Aliases for TRPM4 Gene
External Ids for TRPM4 Gene
Previous GeneCards Identifiers for TRPM4 Gene
The protein encoded by this gene is a calcium-activated nonselective ion channel that mediates transport of monovalent cations across membranes, thereby depolarizing the membrane. The activity of the encoded protein increases with increasing intracellular calcium concentration, but this channel does not transport calcium. [provided by RefSeq, Mar 2016]
GeneCards Summary for TRPM4 Gene
TRPM4 (Transient Receptor Potential Cation Channel Subfamily M Member 4) is a Protein Coding gene. Diseases associated with TRPM4 include Progressive Familial Heart Block, Type Ib and Brugada Syndrome. Among its related pathways are Transport of glucose and other sugars, bile salts and organic acids, metal ions and amine compounds and Ion channel transport. GO annotations related to this gene include calmodulin binding and calcium channel activity. An important paralog of this gene is TRPM5.
UniProtKB/Swiss-Prot for TRPM4 Gene
Calcium-activated non selective (CAN) cation channel that mediates membrane depolarization. While it is activated by increase in intracellular Ca(2+), it is impermeable to it. Mediates transport of monovalent cations (Na(+) > K(+) > Cs(+) > Li(+)), leading to depolarize the membrane. It thereby plays a central role in cadiomyocytes, neurons from entorhinal cortex, dorsal root and vomeronasal neurons, endocrine pancreas cells, kidney epithelial cells, cochlea hair cells etc. Participates in T-cell activation by modulating Ca(2+) oscillations after T lymphocyte activation, which is required for NFAT-dependent IL2 production. Involved in myogenic constriction of cerebral arteries. Controls insulin secretion in pancreatic beta-cells. May also be involved in pacemaking or could cause irregular electrical activity under conditions of Ca(2+) overload. Affects T-helper 1 (Th1) and T-helper 2 (Th2) cell motility and cytokine production through differential regulation of calcium signaling and NFATC1 localization. Enhances cell proliferation through up-regulation of the beta-catenin signaling pathway.