Overview
- Peptide (C)ENSYRSEVKARQDVK, corresponding to amino acid residues 1066-1080 of mouse MAGI2 (Accession Q9WVQ1). Intracellular, C-terminus.
- Rat and mouse brain lysates; human SH-SY5Y neuroblastoma cell lysates (1:200-1:2000).
- Western blot analysis of mouse brain lysate:1. Anti-MAGI2/AIP1 Antibody (#APZ-052), (1:400).
2. Anti-MAGI2/AIP1 Antibody, preincubated with MAGI2/AIP1 Blocking Peptide (#BLP-PZ052).
MAGI2 is a member in the Membrane-associated guanylate kinase with an inverted arrangement of protein-protein interaction domains (MAGI) family, and includes two additional family members, MAGI1 and MAGI31.
MAGI proteins are essential for efficient cell signaling as they function as scaffolds for assembling cell adhesion molecules, receptors and signaling molecules and linking them to the cytoskeleton2.
MAGI2 has a guanylate kinase, 2 WW, and 6 PDZ domains (PDZ0-PDZ5). It interacts with cytoskeleton-associated proteins: guanylate-kinase-associated protein (GKAP), Postsynaptic density-95 (PSD-95)/synapse-associated protein 90 (SAP90), Stargazin/transmembrane AMPAR regulatory proteins (TARPs). MAGI2 also interacts with N-methyl-D-aspartate (NMDA) receptors, δ2 Glutamate receptor, β1AR, VPAC1, Brain-specific angiogenesis inhibitor-1, Activin Type II receptors, Neuroligins, β-Dystroglycan, Dendrite arborization and synapse maturation 1 (Dasm1)/IgSF9b, Nectins and Nephrin receptors and cell adhesion proteins, respectively1,3.
MAGI2 expression is almost exclusively in brain, deletion of MAGI2 causes infantile spasm and increased cognitive impairment in schizophrenia patients4.
In non-neuronal tissues, MAGI2 enhances the ability of PTEN to suppress Akt activation in the PI3-kinase/Akt pathway. PTEN binds to MAGI2 through the PDZ domains, thus enhancing PTEN stability and improves the efficiency of PTEN signalling, allowing for efficient tumor suppression by PTEN1,5.