| Annotated protein: | Kinesin-like protein KIF2C (Mitotic centromere-associated kinesin) (MCAK). Gene symbol: KIF2C. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q922S8 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ KIF2C |
| Ontology domain: | Biological Process |
| SynGO term: | regulation of neurotransmitter receptor localization to postsynaptic specialization membrane (GO:0098696) |
| Synapse type(s): | hippocampus, glutamatergic |
| Annotated paper: | Zheng R, et al. "KIF2C regulates synaptic plasticity and cognition in mice through dynamic microtubule depolymerization" Elife. 2022 Feb 9;11:e72483 PMID:35138249 |
| Figure(s): | Figures 2-6 |
| Annotation description: | Figure 2: KIF2C knockdown affects spine morphology, synaptic transmission and long-term potentiation in vitro and in vivo. Figure 3-4: KIF2C knockout affects spine morphology, synaptic transmission, and long-term potentiation in vivo. Figure 5: "Result showed a decreased ratio NMDAR/AMPAR in cKO mice (Figure 5C). The amplitude of NMDAR-mediated EPSCs was comparable under various stimulation, while AMPAR-mediated EPSCs was increased (Figure 5D-E), indicating a specific defect in AMPAR-mediated synaptic currents. In addition, we performed cell-surface biotinylation experiments to examine the surface expression of these two receptors. The level of surface AMPA receptors was significantly increased in the cKO hippocampus (Figure 5F), which coincided with the electrophysiological abnormalities in AMPAR-mediated synaptic transmission in cKO mice." Figure 6: KIF2C regulates synaptic transmission and plasticity by mediating dynamic microtubule depolymerization in dendrites and spines. "In this study, we find that KIF2C, a dynamic microtubule depolymerization protein without known function in the nervous system, plays a pivotal role in the structural and functional plasticity of synapses and regulates cognitive function in mice. Through its microtubule depolymerization capability, KIF2C regulates microtubule dynamics in dendrites, and regulates microtubule invasion of spines in neurons in a neuronal activity-dependent manner. Using RNAi knockdown and conditional knockout approaches, we showed that KIF2C regulates spine morphology and synaptic membrane expression of AMPA receptors. Moreover, KIF2C deficiency leads to impaired excitatory transmission, long-term potentiation, and altered cognitive behaviors in mice." |
| Evidence tracking, Biological System: | Cultured neurons Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) RNAi / shRNA |
| Evidence tracking, Experiment Assay: | Confocal Whole-cell patch clamp Electron Microscopy |
| Annotator(s): | Frank Koopmans (ORCID:0000-0002-4973-5732) Guus Smit (ORCID:0000-0002-2286-1587) Matthijs Verhage (ORCID:0000-0002-2514-0216) |
| Lab: | Department of Functional Genomics, Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands |
| SynGO annotation ID: | 5443 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |