title: The LGI1-ADAM22 protein complex in synaptic transmission and synaptic disorders.
abstract: Physiological functioning of the brain requires fine-tuned synaptic transmission, and its dysfunction causes various brain disorders such as autism, dementia, and epilepsy. It is therefore extremely important to identify and characterize key regulators of synaptic function. In particular, disease-related synaptic proteins, such as autism-related neurexin-neuroligin and psychiatric disorder-related NMDA receptor, have attracted considerable attention. Recent basic and clinical research has highlighted critical roles of a ligand-receptor complex, LGI1-ADAM22, in synaptic transmission and brain function, as mutations in the LGI1 gene cause autosomal dominant lateral temporal lobe epilepsy and autoantibodies to LGI1 cause limbic encephalitis which is characterized by memory loss and seizures. Here, we will review our current knowledge about LGI1 and ADAM22, and discuss their patho-physiological roles in synaptic transmission and synaptic disorders.
authors.affiliation: Division of Membrane Physiology, Department of Molecular and Cellular Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki 444-8787, Japan; Department of Physiological Sciences, School of Life Science, SOKENDAI (The Graduate University for Advanced Studies), Okazaki 444-8787, Japan.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Fukata
authors.affiliation: Division of Membrane Physiology, Department of Molecular and Cellular Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki 444-8787, Japan; Department of Physiological Sciences, School of Life Science, SOKENDAI (The Graduate University for Advanced Studies), Okazaki 444-8787, Japan.
authors.forename: Norihiko
authors.initials: N
authors.lastname: Yokoi
authors.affiliation: Division of Membrane Physiology, Department of Molecular and Cellular Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki 444-8787, Japan; Department of Physiological Sciences, School of Life Science, SOKENDAI (The Graduate University for Advanced Studies), Okazaki 444-8787, Japan.
authors.forename: Yuri
authors.initials: Y
authors.lastname: Miyazaki
authors.affiliation: Division of Membrane Physiology, Department of Molecular and Cellular Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki 444-8787, Japan; Department of Physiological Sciences, School of Life Science, SOKENDAI (The Graduate University for Advanced Studies), Okazaki 444-8787, Japan. Electronic address: mfukata@nips.ac.jp.
authors.forename: Masaki
authors.initials: M
authors.lastname: Fukata
mesh_terms: D051722:ADAM Proteins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D001927:Brain Diseases / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D051379:Mice; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D011506:Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D009435:Synaptic Transmission
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; C116499:LGI1 protein, human; C492120:Lgi1 protein, mouse; D009419:Nerve Tissue Proteins; D011506:Proteins; D051722:ADAM Proteins; C498474:ADAM22 protein, human; C121258:Adam22 protein, mouse
keywords: ADAM22; AMPA receptor; Epilepsy; LGI1; Limbic encephalitis; Synapse