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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

GAK (E7W7Z) Rabbit mAb #51509

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 175
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    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

    GAK (E7W7Z) Rabbit mAb recognizes endogenous levels of total GAK protein. A band of unknown origin is detected at ~45 kDa and at ~20kDa.


    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro758 of human GAK protein.

    Background

    Cyclin-G-associated kinase (GAK) is the ubiquitous form of the neuronal-specific protein auxilin 1 (1) and is an essential cofactor for Hsc70-dependent uncoating of clathrin-coated vesicles in non-neuronal cells (2). The recruitment of GAK to clathrin-coated pits during endocytosis is dependent on its PTEN-like domain, which has been shown to bind to phospholipids (3). It has been postulated that the JAK inhibitor baricitinib may impair entry of the SARS-CoV-2 virus by inhibiting AAK1- and GAK-mediated endocytosis via ACE2 (4). In the nucleus, GAK forms complexes with cyclin G1 and other nuclear proteins (5) and plays an essential role in proper mitotic progression by maintaining centrosome structure (6). GAK is also required for the regulation of basal, PRKN-independent mitophagy by modifying the mitochondrial network and lysosomal morphology that compromise efficient transport of mitochondria for degradation (7,8).

    For Research Use Only. Not For Use In Diagnostic Procedures.
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