| Annotated protein: | Pro-neuregulin-1, membrane-bound isoform (Pro-NRG1) [Cleaved into: Neuregulin-1 (Acetylcholine receptor-inducing activity) (ARIA) (Breast cancer cell differentiation factor p45) (Glial growth factor) (Heregulin) (HRG) (Neu differentiation factor) (Sensory and motor neuron-derived factor)]. Gene symbol: NRG1. Taxonomy: Homo sapiens (Human). Uniprot ID: Q02297-6 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ NRG1 |
| Ontology domain: | Biological Process |
| SynGO term: | regulation of postsynaptic neurotransmitter receptor endocytosis (GO:0099149) |
| Synapse type(s): | hippocampus, glutamatergic |
| Annotated paper: | Kwon OB, et al. "Neuregulin-1 reverses long-term potentiation at CA1 hippocampal synapses" J Neurosci. 2005 Oct 12;25(41):9378-83 PMID:16221846 |
| Figure(s): | Fig.1, 2, 3, 4 |
| Annotation description: | Fig.1: "NRG-1β depotentiates LTP at CA1 synapses." Fig.2: "NRG-1β-mediated LTP reversal shares similarities with activity-dependent depotentiation" Fig.3: "NRG-1β acts postsynaptically on AMPA receptors to reverse LTP" Fig.4: "Effects of NRG-1 on transfected and native surface GluR1 AMPARs in hippocampal neurons. " - "Hippocampal neurons were cotransfected with untagged GluR2 and a GluR1 construct fused at its N-terminal extracellular domain to seGFP to monitor in real time its surface expression (Ashby et al., 2004), exploiting the pH sensitivity of seGFP that renders it ~20-fold more fluorescent at the cell surface (pH ~ 7.4) than in endocytic vesicles (pH ~ 5.5)." - "NRG-1β caused a significant reduction in fluorescence at receptor clusters and in neurites (Fig. 4A, top), starting ~2 min after the onset of perfusion, as shown in the line graphs of the entire recording session (Fig. 4B, left). Five minutes after NRG-1β application (Fig. 4C, left), the levels of surface GluR1 receptors were reduced significantly (68.6 ± 5.3%) relative to those in chemLTP cultures (set to 100%). The NRG-1β-induced reduction of surface seGFP-GluR1 requires ErbB receptor activation, because the effect was blocked by PD158780 (Fig. 4A-C, right). " - "As shown in Figure 4D (images are in supplemental material, available at www.jneurosci.org), chemLTP induction by glycine increased surface expression of GluR1-containing AMPARs (213 ± 29%) but not of NMDARs (120 ± 18%). Treatment of chemLTP cultures with NRG-1β reduced surface GluR1-containing AMPARs (106 ± 15%) to pre-chemLTP levels (Fig. 4D, left), and this was blocked by PD158780 (195 ± 26%). No changes in NMDAR surface levels were observed for any treatment (Fig. 4D, right), indicating that NRG-1β promotes the selective removal of surface AMPARs." Note: PD158780 is an ErbB receptor blocker. |
| Evidence tracking, Biological System: | Intact tissue Cultured neurons |
| Evidence tracking, Protein Targeting: | Over-expression |
| Evidence tracking, Experiment Assay: | Confocal Whole-cell patch clamp Field recordings |
| 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: | 2776 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |