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Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior

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Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior. / Gromova, Kira V; Muhia, Mary; Rothammer, Nicola; Gee, Christine E; Thies, Edda; Schaefer, Irina; Kress, Sabrina; Kilimann, Manfred W; Shevchuk, Olga; Oertner, Thomas G; Kneussel, Matthias.

in: CELL REP, Jahrgang 23, Nr. 9, 29.05.2018, S. 2705-2717.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Gromova, KV, Muhia, M, Rothammer, N, Gee, CE, Thies, E, Schaefer, I, Kress, S, Kilimann, MW, Shevchuk, O, Oertner, TG & Kneussel, M 2018, 'Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior', CELL REP, Jg. 23, Nr. 9, S. 2705-2717. https://doi.org/10.1016/j.celrep.2018.04.112

APA

Gromova, K. V., Muhia, M., Rothammer, N., Gee, C. E., Thies, E., Schaefer, I., Kress, S., Kilimann, M. W., Shevchuk, O., Oertner, T. G., & Kneussel, M. (2018). Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior. CELL REP, 23(9), 2705-2717. https://doi.org/10.1016/j.celrep.2018.04.112

Vancouver

Gromova KV, Muhia M, Rothammer N, Gee CE, Thies E, Schaefer I et al. Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior. CELL REP. 2018 Mai 29;23(9):2705-2717. https://doi.org/10.1016/j.celrep.2018.04.112

Bibtex

@article{52716a566dee40a3aa61231e0da1dab6,
title = "Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior",
abstract = "Autism spectrum disorders (ASDs) are associated with mutations affecting synaptic components, including GluN2B-NMDA receptors (NMDARs) and neurobeachin (NBEA). NBEA participates in biosynthetic pathways to regulate synapse receptor targeting, synaptic function, cognition, and social behavior. However, the role of NBEA-mediated transport in specific trafficking routes is unclear. Here, we highlight an additional function for NBEA in the local delivery and surface re-insertion of synaptic receptors in mouse neurons. NBEA dynamically interacts with Rab4-positive recycling endosomes, transiently enters spines in an activity-dependent manner, and regulates GluN2B-NMDAR recycling. Furthermore, we show that the microtubule growth inhibitor kinesin KIF21B constrains NBEA dynamics and is present in the NBEA-recycling endosome-NMDAR complex. Notably, Kif21b knockout decreases NMDAR surface expression and alters social behavior in mice, consistent with reported social deficits in Nbea mutants. The influence of NBEA-KIF21B interactions on GluN2B-NMDAR local recycling may be relevant to mechanisms underlying ASD etiology.",
keywords = "Journal Article",
author = "Gromova, {Kira V} and Mary Muhia and Nicola Rothammer and Gee, {Christine E} and Edda Thies and Irina Schaefer and Sabrina Kress and Kilimann, {Manfred W} and Olga Shevchuk and Oertner, {Thomas G} and Matthias Kneussel",
note = "Copyright {\textcopyright} 2018 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2018",
month = may,
day = "29",
doi = "10.1016/j.celrep.2018.04.112",
language = "English",
volume = "23",
pages = "2705--2717",
journal = "CELL REP",
issn = "2211-1247",
publisher = "Elsevier",
number = "9",

}

RIS

TY - JOUR

T1 - Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior

AU - Gromova, Kira V

AU - Muhia, Mary

AU - Rothammer, Nicola

AU - Gee, Christine E

AU - Thies, Edda

AU - Schaefer, Irina

AU - Kress, Sabrina

AU - Kilimann, Manfred W

AU - Shevchuk, Olga

AU - Oertner, Thomas G

AU - Kneussel, Matthias

N1 - Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2018/5/29

Y1 - 2018/5/29

N2 - Autism spectrum disorders (ASDs) are associated with mutations affecting synaptic components, including GluN2B-NMDA receptors (NMDARs) and neurobeachin (NBEA). NBEA participates in biosynthetic pathways to regulate synapse receptor targeting, synaptic function, cognition, and social behavior. However, the role of NBEA-mediated transport in specific trafficking routes is unclear. Here, we highlight an additional function for NBEA in the local delivery and surface re-insertion of synaptic receptors in mouse neurons. NBEA dynamically interacts with Rab4-positive recycling endosomes, transiently enters spines in an activity-dependent manner, and regulates GluN2B-NMDAR recycling. Furthermore, we show that the microtubule growth inhibitor kinesin KIF21B constrains NBEA dynamics and is present in the NBEA-recycling endosome-NMDAR complex. Notably, Kif21b knockout decreases NMDAR surface expression and alters social behavior in mice, consistent with reported social deficits in Nbea mutants. The influence of NBEA-KIF21B interactions on GluN2B-NMDAR local recycling may be relevant to mechanisms underlying ASD etiology.

AB - Autism spectrum disorders (ASDs) are associated with mutations affecting synaptic components, including GluN2B-NMDA receptors (NMDARs) and neurobeachin (NBEA). NBEA participates in biosynthetic pathways to regulate synapse receptor targeting, synaptic function, cognition, and social behavior. However, the role of NBEA-mediated transport in specific trafficking routes is unclear. Here, we highlight an additional function for NBEA in the local delivery and surface re-insertion of synaptic receptors in mouse neurons. NBEA dynamically interacts with Rab4-positive recycling endosomes, transiently enters spines in an activity-dependent manner, and regulates GluN2B-NMDAR recycling. Furthermore, we show that the microtubule growth inhibitor kinesin KIF21B constrains NBEA dynamics and is present in the NBEA-recycling endosome-NMDAR complex. Notably, Kif21b knockout decreases NMDAR surface expression and alters social behavior in mice, consistent with reported social deficits in Nbea mutants. The influence of NBEA-KIF21B interactions on GluN2B-NMDAR local recycling may be relevant to mechanisms underlying ASD etiology.

KW - Journal Article

U2 - 10.1016/j.celrep.2018.04.112

DO - 10.1016/j.celrep.2018.04.112

M3 - SCORING: Journal article

C2 - 29847800

VL - 23

SP - 2705

EP - 2717

JO - CELL REP

JF - CELL REP

SN - 2211-1247

IS - 9

ER -