Neurotensin receptors are a type of transmembrane receptors responsible for transmitting the signaling of neurotensin. There are three subtypes: NTSR1, NTSR2, and NTSR3. NTSR1 and NTSR2 feature seven transmembrane helices and belong to GPCRs. The third receptor NTSR3, also called sortilin, has a single transmembrane domain. Every one of them is implicated in the development of several cancers, including prostate cancer, lung cancer, pancreatic cancer, and others. Consequently, identifying the contribution of neurotensin receptors in the underlying molecular mechanisms of distinct cancers could potentially encourage the development of drugs and the personalization of therapy.
Fig.1 Schematic representation of NTS oncogenic effects.1
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Our Magic™ in vitro cell-based neurotensin receptor functional assay service measures the calcium flux in cellular in response to the activation of G protein caused by neurotensin receptors reacting to their ligands. Accordingly, we can analyze the signaling pathway of neurotensin receptors, as well as examine candidate samples and their functions. To ensure global customers' projects run smoothly, we provide a full around of top-notch customized services.
Fig.2 Simplified scheme of the NTS signaling pathways involving NTSR1 and sortilin, and biological effects associated.2
Our Magic™ in vitro cell-based neurotensin receptor functional assay service breaks the limitation of conventional neurotensin receptor functional assays and has succeeded in achieving innovative developments in technology, applications, and other aspects. Simultaneously, our Magic™ in vitro cell-based neurotensin receptor functional assay service can deliver significant benefits to global customers:
Fig.3 Advantages of our Magic™ in vitro cell-based neurotensin receptor functional assay service.
DATA 1: Through this investigation, the results found that neurotensin receptor 2 (NTSR2) is a critical factor in apoptosis resistance in B-CLL. While B-CLL cells and patient plasma showed high amounts of NTSR2, modest levels of its natural ligand- neurotensin (NTS) were detected. Instead of being the product of a mutation-induced gain-of-function, NTSR2's surprisingly sustaining active phosphorylation state was the result of a collaboration with the oncogenic tyrosine kinase receptor TrkB. In contrast to NTS, B-CLL cells produce high levels of brain-derived neurotrophic factor (BDNF), making the NTSR2-TrkB interaction a conditional oncogenic driver.
Fig.4 The phosphorylation of NTSR2 in B-CLL and Giα proteins recruitment.3
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References
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