Render Target: SSR
Render Timestamp: 2024-12-19T21:16:09.519Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:59:52.029
Product last modified at: 2024-12-02T17:15:09.609Z
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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.

GOT2 (F4P3R) Rabbit mAb #39627

Filter:
  • WB
  • IHC
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 41
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:10 - 1:50
    Immunohistochemistry (Paraffin) 1:50 - 1:200
    Immunofluorescence (Immunocytochemistry) 1:100 - 1:400

    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.

    For a carrier free (BSA and azide free) version of this product see product #66911.

    Protocol

    Specificity / Sensitivity

    GOT2 (F4P3R) Rabbit mAb recognizes endogenous levels of total GOT2 protein. This antibody does not cross-react with GOT1 protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly39 of human GOT2 protein.

    Background

    Glutamate oxaloacetate transaminase 2 (GOT2), a mitochondrial enzyme, catalyzes the conversion of oxaloacetate to aspartate. Studies show that the metabolite pyridoxal phosphate (PLP) is selectively required by acute myeloid leukemia. PLP-dependent GOT2 selectively sustains leukemic cell proliferation. Depletion of GOT2 suppresses the proliferation of acute myeloid leukemia cells (1). In addition, mouse hematopoietic stem cells are dependent on cell-autonomous aspartate synthesis. Got2 deletion leads to decreased aspartate levels and reduced hematopoietic stem cell function (2). Furthermore, GOT2-dependent aspartate synthesis is also necessary for protein and collagen biosynthesis in chondrocytes and is critical for chondrocyte proliferation and growth (3).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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