Tachykinin receptors are receptors that bind to the tachykinins, which are a family of structurally-related neuropeptides that derive from alternate gene processing. In mammals, the major tachykinins are substance P (SP), neurokinin A (NKA), and neurokinin B (NKB). These tachykinins interact with three neurokinin G protein-coupled receptors: NK1, NK2, and NK3. Moreover, they have exhibited a lack of selectivity to their receptors. All tachykinins interact with all the three-receptor subtypes with SP preferring NK1, NKA preferring NK2, and NKB preferring NK3. As a result, tachykinins and their receptors have been shown to elicit a broad spectrum of activities such as powerful vasodilatation, hypertensive action, and stimulation of extravascular smooth muscle, and are known to be involved in a variety of clinical conditions including chronic pain, Parkinson's disease, Alzheimer's disease, depression, rheumatoid arthritis, irritable bowel syndrome, and asthma.
Consequently, antagonists of tachykinin receptors that are selective, potent, and show efficacy in disease models have been developed to treat diseases, such as nausea and vomiting. The therapeutic potential of these receptors has been actively studied and multiple ongoing clinical trials of NKR antagonists are being undertaken. Here, we give an introduction of the currently known information about the signaling, trafficking, and properties of NKRs.
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