Description
This Human Cystatin M (CST6) ELISA Kit is intended for quantitative detection of human Cystatin M/CST6 in cell culture supernates, serum and plasma (heparin, EDTA). Strip well format. Reagents for up to 96 tests.
This human Cystatin M/CST6 ELISA Kit was based on standard sandwich enzyme-linked immune-sorbent assay technology. A monoclonal antibody from mouse specific for Cystatin M/CST6 has been precoated onto 96-well plates. Standards (Expression system for standard: E Coli, Immunogen sequence: R29-M149) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for Cystatin M/CST6 is added subsequently and then followed by washing with PBS or TBS buffer. Avidin-Biotin-Peroxidase Complex was added and unbound conjugates were washed away with PBS or TBS buffer. HRP substmousee TMB was used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the human Fibronectin amount of sample captured in plate.
The capture antibody is a monoclonal antibody from mouse, the detection antibody is a biotinylated detection polyclonal antibody from goat. Expression system for standard: Cystatin-M is a protein that in humans is encoded by the CST6 gene. It is mapped to 11q13.1. The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors, while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and the kininogens. The type 2 cystatin proteins are a class of cysteine proteinase inhibitors found in a variety of human fluids and secretions, where they appear to provide protective functions. This gene encodes a cystatin from the type 2 family, which is down-regulated in metastatic breast tumor cells as compared to primary tumor cells. Loss of expression is likely associated with the progression of a primary tumor to a metastatic phenotype