DLK1, Soluble (human) ELISA Kit

CHF 740.00
In stock
AG-45A-0032YEK-KI0196 wellsCHF 740.00
More Information
Product Details
Synonyms Protein Delta Homolog 1; pG2; Fetal Antigen 1; FA 1
Product Type Kit
Properties
Application Set Quantitative ELISA
Specificity Detects human DLK1. Does not cross-react with human DLL1 or human DNER.
Crossreactivity Human
Quantity 1 x 96 wells
Sensitivity 336pg/ml
Range 0.47 to 30ng/ml
Sample Type Cell Culture Supernatant
Serum
Assay Type Sandwich
Detection Type Colorimetric
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage +4°C
Handling Advice After standard reconstitution, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
Plate and reagents should reach room temperature before use.
Use/Stability 12 months after the day of manufacturing. See expiry date on ELISA Kit box.
Documents
Manual Download PDF
MSDS Download PDF
Product Specification Sheet
Datasheet Download PDF

The Notch signaling pathway is essential for appropriate cell differentiation and cell fate decisions. DLK1 (Protein delta homolog 1; Preadipocyte factor 1; Pref-1) is a regulator of adipocyte differentiation found in serum and urine. DLK1 shifts nutrient metabolism towards FA oxidation. Serum or plasma levels of soluble DLK1 affect negatively or positively adipogenesis and control mesenchymal cell fate. DLK1 is frequently upregulated in myelodysplastic syndrome (MDS) patients compared to non-leukemic individuals. Fetus is the source of maternal circulating DLK1 during pregnancy. It has been recently reported that measurement of DLK1 in maternal blood may be a valuable method for diagnosing human disorders associated with impaired DLK1 expression, and to predict poor intrauterine growth and complications of pregnancy. 

 

Product References
  1. Identification of adipokine clusters related to parameters of fat mass, insulin sensitivity and inflammation: G. Flehmig, et al.; PLos One 9, e99785 (2014)
  2. Fetus-derived DLK1 is required for maternal metabolic adaptations to pregnancy and is associated with fetal growth restriction: M. Cleaton, et al.; Nat. Genet. 48, 1473 (2016)
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