest binder was further modified by N-terminal acetylation to optimize pharmacokinetics. The synthesized compounds were compared against [Ga]-Ga-NT-20.3, a clinically investigated agent. Based on an competition radioligand-binding assay using PC-3 cells, Ga-SK01001 and Ga-SK01014, among the tested NT(6-13) analogs, exhibit binding affinity values in the low-nanomolar range ( < 2 nM). Ga-labeling was conducted in HEPES (2 M, pH 5.0) buffer, and the radiolabeled products were obtained in 22-60% decay-corrected radiochemical yields with >190 GBq/μmol molar activity and >95% radiochemical purity. [Ga]-Ga-SK01014 demonstrated significantly higher internalization and reduced efflux compared to [Ga]-Ga-NT-20.3 (reference tracer). In vivo PET imaging in PC-3 tumor-bearing NRG mice revealed that [Ga]-Ga-SK01014 had similar tumor uptake compared to [Ga]-Ga-NT-20.3 (10.0 ± 2.48 vs 9.43 ± 0.73%ID/g at 1 h postinjection), while demonstrating a marked reduction in renal accumulation (2.88 ± 0.64 vs 9.65 ± 1.15%ID/g, < 0.01). Receptor specificity was validated by blocking studies, which resulted in a 92.7% reduction in tumor uptake. Notably, despite exhibiting lower plasma stability at 15 min postinjection (34.0 ± 5.5% intact for [Ga]-Ga-SK01014 vs 64.1 ± 5.9% for [Ga]-Ga-NT-20.3), [Ga]-Ga-SK01014 maintained efficient tumor targeting. This suggests that, in addition to metabolic stability, both early receptor engagement and rapid internalization also play a critical role in determining tumor uptake. Overall, this study identifies [Ga]-Ga-SK01014 as a promising NTSR1-targeted imaging agent with improved renal clearance and provides insight into the balance between stability and receptor-driven tumor uptake, guiding the future design of neurotensin-based theranostic agents. - Source: PubMed
Publication date: 2026/04/29
Kaur SimranjeetMair StefanLau Wing SumZeisler JuttaBénard FrançoisLin Kuo-ShyanLau Joseph