Anti-TRPC3 antibody [EPR25056-56]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The TRPC3 protein also known as transient receptor potential cation channel subfamily C member 3 is a fundamental component of the plasma membrane and participates in forming a non-selective cation channel. With a molecular mass of approximately 97 kDa TRPC3 channels are widely expressed in the brain heart and vascular smooth muscle. These channels mediate calcium and to a less degree sodium influx when activated facilitating various cellular responses. Additionally TRPC3 channels can interact with other proteins within the same family shaping the channel's functional properties.

Biological function summary

Transient receptor potential channels like TRPC3 play important roles in cellular calcium signaling with direct implications in neuronal cardiac and smooth muscle functions. TRPC3 proteins can assemble into heteromultimeric complexes with other TRPC family members often modulating their biophysical characteristics and responsiveness to stimuli. In neurons TRPC3 channels contribute to synaptic transmission and plasticity by influencing intracellular calcium levels. In smooth muscle cells TRPC3 activity influences contraction and relaxation processes affected by calcium flux regulation.

Pathways

Inositol triphosphate (IP3) and phospholipase C (PLC) pathways notably involve TRPC3 activity. TRPC3 cooperates with the IP3 receptor to mediate calcium release from the endoplasmic reticulum enhancing cellular calcium entry. This interaction ties TRPC3 functionally to the regulation of important physiological processes like cardiac hypertrophy and vascular tone. Additionally TRPC3's relationship with proteins such as calmodulin and STIM1 further illustrates its role in calcium signaling pathways.

Associated diseases and disorders

Altered TRPC3 activity relates to conditions such as cardiac hypertrophy and neurodegenerative diseases. The protein's dysregulation can result in disrupted calcium homeostasis contributing to excessive cardiac cell growth and potential heart failure. In the nervous system TRPC3 has links to Huntington's disease where its abnormal function associates with neuronal survival and synaptic alterations. The interaction of TRPC3 with proteins such as huntingtin in these pathological contexts highlights its participation in disease development and progression.