Short transient receptor potential channel 6 (TRPC6) belongs to the subfamily C of transient receptor potential cation channel (TRP channels). TRPC6 is a nonselective cation channel that allows the influx of Ca²⁺ and Na⁺ ions into the cells via a pore between the fifth and sixth transmembrane domains (TM5-TM6). The cytoplasmic N terminus of TRPC6 has four ankyrin repeats, while the cytoplasmic C terminus has a dystrophin (coiled-coil) domain. It is reported that defects in the TRPC6 gene may contribute to focal segmental glomerulosclerosis 2 (FSGS2).
|Basic Information of TRPC6|
|Protein Name||Short transient receptor potential channel 6|
|Aliases||Transient receptor protein 6, FSGS2, TRP6|
|Organism||Homo sapiens (Human)|
TRPC6 can assemble with other TRPCs or itself to form a nonselective cation channel enabling Ca²⁺ influx into cells. It can be activated by diacylglycerol to transform into an open state. In addition, nephrin is shown to bind to phosphorylated TRPC6 via its cytoplasmic domain, competitively inhibiting TRPC6 expression and activation. TRPC6 is supposed to have a fundamental role in the regulation of smooth muscle tone in blood vessels and lung, and it might act as an important mediator for sensing the extracellular signals that affect synaptic and behavioral plasticity. Different from other members of transient receptor potential cation channel subfamily C, activation of TRPC6 ion channel occurs independently of protein kinase C and it cannot be triggered by depletion of intracellular calcium. TRPC6 is also involved in multiple other biological processes, such as manganese ion transport, regulation of dendrite morphogenesis, neuron differentiation, regulation of cytosolic calcium ion concentration, regulation of peptidyl-threonine phosphorylation, and so on. TRPC6 has been associated with depression and anxiety, as well as with focal segmental glomerulosclerosis (FSGS).
Fig.1 Cryo-EM structure of human TRPC6 at 3.8A resolution. (Tang, 2018)
This article finds that down-regulation of TRPC6 by using either a TRPC6 blocker or TRPC6 siRNA can lead to the reduced expression of adenosine monophosphate-activated protein kinase (AMPK), suggesting that the involvement of TRPC6 in hypoxia-induced autophagy in podocytes is associated with AMPK signaling.
This article provides an overview of the interactions between inflammation and ion exchanges with a focus on the pathogenesis of potential future therapeutic implications and immune-mediated diseases.
This article suggests that miR-200 b-3p inhibition can reduce the currents of TRPC6, which then can lead to a decrease of the concentration of intracellular Ca²⁺ and consequently result in the down-regulation of BKCa currents.
This article suggests that TRPC6 and/or calpain-1 repression could be options of future therapeutics to treat patients with focal segmental glomerulosclerosis (FSGS) or other podocytopathies.
This article indicates that repression of TRPC6 channel may have, at least partial, renoprotective effects, which could contribute to the development of new pharmacological tools to prevent or treat the progression of diabetic kidney disease.
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