title: Auxiliary subunits of the CKAMP family differentially modulate AMPA receptor properties.
abstract: AMPA receptor (AMPAR) function is modulated by auxiliary subunits. Here, we report on three AMPAR interacting proteins-namely CKAMP39, CKAMP52 and CKAMP59-that, together with the previously characterized CKAMP44, constitute a novel family of auxiliary subunits distinct from other families of AMPAR interacting proteins. The new members of the CKAMP family display distinct regional and developmental expression profiles in the mouse brain. Notably, despite their structural similarities they exert diverse modulation on AMPAR gating by influencing deactivation, desensitization and recovery from desensitization, as well as glutamate and cyclothiazide potency to AMPARs. This study indicates that AMPAR function is very precisely controlled by the cell-type specific expression of the CKAMP family members.
authors.affiliation: Synaptic Signalling and Neurodegeneration, German Cancer Research Center, Heidelberg, Germany.|Synaptic Signalling and Neurodegeneration, German Center for Neurodegenerative Diseases, Bonn, Germany.
authors.forename: Paul
authors.initials: P
authors.lastname: Farrow
authors.affiliation: Department of Clinical Neurobiology, Medical Faculty of Heidelberg University, Heidelberg, Germany.|German Cancer Research Center, Heidelberg, Germany.
authors.forename: Konstantin
authors.initials: K
authors.lastname: Khodosevich
authors.affiliation: Department of Biochemistry and Molecular Biology, Institute for Medical Research - Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
authors.forename: Yechiam
authors.initials: Y
authors.lastname: Sapir
authors.affiliation: Department of Clinical Neurobiology, Medical Faculty of Heidelberg University, Heidelberg, Germany.|German Cancer Research Center, Heidelberg, Germany.
authors.forename: Anton
authors.initials: A
authors.lastname: Schulmann
authors.affiliation: Synaptic Signalling and Neurodegeneration, German Cancer Research Center, Heidelberg, Germany.|Synaptic Signalling and Neurodegeneration, German Center for Neurodegenerative Diseases, Bonn, Germany.
authors.forename: Muhammad
authors.initials: M
authors.lastname: Aslam
authors.affiliation: Department of Biochemistry and Molecular Biology, Institute for Medical Research - Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
authors.forename: Yael
authors.initials: Y
authors.lastname: Stern-Bach
authors.affiliation: Department of Clinical Neurobiology, Medical Faculty of Heidelberg University, Heidelberg, Germany.
authors.forename: Hannah
authors.initials: H
authors.lastname: Monyer
authors.affiliation: Synaptic Signalling and Neurodegeneration, German Cancer Research Center, Heidelberg, Germany.|Synaptic Signalling and Neurodegeneration, German Center for Neurodegenerative Diseases, Bonn, Germany.
authors.forename: Jakob
authors.identifier: http://orcid.org/0000-0003-3861-3294
authors.initials: J
authors.lastname: von Engelhardt
mesh_terms: D000818:Animals; D001581:Benzothiadiazines / Q000378:metabolism; D001921:Brain / Q000196:embryology*; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D011485:Protein Binding; D018091:Receptors, AMPA / Q000819:agonists / Q000378:metabolism*; D017422:Sequence Analysis, DNA
chemical_list: D001581:Benzothiadiazines; C000611431:CKAMP39 protein, mouse; C000611432:CKAMP52 protein, mouse; C000611433:CKAMP59 protein, mouse; D002352:Carrier Proteins; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D018091:Receptors, AMPA; D018698:Glutamic Acid; C004639:cyclothiazide
keywords: AMPA receptors; auxiliary subunits; deactivation; desensitization; mouse; neuroscience