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Literature summary for 3.4.21.2 extracted from

  • Szmola, R.; Sahin-Toth, M.
    Pancreatitis-associated chymotrypsinogen C (CTRC) mutant elicits endoplasmic reticulum stress in pancreatic acinar cells (2010), Gut, 59, 365-372.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine carriers of CTRC mutations may be at a higher risk of developing endoplasmic reticulum stress in the exocrine pancreas. Endoplasmic reticulum stress may contribute to parenchymal damage in chronic pancreatitis through acinar cell apoptosis Homo sapiens

Cloned(Commentary)

Cloned (Comment) Organism
cDNAs for the wild-type CTRC and the p.A73T mutant carrying a Glu-Glu epitope tag excised from pcDNA3.1(-)_CTRC expression plasmids with XhoI and EcoRI and subcloned into the VQ Ad5CMV shuttle vector under the control of a CMV promoter. Dexamethasone-differentiated AR42J rat acinar cells and freshly isolated mouse acini transfected with recombinant adenovirus carrying wild-type CTRC or the p.A73T pancreatitis-associated mutant Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Synonyms

Synonyms Comment Organism
chymotrypsinogen C
-
Homo sapiens
CTRC
-
Homo sapiens

Expression

Organism Comment Expression
Homo sapiens in AR42J cells and mouse acini, CTRC is transiently expressed in its inactive zymogen form up

General Information

General Information Comment Organism
malfunction pancreatitis-associated CTRC mutations can markedly increase the propensity of chymotrypsinogen C to elicit endoplasmic reticulum stress in pancreatic acinar cells. Diminished secretion and intracellular retention/degradation of the p.A73T CTRC mutant. Endoplasmic reticulum stress in AR42J cells is proportional to intracellular levels of the p.A73T CTRC mutant. No activation of the PERK pathway and NFkappaB in acinar cells expressing the p.A73T CTRC mutant. Apoptotic cell death in AR42J cells expressing the p.A73T CTRC mutant Homo sapiens