Neurotensin Family Related Drug Discovery Products
Creative Biolabs has the assays you can rely on for high throughput screening, lead optimization, characterizing and discovering targets, and uncovering the complexity of disease pathways. We can offer membrane protein in vitro assay kits that save valuable laboratory time and is ideal for high throughput screening.
Membrane protein stable cell lines are widely used in many areas of biomedical research. Creative Biolabs can offer membrane protein stable cell lines to stablish in vitro models for High Throughput Screening.
Creative Biolabs offers high-quality, innovative tools to help research groups accelerate membrane protein drug discovery. They can be found by targets. If there is no product that meets your needs, please contact us.
Neurotensin (NTS) is a tridecapeptide that acts as a neurotransmitter or neuromodulator in the central nervous system (CNS). It has been linked to CNS physiology and pathology, including Parkinson's disease, schizophrenia, potent hypothermia, and opioid-independent analgesia. In the peripheral nervous system, NTS functions as a local hormone, which has a negative impact by promoting fat storage, obesity, and metabolic disorders. One of the many biological impacts of NTS is its capacity to stimulate tissue growth. This result not only points to a role for NTS in the regulation of normal tissue growth, but also raises the possibility that NTS may aid in the development of malignancies. High-affinity neurotensin receptor 1 (NTSR1) and low-affinity neurotensin receptor (NTSR2) are the two GPCRs that neurotensin principally uses to exert its effects.
Fig.1. Peptide sequence of neurotensin. (Myers, 2009)
Creative Biolabs can offer high-quality neurotensin family in vitro assays and related products to meet the needs of drug discovery:
Overview of Neurotensin Family
- NTSR1
NTSR1 plays a role as a potential prognostic biomarker or pharmaceutical target in specific cancers since it is more accountable for tumor progression. In colonic adenomas, for instance, the mutation or loss of Adenomatous Polyposis Coli (APC) frequently results in the cytosolic accumulation of β-catenin. β-catenin then translocates to the nucleus and associates with the transcription factor T cell factor (Tcf), which in turn activates NTSR1 gene transcription by binding to the functional consensus DNA binding site for Tcf in the NTSR1. Moreover, NTS stimulation increases NTSR1 expression via inhibiting glycogen synthase kinase (GSK-3β), while GSK-3β inhibition significantly increases NTSR1 mRNA expression, indicating GSK-3β, in the Wnt pathway, is thought to be responsible for the dysregulation of NTSR1 expression in colon cancer.
- NTSR2
The 410 amino acid long NTSR2 receptor has a 64% similarity to the NTSR113 receptor. Compared to NTSR1, the NTSR2 receptor has a lesser affinity for NTS. Prostatic malignancy, B cells from chronic lymphocytic leukemia (CLL), and glioma have all been documented to express NTSR2. The biofunction and underlying mechanisms of NTSR2 activation in NTS-induced cancer progression are poorly understood.
Fig.2. Simplified signaling pathway. (Ouyang, 2017)
Neurotensin Family Drug Discovery
A few oncological situations can be better understood thanks to the NTS and NTSR systems. Many tumors have elevated levels of neurotensin and NTSRs, which have been linked to every stage of cancer growth. As a result, they could serve as both diagnostic and prognostic indicators as well as possible targets for chemotherapy. To further understand the properties of NTS and NTSRs as prognostic or diagnostic markers, future research should concentrate on the widespread expression of NTS/NTSRs in various malignancies. NTS/NTSRs may potentially be thought of as therapeutic targets for therapeutic purposes.
References
- Myers, R. M.; et al. Cancer, chemistry, and the cell: molecules that interact with the neurotensin receptors. ACS chemical biology. 2009, 4(7): 503-525.
- Ouyang, Q.; et al. Oncogenic role of neurotensin and neurotensin receptors in various cancers. Clinical and Experimental Pharmacology and Physiology. 2017, 44(8): 841-846.
