Cat. # | Size | Qty. | Price |
---|---|---|---|
74969S | 100 µl |
|
REACTIVITY | H Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 70 |
Source/Isotype | Rabbit IgG |
Product Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Loading of prestained molecular weight markers (#59329, 10 µl/lane) to verify electrotransfer and biotinylated protein ladder (#7727, 10 µl/lane) to determine molecular weights are recommended.
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
Human, Monkey
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro301 of human PAPSS2 protein.
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).
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