Annotated protein:PDZ domain-containing protein GIPC1 (GAIP C-terminus-interacting protein) (RGS-GAIP-interacting protein) (RGS19-interacting protein 1) (SemaF cytoplasmic domain-associated protein 1) (SEMCAP-1) (Synectin). Gene symbol: GIPC1. Taxonomy: Mus musculus (Mouse). Uniprot ID: Q9Z0G0
antibody wiki:
SynGO gene info:SynGO data @ GIPC1
Ontology domain:Biological Process
SynGO term:presynaptic modulation of chemical synaptic transmission (GO:0099171)
Synapse type(s):hippocampus, glutamatergic
Schaffer collateral synapse (CA3->CA1)
Annotated paper:Yano H, et al. "BDNF-mediated neurotransmission relies upon a myosin VI motor complex" Nat Neurosci. 2006 Aug;9(8):1009-18 PMID:16819522
Figure(s):Fig3, 4, 5, 8 and supplementary figure 3
Annotation description:Fig3A shows that basal neurotransmission in the Schaffer collateral-CA1 synapse is impaired in GIPC1 null mice. Fig4 shows that paired-pulse facilitation is impaired in GIPC1 null mice, while LTP is normal (Fig S3), suggesting that presynaptic plasticity is impaired. Fig5 shows that BDNF-induced potentiation and synaptic vesicle release (Fig8) are absent in GIPC1 null mice, suggesting that this presynaptic signalling of this neuropeptide is impaired.

26/10/2017 Pim
Literal: "The actions of BDNF upon synaptic plasticity occur through increased Bdnf gene expression, processing and release, leading to binding and activation of TrkB receptors in both pre- and postsynaptic sites3,4. Here we demonstrate that BDNF-induced neurotransmitter release relies upon Myo6 and the GIPC1 adaptor protein. GIPC1 binds directly to the Trk receptor24 as well as to Myo6 (refs. 28,30). A notable colocalization of GIPC1 and Myo6 exists in hippocampal neurons, which overlapped with the expression of TrkB receptors. Loss of either GIPC1 or Myo6 protein led to similar defects in presynaptic properties, as measured by PPF and PTP. In addition to hippocampal slice measurements, electrophysiological and FM 1-43 staining experiments using primary hippocampal cultures verified that Myo6 and GIPC1 were required for vesicle recycling in response to BDNF. Hence, BDNF can use GIPC1 and the Myo6 actin motor to modulate neurotransmitter release at presynaptic locations."
Evidence tracking, Biological System:Intact tissue
Evidence tracking, Protein Targeting:Genetic transformation (eg; knockout, knockin, mutations)
Evidence tracking, Experiment Assay:Field recordings
Annotator(s):Jan van Weering (ORCID:0000-0001-5259-4945)
Matthijs Verhage (ORCID:0000-0002-2514-0216)
Lab:Department of Functional Genomics, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands
SynGO annotation ID:1683
Dataset release (version):20231201
View annotation as GO-CAM model:Gene Ontology