Overview
- Peptide (C)EHQMAKISVAEDGR, corresponding to amino acid residues 131-144 of rat Connexin-37 (Accession Q03190). Intracellular loop.
- Mouse heart and lung, rat lung lysates and human MCF-7 breast adenocarcinoma cell lysate (1:200-1:2000).
- Western blot analysis of mouse heart lysate (lanes 1 and 4), rat lung membranes (lanes 2 and 5) and mouse lung lysate (lanes 3 and 6):1-3. Anti-Connexin-37 Antibody (#ACC-204), (1:400).
4-6. Anti-Connexin-37 Antibody, preincubated with Connexin-37 Blocking Peptide (#BLP-CC204). - Western blot analysis of human MCF-7 breast adenocarcinoma cell lysate:1. Anti-Connexin-37 Antibody (#ACC-204), (1:200).
2. Anti-Connexin-37 Antibody, preincubated with Connexin-37 Blocking Peptide (#BLP-CC204).
Connexins (Cxs) are a family of transmembrane proteins comprising 21 members in humans that forms gap junction channels (GJCs). Connexins are divided in four groups: α, β, γ and δ. Cx37 is also named α4 since it is the fourth connexin of the alpha group that was identified1,2.
Connexins do not function as single proteins; six connexins assemble into connexons (hemi-channels), and two connexons from neighboring cells dock in the extracellular space to form a full gap junction channel. Connexins are responsible for mediating direct communication between adjacent cells by the exchange of ions and small signaling molecules and cytosolic factors1,3. Their structure consists of four transmembrane helices, two extracellular loops, a cytoplasmic loop, a cytoplasmic NH2- and COOH-termini1,2.
Connexin-37 is encoded by the GJA4 gene and is expressed in vascular endothelial cells. The protein is responsible for regulating and controlling the growth, proliferation and regeneration of the vascular endothelium by mediating the signal transduction between smooth muscle and endothelial cells. Cx37 knockout mice have a tendency for developing endarterium atheromatous plaques4. Also, a polymorphism in the gene that encodes for Cx37, is associated with increased risk for atherosclerosis and myocardial infarction1.