Anti-Connexin 43 Antibody, CT Antibody, clone 1C5.1 Antibody, Alexa Fluor(R) 488 Conjugate clone 1C5.1, from mouse, ALEXA FLUOR(R) 488

Gap junction alpha-1 protein (UniProt: P17302; also known as Connexin-43, Cx43, Gap junction 43 kDa heart protein) is encoded by the GJA1 (also known as GJAL) gene (gene ID: 2697) in human. Cx43 is a member of the connexin family of proteins and a component of gap junctions. Connexins belong to a family of integral membrane proteins that assemble as hexamers (connexons) to form gap junctions, which are specialized sites of cell-cell contact. Gap junctions allow the passage of ions, metabolites and low molecular weight messenger molecules to pass from one cell to the other. Cx43 undergoes rapid turnover in the cell and its monomers may reside in the ER/Golgi network, forming a reservoir available for assembly upon degradation of existing connexin-43 channels. Cx43 may play a critical role in the physiology of hearing by participating in the recycling of potassium to the cochlear endolymph. It also acts as a negative regulator of bladder functional capacity by enhancing intercellular electrical and chemical transmission, thus sensitizing bladder muscles to cholinergic stimuli and causing them to contract. Cx43 is reported to be essential for normal cardiac development. Mice lacking Cx43 die soon after birth due to cardiac malformations and obstruction of the pulmonary artery. Cx43 has been detected in a variety of tissues including: atrial and ventricular myocytes, granulose cells, astrocytes, fibroblasts, leptomeningeal cells, brain, lung, smooth muscle, uterine muscle, kidney, lens, epithelium, cornea, and testis. Cx43 is phosphorylated at Ser368 by PKC gamma; which leads to disassembly of gap junction plaques and inhibition of gap junction activity. Mutations in GJA1 gene are reported to cause Oculodentodigital dysplasia and Hallermann-Streiff syndrome.