Render Target: STATIC
Render Timestamp: 2024-12-02T12:31:01.204Z
Commit: cd2fae6ca3f811b1ddb1df24ac291ed56d5d501b
XML generation date: 2024-08-01 15:28:21.904
Product last modified at: 2024-11-24T18:00:08.440Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

ARL8B Antibody #56085

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 21
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    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

    ARL8B Antibody recognizes endogenous levels of total ARL8B protein. This antibody does not cross-react with ARL8A.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala137 of human ARL8B protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    The small GTPases of the Arf and Rab families have critical roles in cytoskeletal organization and membrane/vesicular transport (1,2). The related ADP-ribosylation factor-like (ARL) family member ARL8, including two paralogs ARL8A and ARL8B, has emerged as an important regulator of lysosomal transport to the cell periphery (3,4). Lysosome positioning is a critical determinant of a number of physiological processes including plasma membrane repair, cell migration, antigen presentation, and response to nutrient availability. Membrane association of ARL8B is regulated by the BLOC-one related complex (BORC), a multi-subunit complex under the control of the mTOR pathway (5,6). Effectors of GTP-bound ARL8B include PLEKHM2/SKIP and the Vps41 subunit of the HOPS complex (7). Studies have found that ARL8B may be a critical factor for NK-mediated cytotoxicity by driving polarization of lytic granules toward the immune synapse (8). In addition, ARL8B has been shown to act as a negative regulator of autophagy (9). Knockdown of ARL8B resulted in increased fusion of autophagosomes with lysosomes. Furthermore, ARL8B depleted cells had reduced levels of pathogenic substrates associated with neurodegenerative diseases.
    For Research Use Only. Not For Use In Diagnostic Procedures.
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