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The main focus of his research program is to provide molecular evidence that genetic alterations in the three human trypsinogen isoforms (PRSS1, PRSS2 and PRSS3 genes) and the pancreatic secretory trypsin inhibitor (SPINK1 gene) can influence the susceptibility for the development of pancreatitis. Thus, gain-of-function mutations in cationic trypsinogen can cause pancreatitis, while loss of function mutations in anionic trypsinogen can protect against pancreatitis. The following specific projects are studied. (1) The role of human mesotrypsin in pancreatitis. Mesotrypsin is a unique protease specialized for the degradation of trypsin inhibitors. Premature mesotrypsinogen activation might lower protective SPINK1 levels in the pancreas and contribute to the pathogenesis of pancreatitis. (2) Characterization of pancreatitis-associated cationic trypsinogen (PRSS1) mutants and identification of novel mutation-dependent biochemical defects that lead to hereditary pancreatitis (3) Functional analysis of anionic trypsinogen (PRSS2) mutants that afford protection against pancreatitis. The concept that loss-of-function trypsinogen mutations can protect against pancreatitis provides independent evidence for the central role of trypsin in this disease. (4) Identification of the disease-causing biochemical defects in pancreatitis-associated SPINK1 mutants. More recently, Dr. Sahin-Toth succeeded in developing preclinical mouse models of chronic pancreatitis driven by human mutations in mouse digestive proteases.
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论文共 239 篇作者统计合作学者相似作者
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Gergő Berke,Miklós Sahin-Tóth
Gutpp.gutjnl-2024, (2024)
GUTpp.gutjnl-331105, (2023)
Pancreatology (2023): e63-e63
Zsofia Gabriella Pesei, Reka Hegede,Gergo Berke,Balazs Csaba Nemeth,Balint Eross, Vera Sahin-Toth,Gyula Farkas,Andrea Szentesi,Laszlo Czako,Miklos Sahin-Toth,Peter Hegyi,Eszter Hegyi
Pancreatology (2023): e31-e32
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Pancreatologyno. 2 (2023): 131-142
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