Render Target: STATIC
Render Timestamp: 2024-11-07T10:50:59.817Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-08-01 15:28:26.923
Product last modified at: 2024-05-30T07:11:48.804Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

DUSP9 Antibody #59277

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 44, 46
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100

    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

    DUSP9 Antibody recognizes endogenous levels of total DUSP9 protein.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human DUSP9 protein. Antibodies are purified by peptide affinity chromatography.

    Background

    MAP kinases are inactivated by dual-specificity protein phosphatases (DUSPs) that differ in their substrate specificity, tissue distribution, inducibility by extracellular stimuli, and cellular localization. DUSPs, also known as MAPK phosphatases (MKPs), specifically dephosphorylate both threonine and tyrosine residues in MAPK P-loops and have been shown to play important roles in regulating the function of the MAPK family (1,2). At least 13 members of the family (DUSP1-10, DUSP14, DUSP16, and DUSP22) display unique substrate specificities for various MAP kinases (3). MAPK phosphatases typically contain an amino-terminal rhodanese-fold responsible for DUSP docking to MAPK family members and a carboxy-terminal catalytic domain (4). These phosphatases can play important roles in development, immune system function, stress responses, and metabolic homeostasis (5). In addition, research studies have implicated DUSPs in the development of cancer and the response of cancer cells to chemotherapy (6).

    DUSP9 has been implicated in cancer, although expression level and effect on downstream signaling pathways are varied. In colorectal carcinoma, for example, it has been shown that the levels of DUSP9 are reduced in cancerous tissue compared to normal adjacent tissue (7), and in clear cell renal carcinoma cell line and xenograft experiments decreased DUSP9 was also observed, suggesting that it may be a tumor suppressor in some cell types (8). In contrast, in some difficult to treat triple negative breast cancers, experiments suggest DUSP9 activity and expression is abnormally elevated, particularly in cancer-like stem cells in these tumors (9).

    DUSP9 has also been shown to be a key suppressor of high-fat diet-induced hepatic steatosis and inflammatory responses in liver. Since no drugs have yet to be approved for NAFLD and NASH, therapeutics to increase expression of DUSP9 in liver are of interest (10).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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