Asprosin (AA 2732-2871) protein (His tag)

Catalog No. ABIN5564356

This Recombinant Asprosin protein is produced in Escherichia coli (E. coli).

Quick Overview for Asprosin (AA 2732-2871) protein (His tag) (ABIN5564356)

Target: Asprosin

Protein Type: Recombinant

Origin: Human

Source: Escherichia coli (E. coli)

Application: SDS-PAGE (SDS)

Purity: >95 % (SDS-PAGE)

Product Details

Protein Characteristics: AA 2732-2871

Purification tag / Conjugate: His tag

Purpose: Asprosin (human) (rec.) (His)

Cross-Reactivity: Human

Characteristics: Human asprosin (aa 2732-2871) is fused at the C-terminus to a His-tag.

Sterility: Sterile filtered

Endotoxin Level: <0.1EU/μg purified protein (LAL test).

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

Format: Lyophilized

Concentration: Lot specific

Buffer: Lyophilized from 0.2μm-filtered solution in 50 mM Tris-HCl( pH 8.2), 200 mM NaCl.

Handling Advice: After reconstitution, prepare aliquots and store at -20 °C. Avoid freeze/thaw cycles. Centrifuge lyophilized vial before opening and reconstitution.

Storage: 4 °C,-20 °C

Storage Comment:

Short Term Storage: +4°C

Long Term Storage: -20°C

Use & Stability: Stable for at least 6 months after receipt when stored at -20°C.Working aliquots are stable for up to 3 months when stored at -20°C.

Expiry Date: 6 months

Target Details

Target: Asprosin

Background:

Fibrillin-1 C-terminal Cleavage Product, FBN1 C Terminal Cleavage Product

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 pro-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. Endogenous asprosin runs on SDS-PAGE at ~30 kDa, while bacterially expressed recombinant asprosin runs at 18 kDa. The difference of migration is probably due to predicted three N-linked glycosylation sites and potentially other post-translational modifications that are lacking in bacteria. Bacterially expressed recombinant asprosin retains the biological activity displayed by its endogenously expressed counterpart.

Molecular Weight: ~18kDa (SDS-PAGE)

UniProt: P35555