Annotated protein:SUMO-conjugating enzyme UBC9 (EC 2.3.2.-) (RING-type E3 SUMO transferase UBC9) (SUMO-protein ligase) (Ubiquitin carrier protein 9) (mUBC9) (Ubiquitin carrier protein I) (Ubiquitin-conjugating enzyme E2 I) (Ubiquitin-protein ligase I). Gene symbol: UBE2I. Taxonomy: Mus musculus (Mouse). Uniprot ID: P63280
antibody wiki:
SynGO gene info:SynGO data @ UBE2I
Ontology domain:Biological Process
SynGO term:modulation of chemical synaptic transmission (GO:0050804)
Synapse type(s):Schaffer collateral synapse (CA3->CA1)
Annotated paper:Lee L, et al. "Regulation of synaptic plasticity and cognition by SUMO in normal physiology and Alzheimer's disease" Sci Rep. 2014 Dec 2;4:7190 PMID:25448527
Figure(s):Figure 2
Annotation description:"With the development of the TAT-Ubc9 transduction enzymes, we were able to investigate this issue by specifically inhibiting SUMOylation in acute hippocampal slices and observing the effects on LTP. When TAT-Ubc9(DN) (100 nM) was perfused onto slices for 1 hour prior to induction, LTP was significantly reduced compared to interleaved vehicle, TAT-Ubc9 or TAT-GFP controls (Fig. 2a, 2b). Baseline transmission was not altered during the TAT protein perfusions, and input-output curves were not affected by TAT-Ubc9 or TAT-Ubc9(DN) (Fig. 2c). In addition, we performed whole cell patch clamp experiments to investigate potential effects of SUMO inhibition on glutamate receptors known to underlie LTP. However, current-voltage curves for neither AMPA receptors nor NMDA receptors were altered by TAT-Ubc9(DN) (Fig. S2c, S2d). The effects of acute SUMOylation inhibition appear to be specific for long-term synaptic plasticity and do not impact basal transmission.
...
While long-term synaptic plasticity in the form of LTP was significantly impaired by SUMO inhibition/deconjugation, we also investigated a form of short-term synaptic plasticity, paired-pulse facilitation (PPF), that is thought to be expressed presynaptically. TAT-Ubc9(DN) did not significantly affect PPF at any of the inter-stimulus intervals examined (Fig. 2f)."
Evidence tracking, Biological System:Intact tissue
Evidence tracking, Protein Targeting:Over-expression
Evidence tracking, Experiment Assay:Whole-cell patch clamp
Field recordings
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
Additional literature:Increasing synaptic activity with a GABAA receptor antagonist or directly activating mGlu5R increases the synaptic residency time of Ubc9 via a Gαq/PLC/Ca2+/PKC cascade. This activation promotes a transient synaptic trapping of Ubc9 through a PKC phosphorylation-dependent increase of Ubc9 recognition to phosphorylated substrates and consequently leads to the modulation of synaptic sumoylation. @ PMID:25311713

overexpression of a dominant-negative Ubc9 mutant modulated AMPAR trafficking and LTP @ PMID:23326329
SynGO annotation ID:5140
Dataset release (version):20231201
View annotation as GO-CAM model:Gene Ontology