{"publist_id":"4423","volume":110,"date_created":"2018-12-11T11:57:54Z","intvolume":"       110","year":"2013","publisher":"National Academy of Sciences","status":"public","quality_controlled":0,"title":"Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling","publication":"PNAS","author":[{"full_name":"Budreck, Elaine C","last_name":"Budreck","first_name":"Elaine"},{"last_name":"Kwon","first_name":"Oh","full_name":"Kwon, Oh-Bin"},{"full_name":"Jung, Jung-Hoon","first_name":"Jung","last_name":"Jung"},{"first_name":"Stéphane","last_name":"Baudouin","full_name":"Baudouin, Stéphane J"},{"last_name":"Thommen","first_name":"Albert","full_name":"Thommen, Albert"},{"last_name":"Kim","first_name":"Hye","full_name":"Kim, Hye-Sun"},{"last_name":"Fukazawa","first_name":"Yugo","full_name":"Fukazawa, Yugo"},{"orcid":"0000-0001-7429-7896","first_name":"Harumi","last_name":"Harada","id":"2E55CDF2-F248-11E8-B48F-1D18A9856A87","full_name":"Harumi Harada"},{"full_name":"Tabuchi, Katsuhiko","first_name":"Katsuhiko","last_name":"Tabuchi"},{"full_name":"Ryuichi Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","last_name":"Shigemoto","orcid":"0000-0001-8761-9444"},{"last_name":"Scheiffele","first_name":"Peter","full_name":"Scheiffele, Peter"},{"full_name":"Kim, Joung-Hun","last_name":"Kim","first_name":"Joung"}],"day":"08","doi":"10.1073/pnas.1214718110","page":"725 - 730","type":"journal_article","date_updated":"2021-01-12T06:57:43Z","month":"01","issue":"2","extern":1,"publication_status":"published","citation":{"ama":"Budreck E, Kwon O, Jung J, et al. Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling. <i>PNAS</i>. 2013;110(2):725-730. doi:<a href=\"https://doi.org/10.1073/pnas.1214718110\">10.1073/pnas.1214718110</a>","apa":"Budreck, E., Kwon, O., Jung, J., Baudouin, S., Thommen, A., Kim, H., … Kim, J. (2013). Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1214718110\">https://doi.org/10.1073/pnas.1214718110</a>","chicago":"Budreck, Elaine, Oh Kwon, Jung Jung, Stéphane Baudouin, Albert Thommen, Hye Kim, Yugo Fukazawa, et al. “Neuroligin-1 Controls Synaptic Abundance of NMDA-Type Glutamate Receptors through Extracellular Coupling.” <i>PNAS</i>. National Academy of Sciences, 2013. <a href=\"https://doi.org/10.1073/pnas.1214718110\">https://doi.org/10.1073/pnas.1214718110</a>.","ista":"Budreck E, Kwon O, Jung J, Baudouin S, Thommen A, Kim H, Fukazawa Y, Harada H, Tabuchi K, Shigemoto R, Scheiffele P, Kim J. 2013. Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling. PNAS. 110(2), 725–730.","short":"E. Budreck, O. Kwon, J. Jung, S. Baudouin, A. Thommen, H. Kim, Y. Fukazawa, H. Harada, K. Tabuchi, R. Shigemoto, P. Scheiffele, J. Kim, PNAS 110 (2013) 725–730.","mla":"Budreck, Elaine, et al. “Neuroligin-1 Controls Synaptic Abundance of NMDA-Type Glutamate Receptors through Extracellular Coupling.” <i>PNAS</i>, vol. 110, no. 2, National Academy of Sciences, 2013, pp. 725–30, doi:<a href=\"https://doi.org/10.1073/pnas.1214718110\">10.1073/pnas.1214718110</a>.","ieee":"E. Budreck <i>et al.</i>, “Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling,” <i>PNAS</i>, vol. 110, no. 2. National Academy of Sciences, pp. 725–730, 2013."},"date_published":"2013-01-08T00:00:00Z","abstract":[{"lang":"eng","text":"Despite the pivotal functions of the NMDA receptor (NMDAR) for neural circuit development and synaptic plasticity, the molecular mechanisms underlying the dynamics of NMDAR trafficking are poorly understood. The cell adhesion molecule neuroligin-1 (NL1) modifies NMDAR-dependent synaptic transmission and synaptic plasticity, but it is unclear whether NL1 controls synaptic accumulation or function of the receptors. Here, we provide evidence that NL1 regulates the abundance of NMDARs at postsynaptic sites. This function relies on extracellular, NL1 isoform-specific sequences that facilitate biochemical interactions between NL1 and the NMDAR GluN1 subunit. Our work uncovers NL1 isoform-specific cisinteractions with ionotropic glutamate receptors as a key mechanism for controlling synaptic properties."}],"_id":"2478"}