Render Target: STATIC
Render Timestamp: 2024-12-20T11:37:50.215Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-10-15 21:56:07.098
Product last modified at: 2024-12-17T19:00:46.605Z
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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.

PAPSS2 (E8O2O) Rabbit mAb #74969

Filter:
  • WB

    Supporting Data

    REACTIVITY H Mk
    SENSITIVITY Endogenous
    MW (kDa) 70
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • Mk-Monkey 

    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

    PAPSS2 (E8O2O) Rabbit mAb recognizes endogenous levels of total PAPSS2 protein.

    Species Reactivity:

    Human, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro301 of human PAPSS2 protein.

    Background

    PAPSS2 is a bifunctional enzyme with both ATP sulfurylase and APS kinase activity, which mediates two reactions to generate 3'-Phosphoadenosine-5'-phosphosulfate (PAPS), a critical intermediate in the sulfate activation pathway. PAPS is the sulfate donor co-substrate for all sulfotransferase (SULT) enzymes and is required to catalyze the sulfate conjugation of many endogenous and exogenous compounds (1,2). Mutations in PAPSS2 lead to an autosomal recessive form of spondyloepimetaphyseal dysplasia (SEMD) in humans (3), whereas mutant mice lacking PAPSS2 activity demonstrate defective postnatal skeletal development leading to premature joint degeneration and brachymorphism (4). In conjunction with SULT1E1, PAPSS2 and its paralogue PAPSS1 are responsible for sulfation and subsequent inactivation of estrogen in target tissues. Expression levels of PAPSS2 were found to be significantly higher in tumorous breast and endometrial tissues than in adjacent normal tissues, suggesting that targeting PAPSS2 could be an important approach for estrogen-dependent cancers (5). Additionally, PAPSS2 provides the universal sulfate donor PAPS to SULT2A1, which is responsible for sulfation of the crucial androgen precursor dehydroepiandrosterone (DHEA) (6). TGF-β signaling has been shown to regulate the expression of PAPSS2 via stabilization of SOX9 protein in mouse articular cartilage and bovine chondrocytes (7,8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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