The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent dilution.
Plays an important role in the final stage of carbohydrate digestion.
Expressed in the poorly differentiated crypt cells of the small intestine as well as in the mature villous cells. Expressed at very low levels in the colon.
Defects in SI are the cause of congenital sucrase-isomaltase deficiency (CSID) [MIM:222900]; also known as disaccharide intolerance I. CSID is an autosomal recessive intestinal disorder that is clinically characterized by fermentative diarrhea, abdominal pain, and cramps upon ingestion of sugar. The symptoms are the consequence of absent or drastically reduced enzymatic activities of sucrase and isomaltase. The prevalence of CSID is 0.02 % in individuals of European descent and appears to be much higher in Greenland, Alaskan, and Canadian native people. CSID arises due to post-translational perturbations in the intracellular transport, polarized sorting, aberrant processing, and defective function of SI.
Belongs to the glycosyl hydrolase 31 family. Contains 2 P-type (trefoil) domains.
The precursor is proteolytically cleaved when exposed to pancreatic proteases in the intestinal lumen. Sulfated.
Sucrase-isomaltase is composed of 2 polypeptide chains of similar size linked together by noncovalent bonds. The polypeptide chains show a high degree of overlapping substrate specificity and are synthesized as 1 long polypeptide chain which, by means of pancreatic proteases, is later split into the 2 subunits.