Complete analysis of the human mesotrypsinogen gene (PRSS3) in patients with chronic pancreatitis.

doi:10.1159/000243769

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Complete analysis of the human mesotrypsinogen gene (PRSS3) in patients with chronic pancreatitis.

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] - 1 Jan 2010

Rosendahl Jonas, Teich Niels, Kovacs Peter, Szmola Richard, Blüher Matthias, Gress Thomas M, Hoffmeister Albrecht, Keim Volker, Löhr Matthias, Mössner Joachim, Nickel Renate, Ockenga Johann, Pfützer Roland, Schulz Hans-Ulrich, Stumvoll Michael, Wittenburg Henning, Sahin-Tóth Miklós, Witt Heiko

Abstract excerpt

BACKGROUND/AIMS: A sustained imbalance of pancreatic proteases and their inhibitors seems to be important for the development of chronic pancreatitis (CP). Mesotrypsin (PRSS3) can degrade intrapancreatic trypsin inhibitors that protect against CP. Genetic variants that cause higher mesotrypsin activity might increase the risk for CP. METHODS: We analyzed all 5 exons and the adjacent non-coding sequences of PRSS3...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aged, 80 and over

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Child, Preschool

Share to Gene Frequency

Share to Haplotypes

Share to Infant

Share to Infant, Newborn

Share to Pancreatitis, Chronic

Share to Trypsin

Source

Open in PubMed Open full text

Identifiers

PMID: 20484962
DOI: 10.1159/000243769
PMCID: PMC2899151

Genes

PRSS3

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Complete analysis of the human mesotrypsinogen gene (PRSS3) in patients with chronic pancreatitis.PMID 20484962Read ↗

Genetic and biochemical characterization of the E32del polymorphism in human mesotrypsinogen.Semantic proximity Read ↗

Mesotrypsin Signature Mutation in a Chymotrypsin C (CTRC) Variant Associated with Chronic Pancreatitis.Semantic proximity Read ↗

Mouse model suggests limited role for human mesotrypsin in pancreatitis.Semantic proximity Read ↗

Risk of chronic pancreatitis in carriers of loss-of-function CTRC variants: A meta-analysis.Semantic proximity Read ↗

Novel chymotrypsin C (CTRC) variants from real-world genetic testing of pediatric chronic pancreatitis cases.Semantic proximity Read ↗

Loss-of-function variant in chymotrypsin like elastase 3B (CELA3B) is associated with non-alcoholic chronic pancreatitis.Semantic proximity Read ↗

Genetic Analysis of Human Chymotrypsin-Like Elastases 3A and 3B (CELA3A and CELA3B) to Assess the Role of Complex Formation between Proelastases and Procarboxypeptidases in Chronic Pancreatitis.Semantic proximity Read ↗

Human Mesotrypsin Is a Unique Digestive Protease Specialized for the Degradation of Trypsin InhibitorsSemantic proximity Read ↗

Chymotrypsin C (CTRC) variants that diminish activity or secretion are associated with chronic pancreatitis.Semantic proximity Read ↗

Risk of chronic pancreatitis in carriers of the c.180C>T (p.Gly60=) CTRC variant: case-control studies and meta-analysis.Semantic proximity Read ↗

Gene conversion between cationic trypsinogen (PRSS1) and the pseudogene trypsinogen 6 (PRSS3P2) in patients with chronic pancreatitis.Semantic proximity Read ↗

Inactivation of mesotrypsin by chymotrypsin C prevents trypsin inhibitor degradation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.