| Annotated protein: | Receptor tyrosine-protein kinase erbB-4 (EC 2.7.10.1) (Proto-oncogene-like protein c-ErbB-4) [Cleaved into: ERBB4 intracellular domain (4ICD) (E4ICD) (s80HER4)]. Gene symbol: ERBB4. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q61527 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ ERBB4 |
| Ontology domain: | Biological Process |
| SynGO term: | neurotransmitter receptor localization to postsynaptic specialization membrane (GO:0099645) |
| Synapse type(s): | Neuro-muscular junction |
| Annotated paper: | Schmidt N, et al. "Neuregulin/ErbB regulate neuromuscular junction development by phosphorylation of alpha-dystrobrevin" J Cell Biol. 2011 Dec 26;195(7):1171-84 PMID:22184199 |
| Figure(s): | Fig.1, 2 |
| Annotation description: | Fig.1: "Deletion of NRG/ErbB signaling increases removal of recycled receptor from the postsynaptic membrane" Fig.2: "Deletion of NRG/ErbB signaling increases AChR puncta containing recycled but not preexisting AChRs in the perisynaptic membrane." - "Genetic and pharmacological abolishment of ErbBs accelerates the migration of recycled receptors to the perisynaptic membrane" Fig.3: "Structural changes in erbb2/4-/- NMJs" - "High resolution confocal microscopy revealed that mutant mice often have small areas within the synaptic AChR cluster that are devoid of receptors, giving the cluster a perforated appearance (Fig. 3 b)... Receptor holes were covered by presynaptic terminal branches (Fig. 3 f), suggesting that receptor holes are not due to localized withdrawal of the nerve due to a presynaptic defect resulting from the lack of ErbB-dependent back-signaling onto the motor neurons (Bao et al., 2003). Thus, the modified distribution of AChRs is a direct consequence of the loss of NRG/ErbB signaling to the subsynaptic membrane." "To examine whether ErbB-mediated signaling is, instead, involved in regulating the stability of postsynaptic AChRs at the NMJ, the sternomastoid muscle of wild-type and erbb2/4-/- mice (Escher et al., 2005) was labeled to saturation in vivo with fluorescent α-bungarotoxin (α-BTX)-Alexa 594, and the decline in fluorescence of labeled AChRs was monitored over time. In erbb2/4-/- NMJs the residual fluorescence normalized to that at the time of labeling was significantly lower than in wild-type synapses (Fig. 1 a; ~30% vs. 60% at 72 h). This indicates that the lack of ErbB-mediated signaling increases the rate of synaptic AChR removal." |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Confocal |
| Annotator(s): | Pim van Nierop (ORCID:0000-0003-0593-3443) 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: | 3824 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |