Recombinant Human RET (S891A) Protein was resolved with SDS-PAGE under reducing (Lane 1) and non-reducing (Lane 2) conditions.
The activity of RET is based on the MSA technology, and the content and ratio of the substrate and the product are directly separated and detected in real time and dynamically by the different migration rates of the substrate and the product after the enzymatic reaction.
The RET proto-oncogene encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor (GDNF) family of extracellular signalling molecules. In order to activate RET, GDNF-family ligands (GFLs) first need to form a complex with a glycosylphosphatidylinositol (GPI)-anchored co-receptor. The co-receptors themselves are classified as members of the GDNF receptor-α (GFRα) protein family. Different members of the GFRα family (GFRα1, GFRα2, GFRα3, GFRα4) exhibit a specific binding activity for a specific GFLs. Mice deficient in GDNF, GFRα1 or the RET protein itself exhibit severe defects in kidney and enteric nervous system development. This implicates RET signal transduction as key to the development of normal kidneys and the enteric nervous system.
