Trpm5 Protein is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
TRPM5 is a calcium-activated cation channel essential for taste transduction. It is required for sweet, bitter, and umami taste signaling. TRPM5 is also expressed in pancreatic beta-cells and regulates insulin secretion.
TRPM5 Protein is encoded by the TRPM5 gene. It is a Transient receptor potential melastatin 5. The UniProt ID is Q9Z5S6.
- Molecular Weight: 116 kDa
- Localization: Plasma membrane, Taste buds
- PDB Structures: 5W5V
TRPM5 is a calcium-activated cation channel essential for taste transduction. It is required for sweet, bitter, and umami taste signaling. TRPM5 is also expressed in pancreatic beta-cells and regulates insulin secretion.
The protein is expressed in Plasma membrane, Taste buds and plays important roles in cellular physiology.
TRPM5 dysfunction may contribute to metabolic disorders including diabetes.
TRPM5 modulators are being investigated for metabolic diseases.
The study of Trpm5 Protein has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- Protein function in neurodegeneration: Przedborski S, et al. Ann Neurol. 2003;53(4):429-448. PMID:12666111
- Molecular mechanisms of neurodegeneration: Winklhofer KF, Haass C. Nat Rev Neurol. 2010;6(9):463-477. PMID:20740084
- Protein aggregation in disease: Chiti F, Dobson CM. Annu Rev Biochem. 2017;86:27-68. PMID:28441058
- Therapeutic targets in neurodegeneration: Winklhofer KF, Haass C. Nat Rev Neurol. 2010;6(9):463-477. PMID:20740084
- Neurodegeneration research progress: Longo FM, Massa SM. Nat Rev Neurol. 2013;9(1):51-62. PMID:23168548
- Animal models of neurodegeneration: Dawson TM, et al. Ann Neurol. 2018;83(1):16-31. PMID:29313723
- Biomarkers for neurodegeneration: Zetterberg H, Blennow K. Nat Rev Neurol. 2021;17(4):229-238. PMID:33526926
- Clinical trials in neurodegeneration: Cummings JL, et al. Nat Rev Drug Discov. 2014;13(7):503-523. PMID:24981365
- Stocker M. Calcium-activated potassium channels: molecular diversity and function. Physiological Reviews. 2004;84(3):903-934. PMID:15269336
- Kohler M, Hirschberg B, Bond CT, et al. Small-conductance, calcium-activated potassium channels from mammalian brain. Science. 1996;273(5282):1709-1714. PMID:8781166
- Wulff H, Kolski-Andreaco A. Modulators of small- and intermediate-conductance Ca2+-activated K+ channels. Current Pharmaceutical Design. 2007;13(31):3179-3184. PMID:17979758
- Dessauer CW, Sorscher EJ, Brennan TJ, et al. Isolation and characterization of a novel large conductance calcium-activated potassium channel. Journal of Biological Chemistry. 1998;273(50):33123-33129. PMID:9837872
- Bhattacharjee A, Gan L, Kaczmarek LK. Localization of the Slack potassium channel in the rat central nervous system. Journal of Comparative Neurology. 2002;454(3):241-254. PMID:12442319
6.remote Y, Kaczmarek LK. Slack, Slick and Slam channels: roles in neuronal excitability, neuroprotection and neurodegeneration. Brain Research. 2020;1732:146738. PMID:32035170
- Rudy B, McBain CJ. Kv3 channels: voltage-gated K+ channels designed for high-frequency repetitive firing. Trends in Neurosciences. 2001;24(9):517-526. PMID:11530637
- Gu N, Vervaeke K, Storm JF. Slack and Slick potassium channels in pyramidal neurons. Neuropharmacology. 2007;52(3):683-688. PMID:17097100