| Annotated protein: | Rab11 family-interacting protein 5 (Rab11-FIP5) (Rab11-interacting protein Rip11). Gene symbol: RAB11FIP5. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q8R361 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ RAB11FIP5 |
| Ontology domain: | Biological Process |
| SynGO term: | postsynaptic neurotransmitter receptor endocytosis (GO:0098884) |
| Annotated paper: | Bacaj T, et al. "Synaptic Function of Rab11Fip5: Selective Requirement for Hippocampal Long-Term Depression" J Neurosci. 2015 May 13;35(19):7460-74 PMID:25972173 |
| Figure(s): | Figure 9 |
| Annotation description: | "Staining for the AMPAR subunit GluA1 and the postsynaptic protein PSD-95 confirmed that Rab11Fip5 KO cultures had normal density of GluA1 synaptic puncta as well as normal GluA1 puncta size, a measure of synaptic size (Fig. 9A). Together, these observations suggest that basal GluA1 receptor levels are not altered by the KO, which is in agreement with the lack of a phenotype in basal transmission (Fig. 8). The fraction of internalized GluA1 receptors 15 min following NMDA application (Fig. 9B) (Bhattacharyya et al., 2009) was increased by almost twofold in ΔCre-infected Rab11Fip5 cKO cultures but remained unchanged over baseline internalized GluA1 receptors in Cre-infected cultures (Fig. 9C; p < 0.01, ΔCre, 1.8 ± 0.12, n = 6; Cre, 1.07 ± 0.11, n = 6). To determine whether this defect arises from lack of proper internalization as opposed to the inability to retain internalized receptors in endosomal compartments, a shorter chase time was analyzed. After 5 min, internalization of GluA1 receptors was not significantly altered in the absence of Rab11Fip5 (Fig. 9D; p = 0.46, ΔCre, 1.73 ± 0.20, n = 6; Cre, 1.52 ± 0.20, n = 6). Thus, consistent with its requisite role in NMDAR-dependent LTD, Rab11Fip5 is required for the net increase in internalized surface AMPARs following NMDA application in cultured neurons, and it acts primarily by preventing recycling back to the plasma membrane of internalized receptors." Authors conclude: "The most notable result in our present study is that Rab11Fip5 is required for LTD (Fig. 7) and the net internalization of AMPARs during chemically induced LTD (Fig. 9C,D). This is a first demonstration that a Rab11Fip acts as a critical regulator of activity-induced trafficking in the postsynaptic compartment during LTD." |
| Evidence tracking, Biological System: | Cultured neurons |
| Evidence tracking, Protein Targeting: | RNAi / shRNA Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Confocal Electrophysiology (generic) |
| 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: | 4864 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |