Render Target: STATIC
Render Timestamp: 2024-12-02T10:43:57.397Z
Commit: cd2fae6ca3f811b1ddb1df24ac291ed56d5d501b
XML generation date: 2024-09-30 01:57:57.718
Product last modified at: 2024-11-20T21:00:09.239Z
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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.

p19 ARF (E9X4Z) Rabbit mAb #77184

Filter:
  • WB

    Supporting Data

    REACTIVITY M
    SENSITIVITY Endogenous
    MW (kDa) 21
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • M-Mouse 

    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, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    p19 ARF (E9X4Z) Rabbit mAb recognizes endogenous levels of total p19 ARF protein. This antibody does not recognize p16 INK4A protein or human p14 ARF protein.

    Species Reactivity:

    Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu92 of mouse p19 ARF protein.

    Background

    Human p14 ARF (p19 ARF in mouse) is a pro-apoptotic cell cycle regulator frequently inactive in human tumors (1). Basal expression of p14 ARF is low in most cell types, but accumulation of this protein occurs in response to oncogene expression (2,3). Increased p14 ARF levels facilitate MDM2 degradation, leading to increased p53 protein levels and subsequent cell cycle arrest and/or apoptosis (4). While most p14 ARF signaling has traditionally thought to be p53-dependent, more recent reports have described p53-independent p14 ARF signaling leading to cell cycle arrest and apoptosis (5,6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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