The genetic risk factor CEL-HYB1 causes proteotoxicity and chronic pancreatitis in mice

January 1, 2022
Pancreatology
https://pubmed.ncbi.nlm.nih.gov/36379850

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/36379850

Research summary

This study investigates the pathogenic role of the human CEL-HYB1 hybrid gene in chronic pancreatitis. Transgenic mice expressing CEL-HYB1 in the pancreas develop progressive pancreatic damage, ER stress, and inflammation. The study provides evidence that CEL-HYB1 induces proteotoxicity, supporting its role as a risk factor in pancreatitis.

Key outcome of the study

Expression of human CEL-HYB1 in the pancreas induces ER stress, acinar cell damage, immune cell infiltration, and chronic pancreatitis, confirming its pathogenic role in proteotoxic stress and pancreatic disease.

Mouse model

Human CEL-HYB1 transgenic mouse model developed by genOway, with targeted insertion of the transgene into the Rosa26 locus using a Cre-inducible system for pancreas-specific expression.

TARGET:
CEL-HYB1
Carboxyl ester lipase hybrid 1

Keywords

Chronic pancreatitis, ER stress, Proteotoxicity, Digestive disease, Genetic risk factors

Technical specifications

Conditional Knockin model, Rosa26 locus targeting, Cre-loxP system, Human CEL-HYB1 expression, Pancreas-specific expression

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