Asprosin (human) ELISA Kit

INQ
In stock
AG-45B-0010-KI0196 wellsINQ
More Information
Product Details
Synonyms Fibrillin-1 C-terminal Cleavage Product; FBN1 C Terminal Cleavage Product
Product Type Kit
Properties
Application Set Quantitative ELISA
Specificity

Detects human asprosin. Cross-reacts with mouse asprosin.

Crossreactivity Human
Mouse
Quantity

1 x 96 wells

Sensitivity 140pg/ml
Range 0.156 to 10ng/ml
Sample Type Cell Culture Supernatant
Plasma
Assay Type Sandwich
Detection Type Colorimetric
Accession Number P35555
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 No
MSDS No
Product Specification Sheet
Datasheet Download PDF

Asprosin is a new fasting-induced protein hormone that targets the liver to increase plasma glucose levels. Asprosin is the C-terminal cleavage product of the protein Fibrillin-1. Asprosin is secreted from white adipose tissue and increases hepatic glucose production by using cAMP as a second messenger, leading to activation of protein Kinase A. Reduction of asprosin levels protects against metabolic syndrome-associated hyperinsulinism. Asprosin may act as a circulating hunger signal. Indeed, peripherally injected recombinant asprosin can cross the blood-brain barrier and intracerebroventricular (i.c.v.) injection of recombinant asprosin stimulated appetite in wild-type mice, indicating a central mechanism of action. Loss of asprosin in mice and human leads to decreased fat mass and body weight and hypophagia. Mice are also completely protected from the development of diet-induced obesity. Asprosin works by stimulating the orexigenic AgRP+ (Agouti related neuropeptide) neurons via a cAMP-dependent pathway and by inhibiting the anorexigenic neurons POMC+ (pro-opiomelanocortin) neurons in a GABA-dependent manner. Mutation in asprosin in human leads to the pattern of metabolic dysregulation, including partial lipodystrophy, accompanied by reduced plasma insulin. Due to its key role in food regulation, asprosin function could serve as a potentially unique therapeutic target against obesity, diabetes or metabolic diseases.

© 2017 Adipogen Life Sciences. Pictures: © 2012 Martin Oeggerli. All Rights Reserved.