Recombinant Human CMA1/Chymase 1 Protein (His Tag) | PKSH031112

Recombinant Human CMA1/Chymase 1 Protein (His Tag) | PKSH031112 | Gentaur US, UK & Europe Disrtribition

Synonyms: chymase;CYH;MCT1

Active Protein: N/A

Activity: A DNA sequence encoding the human CMA1 (P23946) (Met 1-Asn 247) was fused with a polyhistidine tag at the C-terminus.

Protein Construction: A DNA sequence encoding the human CMA1 (P23946) (Met 1-Asn 247) was fused with a polyhistidine tag at the C-terminus.

Fusion Tag: C-His

Species: Human

Expressed Host: Baculovirus-Insect Cells

Shipping: This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at<-20°C.

Purity: > 92 % as determined by reducing SDS-PAGE.

Endotoxin: < 1.0 EU per µg of the protein as determined by the LAL method.

Stability and Storage: Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.

Molecular Mass: 26.6 kDa

Formulation: Supplied as sterile 20mM Tris, 500mM NaCl, pH 7.4, 10% glycerol

Reconstitution: Not Applicable

Background: Chymotrypsin C (abbreviated for CTRC), also known as caldecrin or elastase4, is a digestive enzyme of the peptidase S1 family. This enzyme is synthesized as an inactivate chymotrypsinogen. On cleavage by trypsin into two parts that activate each other by removing two small peptides in a trans-proteolysis, chymotrypsin C produced. N-linked glycosylation of human CTRC is required for efficient folding and secretion, however, the N-linked glycan is unimportant for enzyme activity or inhibitor binding. It has been proposed that CTRC is a key regulator of digestive zymogen activation and a physiological co-activator of digestive carboxypeptidases proCPA1 and proCPA2. Mutations that abolish activity or secretion of CTRC increase the risk for chronic pancreatitis. It's speculated that CTRC might regulate pancreatic cancer cell migration in relation to cytokeratin 18 expression. The pancreatic cancer cell migration ability was downregulated in pancreatic cancer Aspc-1 cells that overexpressed CTRC, whereas the cell migration ability was upregulated in Aspc-1 cells in which CTRC was suppressed. 

Research Area: Signal Transduction, Cardiovascular, immunology,