Miklos Sahin-Toth


Affiliation: Boston University
Country: USA


  1. Geisz A, Sahin Toth M. A preclinical model of chronic pancreatitis driven by trypsinogen autoactivation. Nat Commun. 2018;9:5033 pubmed publisher
    ..This remarkable model provides in vivo proof of concept that trypsinogen autoactivation can drive onset and progression of chronic pancreatitis and therapy should be directed against intra-pancreatic trypsin. ..
  2. Hegyi E, Sahin Toth M. Trypsinogen isoforms in the ferret pancreas. Sci Rep. 2018;8:15094 pubmed publisher
    ..Intra-pancreatic trypsinogen activation by cathepsin B can occur in ferrets, which might trigger pancreatitis even in the absence of trypsinogen autoactivation. ..
  3. Jancsó Z, Hegyi E, Sahin Toth M. Chymotrypsin Reduces the Severity of Secretagogue-Induced Pancreatitis in Mice. Gastroenterology. 2018;155:1017-1021 pubmed publisher
    ..CTRB1 therefore protects against secretagogue-induced pancreatitis by reducing trypsin activity. Protease inhibitors developed for treatment of pancreatitis should be designed to target trypsin but not chymotrypsin. ..
  4. Derikx M, Geisz A, Kereszturi Ã, Sahin Tóth M. Functional significance of SPINK1 promoter variants in chronic pancreatitis. Am J Physiol Gastrointest Liver Physiol. 2015;308:G779-84 pubmed publisher
    ..Our study lends further support to the notion that sequence evaluation of the SPINK1 promoter region in patients with chronic pancreatitis is justified as part of the etiological investigation. ..
  5. Boros E, Szabó A, Zboray K, Héja D, Pál G, Sahin Tóth M. Overlapping Specificity of Duplicated Human Pancreatic Elastase 3 Isoforms and Archetypal Porcine Elastase 1 Provides Clues to Evolution of Digestive Enzymes. J Biol Chem. 2017;292:2690-2702 pubmed publisher
    ..Thus, increased gene dosage rather than specificity divergence of the CELA3 isoforms may compensate for the loss of CELA1 digestive activity in the human pancreas. ..
  6. Tóth A, Szabo A, Hegyi E, Hegyi P, Sahin Toth M. Detection of human elastase isoforms by the ScheBo Pancreatic Elastase 1 Test. Am J Physiol Gastrointest Liver Physiol. 2017;312:G606-G614 pubmed publisher
    ..We demonstrate that, among the human pancreatic proteinases, the test measures the elastase isoform CELA3B and, to a lesser extent, CELA3A. Genetic variants of the human CELA3 isoforms have no significant effect on test performance. ..
  7. Szabó A, Ludwig M, Hegyi E, Szépeová R, Witt H, Sahin Tóth M. Mesotrypsin Signature Mutation in a Chymotrypsin C (CTRC) Variant Associated with Chronic Pancreatitis. J Biol Chem. 2015;290:17282-92 pubmed publisher
  8. Balázs A, Hegyi P, Sahin Toth M. Pathogenic cellular role of the p.L104P human cationic trypsinogen variant in chronic pancreatitis. Am J Physiol Gastrointest Liver Physiol. 2016;310:G477-86 pubmed publisher
    ..L104P exhibits a variety of phenotypic changes that can increase risk for chronic pancreatitis. Mutation-induced misfolding and associated ER stress are the dominant effects that support a direct pathogenic role in chronic pancreatitis. ..
  9. Párniczky A, Hegyi E, Tóth A, Szucs A, Szentesi A, Vincze A, et al. 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. Int J Mol Sci. 2016;17: pubmed publisher

More Information


  1. Sahin Toth M. Human mesotrypsin defies natural trypsin inhibitors: from passive resistance to active destruction. Protein Pept Lett. 2005;12:457-64 pubmed
    ..Here we review the history and properties of human mesotrypsin, and discuss its function in the digestive degradation of dietary trypsin inhibitors and possible pathophysiological role in pancreatitis. ..
  2. Sahin Toth M, Kukor Z, Nemoda Z. Human cationic trypsinogen is sulfated on Tyr154. FEBS J. 2006;273:5044-50 pubmed
    ..Finally, sequence alignment revealed that the sulfation motif is only conserved in primate trypsinogens, suggesting that typsinogen sulfation is absent in other vertebrates. ..
  3. Jancsó Z, Sahin Toth M. Tighter Control by Chymotrypsin C (CTRC) Explains Lack of Association between Human Anionic Trypsinogen and Hereditary Pancreatitis. J Biol Chem. 2016;291:12897-905 pubmed publisher
    ..This unique biochemical property of anionic trypsinogen explains the lack of association of PRSS2 mutations with hereditary pancreatitis. ..
  4. Szabo A, Pilsak C, Bence M, Witt H, Sahin Toth M. Complex Formation of Human Proelastases with Procarboxypeptidases A1 and A2. J Biol Chem. 2016;291:17706-16 pubmed publisher
    ..Complex formation stabilizes the inhibitory activation peptide of procarboxypeptidases and thereby increases zymogen stability and controls activation. ..
  5. Hegyi E, Sahin Tóth M. Genetic Risk in Chronic Pancreatitis: The Trypsin-Dependent Pathway. Dig Dis Sci. 2017;62:1692-1701 pubmed publisher
    ..Here we review key genetic and biochemical features of the trypsin-dependent pathological pathway in chronic pancreatitis. ..