Fetuin-B Human ELISA

Features

• It is intended for research use only
• The total assay time is less than 4 hours
• The kit measures fetuin-B in human serum and plasma (EDTA, citrate, heparin)
• Assay format is 96 wells
• Standard is recombinant protein based
• Components of the kit are provided ready to use, concentrated or lyophilized

Research topic

Bone and cartilage metabolism, Energy metabolism and body weight regulation, Immune Response, Infection and Inflammation, Oncology, Others

Summary

The protein fetuin-B encoded by the FETUB gene is a member of the fetuin family, part of the cystatin superfamily of cysteine protease inhibitors.
By searching DNA sequence databases, expressed sequence tags encoding human and mouse fetuin-B were identified. The 382 amino acid human fetuin-B protein shares 24% sequence similarity with fetuin-A, the prototypic member of the fetuin protein family.
The human, mouse and rat fetuin-B proteins share 61% amino acid identity.
The expression of fetuin-B is regulated by farnesoid X receptor (FXR), a nuclear receptor that acts as a key factor in the regulation of bile acid, lipid and carbohydrate metabolism.
Functional analysis revealed that fetuin-B, similarly to fetuin-A, is an inhibitor of basic calcium phosphate precipitation, however its activity is lower compared to fetuin-A.
Comparison of the expression levels of fetuin-B and fetuin-A at the RNA level revealed that both fetuin genes are most highly expressed in liver tissue. Like fetuin-A, fetuin-B mRNA was found to be highly expressed in tongue and placenta tissues. Fetuin-B is also expressed at the protein level in sera and several organs of mouse, rat and human. Unlike fetuin-A the amount of fetuin-B protein in human serum varied with gender and was higher in females than in males.
Results obtained from proteomic studies on rats provided a possible relationship between reduced plasma protein levels of fetuin-B and Zinc-alpha2-glycoprotein (ZA2G) and higher risk of diet induced obesity through impaired fatty acid metabolism in hepatocytes.
Plasma fetuin-B along with other proteins was differentially regulated between healthy control and streptozotocin-induced male and female diabetic rats. The proteomic data on gender-dimorphic regulation of plasma proteins can provide valuable information that may be used for evidence-based gender-specific clinical treatment of diabetes.
In a different study, elevated fetuin-B levels were observed in CSF of rats with experimentally induced autoimmune encephalomyelitis (EAE). The EAE model resembles certain aspects of multiple sclerosis, with common features such as motor dysfunction, axonal degradation, and infiltration of T-cells.
The fetuins have also been shown to be subject to inflammation associated changes in hepatic mRNA expression. Fetuin-A and -B are negative acute-phase proteins, meaning that their hepatic expression is down-regulated in response to an inflammatory stimulus. In an in vitro model, fetuin-B was found to be significantly down-regulated in hepatocytes under a high dose of acoustic nanobubbles. In this context, immunohistochemistry detected liver fibrosis and inflammation with nanobubble treatment.
Genetic association studies have reported tumor suppressor activity and that overexpression of fetuin-B in skin squamous carcinoma cells suppresses tumor growth in nude mice.
Targeted gene deletion of fetuin-B in mice causes premature ZP (zona pellucida) hardening and, consequently, female infertility. Transplanting fetuin-B-deficient ovaries into wild-type recipients restores fertility to the ovaries, indicating that plasma fetuin-B is necessary and sufficient for fertilization.

A recent study which analysed differentially expressed proteins in serum between, before and after transection of the anterior cruciate ligament found increased levels of fetuin-B in dogs with osteoarthritis compared to healthy dogs. In dogs, Fetuin B was also identified as one of seven proteins elevated in urine of animals bitten by the European adder.

Areas of investigation:

• Energy metabolism and body weight regulation
• Inflammatory diseases
• Oncology
• Bone metabolism