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SNAP29 (F7Y8J) Rabbit Monoclonal Antibody #53186

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    Product Specifications

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 29
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunofluorescence (Immunocytochemistry) 1:100 - 1:400

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    SNAP29 (F7Y8J) Rabbit Monoclonal Antibody recognizes endogenous levels of total SNAP29 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human SNAP29 protein.

    Background

    Synaptosomal-associated protein 29 (SNAP29) is a versatile member of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) family, and functions as a Q-SNARE, typically providing two of the four alpha-helices required to form the SNARE complex that drives membrane fusion (1). Unlike other family members, which are tethered to specific membranes via fatty acid chains, SNAP29 is primarily a soluble protein and can act as a promiscuous mediator of membrane fusion across multiple cellular pathways (2). SNAP29 plays its most critical role in autophagy by forming a complex with Syntaxin 17 (STX17) and VAMP8 to mediate autophagosome-lysosome fusion (3). SNAP29 also controls protein transport between the endoplasmic reticulum (ER) and Golgi apparatus, regulates endocytic recycling, and maintains proper Golgi morphology (1,4). Additionally, SNAP29 promotes accurate chromosome segregation (5) and has been implicated in the secretion of small extracellular vesicles or exosomes, suggesting a role in intercellular communication (4). Homozygous loss-of-function mutations in the SNAP29 gene are linked to CEDNIK (CErebral Dysgenesis, Neuropathy, Ichthyosis, and palmoplantar Keratoderma) syndrome (6), and decreased levels of neuronal SNAP29 may contribute to impaired autophagic/lysosomal function and altered synaptic protein homeostasis in neurodegenerative conditions (7,8). Recent studies have shown that the SARS-CoV-2 ORF7a protein downregulates SNAP29 to prevent autophagosome-lysosome fusion and promote viral replication (9).

    Alternate Names

    CEDNIK; FLJ21051; SNAP-29; SNAP29; SNP29; Soluble 29 kDa NSF attachment protein; Synaptosomal-associated protein 29; synaptosomal-associated protein, 29kD; synaptosomal-associated protein, 29kDa; synaptosome associated protein 29; synaptosome associated protein 29kDa; Vesicle-membrane fusion protein SNAP-29

    For Research Use Only. Not for Use in Diagnostic Procedures.
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