Connexin 43 Polyclonal Antibody

Product Specific Information

This antibody reacts with connexin 43. On western blots, this antibody detects a 43 kDa protein with mouse brain, rat brain, and human smooth muscle cell extracts. Reactivity with other connexin types has not been observed on western blots (note: samples were not boiled prior to running SDS-PAGE). Positive immunohistostaining is seen with mouse heart and thalamus tissue. Paraffin embedded sections require a heat-induced epitope retrieval (HIER) step. Reactivity of this antibody with connexin 43 is independent of phosphorylation status.

Target Information

Connexin 43 (Cx43) is a member of the gap junction protein family. Connexins assemble as a hexamer and are transported to the plasma membrane to create a hemichannel that can associate with hemichannels on nearby cells to create cell-to-cell channels. Clusters of these channels assemble to make gap junctions. Gap junction communication is important in development and regulation of cell growth. Phosphorylation of Cx43 is important in regulating assembly and function of gap junctions. Ser368 of Cx43 is phosphorylated by protein kinase C (PKC) after activation by phorbol esters, which decreases cell-to-cell communication. Src can interact with and phosphorylate Cx43 to alter gap junction communication. GFAP are membrane-spanning proteins that facilitate the transfer of ions and small molecules between cells. According to sequence similarities at the nucleotide and amino acid levels, the gap junction proteins are divided into two categories, alpha and beta. Connexin 43 is the major protein of gap junctions in the heart, and gap junctions are thought to have a crucial role in the synchronized contraction of the heart and in embryonic development. Connexin 43 is also targeted by several protein kinases that regulate myocardial cell-cell coupling. A related intron-less connexin 43 pseudogene, GJA1P, has been mapped to chromosome 5. Mutations in the GFAP gene cause X-linked Charcot-Marie-Tooth disease, an inherited peripheral neuropathy, oculodentodigital dysplasia and heart malformations. Alternatively spliced transcript variants of GFAP have been found.