TACR - Tachykinin Receptor | Elisa - Clia - Antibody - Protein

Background:

Tachykinin receptors (TACR) are a family of G protein-coupled receptors (GPCRs) that mediate the effects of tachykinins, a family of neuropeptides. Tachykinins, including substance P, neurokinin A, and neurokinin B, are involved in various physiological processes, including neurotransmission, pain signaling, inflammation, and smooth muscle contraction. The primary ligands for TACRs are tachykinins, including substance P, neurokinin A, and neurokinin B. Each receptor subtype has varying affinities for different tachykinins. In summary, Tachykinin Receptors (TACRs) play important roles in neurotransmission, pain signaling, inflammation, and smooth muscle contraction. Dysregulation of TACR signaling is implicated in various diseases, including pain disorders, inflammatory diseases, neurological disorders, and gastrointestinal disorders. Therapeutic targeting of TACRs holds promise for the development of novel treatments across a range of clinical conditions.

Structural Features:

TACRs are seven-transmembrane domain receptors, typical of GPCRs, with an extracellular N-terminus and an intracellular C-terminus. They belong to the rhodopsin-like family of GPCRs.

Subtypes:

There are three known subtypes of TACRs:

• TACR1 (NK1 receptor): Preferentially binds to substance P.
• TACR2 (NK2 receptor): Preferentially binds to neurokinin A.
• TACR3 (NK3 receptor): Preferentially binds to neurokinin B.

Physiological Functions:

1.   Neurotransmission: TACRs are widely distributed in the central and peripheral nervous systems, where they modulate neurotransmitter release, neuronal excitability, and synaptic transmission.

2.   Pain Signaling: Substance P, through activation of TACR1, plays a key role in pain transmission and modulation, particularly in the transmission of nociceptive signals.

3.   Inflammation: Tachykinins contribute to the inflammatory response by promoting vasodilation, plasma extravasation, and immune cell activation through TACR activation.

4.   Smooth Muscle Contraction: Tachykinins induce smooth muscle contraction in various organs, including the respiratory, gastrointestinal, and genitourinary systems, via TACR activation.

Clinical Implications:

1.   Pain Disorders: Dysregulation of TACR signaling is implicated in various pain disorders, including migraine, neuropathic pain, and inflammatory pain conditions.

2.   Inflammatory Diseases: Tachykinins and TACRs are involved in inflammatory diseases such as asthma, rheumatoid arthritis, and inflammatory bowel disease, where they contribute to inflammation and tissue damage.

3.   Neurological Disorders: Substance P and TACR1 have been implicated in psychiatric disorders such as depression, anxiety, and schizophrenia, although their exact roles are still under investigation.

4.   Gastrointestinal Disorders: Tachykinins and TACRs play a role in gastrointestinal disorders such as irritable bowel syndrome (IBS) and gastroparesis, where they influence gastrointestinal motility and visceral sensitivity.

Therapeutic Potential:

1.   TACR Antagonists: Small molecule antagonists targeting TACRs are being investigated as potential therapeutics for pain management, inflammation, and gastrointestinal disorders.

2.   Modulators of Neurotransmission: Modulating TACR signaling could offer novel approaches for the treatment of neurological and psychiatric disorders.

3.   Anti-inflammatory Agents: Inhibiting TACR signaling may have therapeutic potential in inflammatory diseases by reducing inflammation and tissue damage.

4.   Smooth Muscle Relaxants: Modulating TACR-mediated smooth muscle contraction could lead to the development of therapeutics for disorders characterized by abnormal smooth muscle activity, such as asthma and urinary incontinence.