SUMOylation of synapsin Ia maintains synaptic vesicle availability and is reduced in an autism mutation.

doi:10.1038/ncomms8728

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Back to search

Article

SUMOylation of synapsin Ia maintains synaptic vesicle availability and is reduced in an autism mutation.

Nature communications - 15 Jul 2015

Tang Leo T-H, Craig Tim J, Henley Jeremy M

Abstract excerpt

Synapsins are key components of the presynaptic neurotransmitter release machinery. Their main role is to cluster synaptic vesicles (SVs) to each other and anchor them to the actin cytoskeleton to establish the reserve vesicle pool, and then release them in response to appropriate membrane depolarization. Here we demonstrate that SUMOylation of synapsin Ia (SynIa) at K687 is necessary for SynIa function....

Topics

Animals
Autistic Disorder
Cerebral Cortex
Epilepsy
Exocytosis
Hippocampus
Humans
Mutation
Neurons
Rats
Rats, Wistar
Sumoylation
Synapses
Synapsins
Synaptic Transmission
Synaptic Vesicles

Source

Open in PubMed Open full text

Identifiers

PMID: 26173895
DOI: 10.1038/ncomms8728
PMCID: PMC4504226

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 31 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

discussions

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics