Render Target: STATIC
Render Timestamp: 2024-12-20T12:09:52.445Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-08-01 15:27:59.734
Product last modified at: 2024-08-21T12:45:34.537Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Syntaxin 17 Antibody #84592

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 33
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200

    Storage

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

    Protocol

    Specificity / Sensitivity

    Syntaxin 17 Antibody recognizes endogenous levels of total syntaxin 17 protein.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu126 of human syntaxin 17 protein. Antibodies are purified by peptide affinity chromatography.

    Background

    Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents (1,2). Autophagy is generally activated by conditions of nutrient deprivation but has also been associated with a number of physiological processes, including development, differentiation, neurodegeneration, infection, and cancer (3). Syntaxin 17/STX17 is a SNARE factor recruited to autophagosomes and required for autophagosome fusion to lysosomes. Syntaxin 17 interacts with SNAP29 (Qbc-SNARE synaptosome-associated protein 29) and the lysosomal factor VAMP8 (R-SNARE vesicle-associated membrane protein 8), as well as BRUCE, an inhibitor of apoptosis (IAP) protein, which is also involved in autophagosome/lysosome fusion (4,5).Syntaxin 17 promotes initiation of PINK1/Parkin-independent mitophagy, which is regulated by depletion of the mitochondrial outer membrane protein Fis1 (6).
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