detected in CD4+ and CD8+ T cells as well as in human B lymphocytes. TRPV2 is one type of ion channel that directs T cell activation, proliferation, and defense mechanisms. If the TRPV2 channel were absent or not functioning properly in T cells, T cell receptor signaling would not be optimal. TRPV2 also acts as a transmembrane protein on the surface of B cells, negatively controlling B cell activation. Abnormal TRPV2 expression has been reported in hematological diseases including multiple myeloma, myelodysplastic syndrome, Burkitt lymphoma, and acute myeloid leukemia. Metabolic TRPV2 seems to be essential in glucose homeostasis. It is highly expressed in MIN6 cells, which is a β-cell. These cell types are known for releasing insulin, a molecule that functions to keep glucose levels low. Under unstimulated conditions, TRPV2 is localized in the cytoplasm. Activation causes the channel to translocate to the plasma membrane. This triggers the influx of calcium resulting in insulin secretion. Cardiovascular TRPV2 is very important in the structure and function of cardiomyocytes (heart cells). Compared to skeletal muscles, TRPV2 is expressed 10 times as high in cardiomyocytes and is important in current conduction. TRPV2 has been shown to be involved in stretch-dependent responses in heart cells. TRPV2 expression is concentrated in intercalated discs which allows the synchronous contraction of cardiomyocytes. Abnormal expression of TRPV2 results in reduced shortening length, shortening rate, and lengthening rate which ultimately compromise cardiac contractile function. Ligands Agonist Agonists include: Anandamide 2-Arachidonoylglycerol Cannabidiol (CBD) Cannabidivarin (CBDV) Cannabinol (CBN) Cannabigerol (CBG) Cannabigerovarin (CBGV) Tetrahydrocannabinol (THC) Tetrahydrocannabinolic acid (THCA) Tetrahydrocannabivarin (THCV) Nabilone See also Endocannabinoid system Transient receptor potential channel TRPV family Cannabinoids References External links Ion channels