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Mouse Salusin Beta (SALb) ELISA Kit-Competitive

Cat. No.EK5F908

Product TypeAnimal Immunoassay Kits

Size 96T

Product Overview

BioVenic Mouse Salusin Beta (SALb) ELISA Kit-Competitive is designed for the quantitative determination of Mouse SALb in serum, plasma, tissue homogenate, cell culture supernatant, cell lysate, and other biological fluids using a Competitive ELISA method. For research use only.

Specifications

Assay Type ELISA-Competitive
Specificity The assay kit is specific for Mouse Salusin Beta (SALb).
Target Species Mouse
Species Reactivity Mouse
Detection Range 6.25-400 pg/mL
Reproducibility Intra-Assay: CV < 10%; Inter-Assay: CV < 12%
Assay Time Around 90 min
Sample Requirement Serum, plasma, tissue homogenate, cell culture supernatant, cell lysate, and other biological fluids.

Target Information

Salusin Beta in mice is associated with a range of complex functions, including promoting vascular inflammation and atherosclerosis, as well as regulating cardiovascular function, the autonomic nervous system, and antioxidant responses. Salusin Beta contributes to vascular inflammation and atherosclerosis through various mechanisms. For instance, it can induce vascular inflammation in ApoE-deficient mice via the IκBα/NF-κB signaling pathway. Additionally, Salusin Beta facilitates foam cell formation and monocyte adhesion through the NOX2/NF-κB signaling pathway. These findings suggest that Salusin Beta plays a pro-inflammatory and pro-atherosclerotic role in atherosclerotic lesions.

Target/Biomarker Mouse SALb
Target Synonym Salusin Beta

Shipping and Storage

This product is shipped with gel ice packs. It is recommended to store at 2-8 °C (Up to 6 months).

Documents

COA

To request a Certificate of Analysis, please enter the Lot No. in the search box. Note: Certificate of Analysis not available for kits.

The product is for research use only.
Not for commercial, prophylactic, diagnostic, or therapeutic applications.

References

  1. Zhou, Cheng-Hua et al. "Salusin-β not salusin-α promotes vascular inflammation in ApoE-deficient mice via the I-κBα/NF-κB pathway." PloS one vol. 9,3 e91468. 12 Mar. 2014.
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