Render Target: SSR
Render Timestamp: 2024-11-14T22:55:15.949Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:54:38.457
Product last modified at: 2024-10-22T13:00:12.012Z
1% for the planet logo
PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

p14 ARF (4C6/4) Mouse mAb #2407

Filter:
  • WB
  • IHC

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 14
    Source/Isotype Mouse IgG2a
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunohistochemistry (Paraffin) 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

    p14 ARF (4C6/4) Mouse mAb detects endogenous levels of total p14 ARF protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a recombinant His-tagged p14 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.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.