Home Primary Antibodies APG5L/ATG5 Antibody [K12K17]

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APG5L/ATG5 Antibody [K12K17]

Catalog No.: F2856

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000 - 1:10000
    1:20
    1:100 - 1:250
    1:100 - 1:250
    Application
    WB, IP, IHC, IF
    Reactivity
    Mouse, Rat, Human
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    102 kDa,32 kDa 32 kDa, 55 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.

    Datasheet & SDS

    Biological Description

    Specificity
    APG5L/ATG5 Antibody [K12K17] detects endogenous levels of total APG5L/ATG5 protein.
    Clone
    K12K17
    Synonym(s)
    APG5L; ASP; ATG5; Autophagy protein 5; APG5-like; Apoptosis-specific protein
    Background
    ATG5 (Autophagy-related protein 5, also known as APG5L) is a core component of the autophagy machinery essential for autophagosome formation through ubiquitin-like conjugation systems in eukaryotic cells. ATG5 comprises an N-terminal ubiquitin-like domain (UblA), a central helix-rich domain (HR), and a C-terminal ubiquitin-like domain (UblB), connected by two flexible linker regions (L1 and L2), with an α-helix at the N-terminus where lysine residue K130 serves as the conjugation site for ATG12. ATG5 is activated by ATG7 (E1-like enzyme) and conjugated to ATG12 by ATG10 (E2-like enzyme), forming the ATG12-ATG5 conjugate that non-covalently binds ATG16L1 to create an E3-like ligase complex localized to the phagophore membrane. This complex facilitates LC3 lipidation (LC3-I to LC3-II conjugated to phosphatidylethanolamine), driving autophagosome elongation and maturation essential for degradation of damaged organelles and proteins during stress/starvation. ATG5 also exhibits autophagy-independent roles, including pro-apoptotic functions via mitochondrial translocation, cell cycle arrest through CDK1/CHEK2 phosphorylation, and immune regulation. Its dysregulation contributes to neurodegeneration, cancer, and autoinflammatory diseases.
    References
    • https://pubmed.ncbi.nlm.nih.gov/23202584/
    • https://pubmed.ncbi.nlm.nih.gov/30386331/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
    If you have any other enquiries, please leave a message.

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