| Annotated protein: | Brain-enriched guanylate kinase-associated protein. Gene symbol: BEGAIN. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q68EF6 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ BEGAIN |
| Ontology domain: | Biological Process |
| SynGO term: | regulation of postsynaptic neurotransmitter receptor activity (GO:0098962) |
| Synapse type(s): | spinal cord, glutamatergic hippocampus, glutamatergic |
| Annotated paper: | Katano T, et al. "Involvement of Brain-Enriched Guanylate Kinase-Associated Protein (BEGAIN) in Chronic Pain after Peripheral Nerve Injury" eNeuro. 2016 Oct 17;3(5):ENEURO.0110-16.2016 PMID:27785460 |
| Figure(s): | Fig 6 |
| Annotation description: | Fig. 6: In the substantia gelatinosa (SG, lamina II) neurons from BEGAIN-KO mice the rising phase of evoked NMDAR EPSCs, but not that of AMPAR EPSCs is altered. Literal: "We further examined evoked NMDAR EPSCs isolated in the presence of these three antagonists at a holding potential of 40 mV, as previously reported (Katano et al., 2008). The NMDAR EPSCs in BEGAIN-KO mice had a shape of currents different from those in WT mice. The former mice showed relatively slower developing currents and did not have the normal rising phase (left and middle traces in Fig. 6A). Also, the time to peak of NMDAR EPSCs in BEGAIN-KO mice was significantly longer than in WT mice. However, the time to peak and decay time of AMPA EPSCs (evoked EPSCs recorded at -70 mV) did not differ between WT and BEGAIN-KO mice (left graph in Fig. 6B). The delay between times to peak for AMPAR and NMDAR EPSCs elicited in singe SG neurons was also longer in BEGAIN-KO mice than in WT mice (right graph in Fig. 6B). The amplitude of NMDAR EPSCs and the ratio of NMDAR to AMPAR EPSCs amplitude did not differ between WT and BEGAIN-KO mice (Fig. 6C). These results indicate that slower-developing NMDAR EPSCs in the BEGAIN-KO mice resulted in lengthening of the delay between times to peak for AMPAR and NMDAR EPSCs." 8/11/2017 Pim - The authors express uncertainty on the precise nature of the EPSC effect caused by phosphorylation of the GluN2B subunit. The used mutation is known to: "... inhibition of GluN2B phosphorylation in Fyn-knockout mice or in knock-in mice with the Y1472 site of GluN2B mutated to phenylalanine (Y1472F-KI) affects the localization of GluN2B at the center of the postsynapse ..." I have trouble understanding the precise interpretation by the authors in the discussion section. |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Whole-cell patch clamp IP + WB/MSMS Y2H |
| Annotator(s): | Chiara Verpelli (ORCID:0000-0003-2949-9725) Carlo Sala (ORCID:0000-0003-0662-9523) |
| Lab: | CNR Neuroscience Institute Milan and Dept. of Biotechnology and Translational Medicine, University of Milan, 20129 Milan, Italy |
| SynGO annotation ID: | 1715 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |