SNAP29

Protein-coding gene in the species Homo sapiens
title: "SNAP29" type: doc version: 1 created: 2026-02-28 author: "Wikipedia contributors" status: active scope: public tags: ["genes-mutated-in-mice"] description: "Protein-coding gene in the species Homo sapiens" topic_path: "general/genes-mutated-in-mice" source: "https://en.wikipedia.org/wiki/SNAP29" license: "CC BY-SA 4.0" wikipedia_page_id: 0 wikipedia_revision_id: 0
::summary Protein-coding gene in the species Homo sapiens ::
Synaptosomal-associated protein 29 is a protein that in humans is encoded by the SNAP29 gene.
Function
This gene, a member of the SNAP25 gene family, encodes a protein involved in multiple membrane trafficking steps. Two other members of this gene family, SNAP23 and SNAP25, encode proteins that bind a syntaxin protein and mediate synaptic vesicle membrane docking and fusion to the plasma membrane. The protein encoded by this gene binds tightly to multiple syntaxins and is localized to intracellular membrane structures rather than to the plasma membrane. While the protein is mostly membrane-bound, a significant fraction of it is found free in the cytoplasm. Use of multiple polyadenylation sites has been noted for this gene.
Interactions
SNAP29 has been shown to interact with Syntaxin 3 and EHD1.
SNAP29 was shown to interact with CVB3 and EV-D68 viral protease 3C.
References
References
- (December 1998). "Three novel proteins of the syntaxin/SNAP-25 family". The Journal of Biological Chemistry.
- (December 1999). "The DNA sequence of human chromosome 22". Nature.
- "Entrez Gene: SNAP29 synaptosomal-associated protein, 29kDa".
- (August 2001). "Association of insulin-like growth factor 1 receptor with EHD1 and SNAP29". The Journal of Biological Chemistry.
- (March 2018). "Enteroviral Infection Inhibits Autophagic Flux via Disruption of the SNARE Complex to Enhance Viral Replication". Cell Reports.
- (March 2018). "Enteroviruses Remodel Autophagic Trafficking through Regulation of Host SNARE Proteins to Promote Virus Replication and Cell Exit". Cell Reports.
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