| scholarly article | Q13442814 |
| P50 | author | Eva Kereszturi | Q114092430 |
| P2093 | author name string | Miklós Sahin-Tóth | |
| P2860 | cites work | Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene | Q24311652 |
| Hereditary pancreatitis caused by mutation-induced misfolding of human cationic trypsinogen: a novel disease mechanism | Q24650338 | ||
| Mutations of human cationic trypsinogen (PRSS1) and chronic pancreatitis | Q24658116 | ||
| Biochemical models of hereditary pancreatitis | Q24675973 | ||
| Cathepsin B cleavage of the trypsinogen activation peptide | Q24797108 | ||
| Crystal structure of enteropeptidase light chain complexed with an analog of the trypsinogen activation peptide | Q27619707 | ||
| Signal integration in the endoplasmic reticulum unfolded protein response | Q27860577 | ||
| Human mesotrypsin exhibits restricted S1' subsite specificity with a strong preference for small polar side chains | Q33246025 | ||
| Mutations in the cationic trypsinogen gene and evidence for genetic heterogeneity in hereditary pancreatitis. | Q35431882 | ||
| Glucocorticoids increase amylase mRNA levels, secretory organelles, and secretion in pancreatic acinar AR42J cells | Q36212907 | ||
| Why does pancreatic overstimulation cause pancreatitis? | Q36632168 | ||
| Structural reorganization of the rough endoplasmic reticulum without size expansion accounts for dexamethasone-induced secretory activity in AR42J cells | Q36697325 | ||
| Involvement of autophagy in trypsinogen activation within the pancreatic acinar cells | Q37203732 | ||
| From endoplasmic-reticulum stress to the inflammatory response | Q37225354 | ||
| The guinea pig pancreas secretes a single trypsinogen isoform, which is defective in autoactivation. | Q37255493 | ||
| Intracellular trypsin induces pancreatic acinar cell death but not NF-kappaB activation | Q37285222 | ||
| Signal peptide variants that impair secretion of pancreatic secretory trypsin inhibitor (SPINK1) cause autosomal dominant hereditary pancreatitis | Q37395316 | ||
| Chymotrypsin C (caldecrin) stimulates autoactivation of human cationic trypsinogen | Q38290039 | ||
| Stable monomeric form of an originally dimeric serine proteinase inhibitor, ecotin, was constructed via site directed mutagenesis | Q38357958 | ||
| Expression of human cationic trypsinogen with an authentic N terminus using intein-mediated splicing in aminopeptidase P deficient Escherichia coli | Q38605810 | ||
| Expression of mutated cationic trypsinogen reduces cellular viability in AR4-2J cells | Q40394944 | ||
| Human cationic trypsinogen. Role of Asn-21 in zymogen activation and implications in hereditary pancreatitis | Q41734787 | ||
| The tetra-aspartate motif in the activation peptide of human cationic trypsinogen is essential for autoactivation control but not for enteropeptidase recognition | Q41837429 | ||
| Glucocorticoids increase cholecystokinin receptors and amylase secretion in pancreatic acinar AR42J cells. | Q42486585 | ||
| Hereditary pancreatitis caused by a novel PRSS1 mutation (Arg-122 --> Cys) that alters autoactivation and autodegradation of cationic trypsinogen | Q43806616 | ||
| Presence of cathepsin B in the human pancreatic secretory pathway and its role in trypsinogen activation during hereditary pancreatitis | Q43946815 | ||
| Evolution of trypsinogen activation peptides | Q44495545 | ||
| Coupled induction of exocrine proteins and intracellular compartments involved in the secretory pathway in AR4-2J cells by glucocorticoids. | Q44669310 | ||
| Affinity purification of recombinant trypsinogen using immobilized ecotin. | Q46011088 | ||
| Gain-of-function mutations associated with hereditary pancreatitis enhance autoactivation of human cationic trypsinogen | Q46911281 | ||
| Alteration of the specificity of ecotin, an E. coli serine proteinase inhibitor, by site directed mutagenesis. | Q54637404 | ||
| Possible lysosomal activation of pancreatic zymogens. Activation of both human trypsinogens by cathepsin B and spontaneous acid. Activation of human trypsinogen 1 | Q67988505 | ||
| Chronic pancreatitis associated with an activation peptide mutation that facilitates trypsin activation | Q74127323 | ||
| That which does not kill me makes me stronger: adapting to chronic ER stress | Q81405125 | ||
| P433 | issue | 48 | |
| P407 | language of work or name | English | Q1860 |
| P921 | main subject | cell death | Q2383867 |
| P304 | page(s) | 33392-33399 | |
| P577 | publication date | 2009-09-29 | |
| P1433 | published in | Journal of Biological Chemistry | Q867727 |
| P1476 | title | Intracellular autoactivation of human cationic trypsinogen mutants causes reduced trypsinogen secretion and acinar cell death | |
| P478 | volume | 284 |
| Q37591305 | Cerulein-induced chronic pancreatitis does not require intra-acinar activation of trypsinogen in mice |
| Q27693296 | Chymotrypsin C mutations in chronic pancreatitis |
| Q43146280 | Digesting new information about the role of trypsin in pancreatitis |
| Q34283421 | Endoplasmic reticulum stress is chronically activated in chronic pancreatitis |
| Q93000610 | Engineering mouse cationic trypsinogen for rapid and selective activation by cathepsin B |
| Q92704497 | Etiology and Risk Factors of Acute and Chronic Pancreatitis |
| Q35986635 | Expression of XBP1s in bone marrow stromal cells is critical for myeloma cell growth and osteoclast formation |
| Q33654180 | Expression of human cationic trypsinogen (PRSS1) in murine acinar cells promotes pancreatitis and apoptotic cell death |
| Q26801332 | Framework for interpretation of trypsin-antitrypsin imbalance and genetic heterogeneity in pancreatitis |
| Q33843764 | Genetic Risk in Chronic Pancreatitis: The Trypsin-Dependent Pathway |
| Q39398523 | Genetic risk in chronic pancreatitis: the misfolding-dependent pathway |
| Q37629167 | Human cationic trypsinogen (PRSS1) variants and chronic pancreatitis |
| Q41628354 | Intra-acinar trypsinogen activation mediates early stages of pancreatic injury but not inflammation in mice with acute pancreatitis |
| Q35005784 | Intracellular activation of trypsinogen in transgenic mice induces acute but not chronic pancreatitis |
| Q55514770 | Intracellular rupture, exocytosis and actin interaction of endocytic vacuoles in pancreatic acinar cells: initiating events in acute pancreatitis. |
| Q34936085 | Intragenic duplication: a novel mutational mechanism in hereditary pancreatitis |
| Q34501606 | Molecular and cellular mechanisms of pancreatic injury |
| Q37918238 | Molecular mechanisms of pancreatic injury |
| Q37602778 | New insights into the pathogenesis of pancreatitis |
| Q55059406 | PRSS1 mutations and the proteinase/antiproteinase imbalance in the pathogenesis of pancreatic cancer. |
| Q38034035 | Pathogenic mechanisms of acute pancreatitis |
| Q41953583 | Preclinical evaluation of Som230 as a radiation mitigator in a mouse model: postexposure time window and mechanisms of action |
| Q27676187 | Quantitative Characterization of the Activation Steps of Mannan-binding Lectin (MBL)-associated Serine Proteases (MASPs) Points to the Central Role of MASP-1 in the Initiation of the Complement Lectin Pathway |
| Q42145402 | Robust autoactivation, chymotrypsin C independence and diminished secretion define a subset of hereditary pancreatitis-associated cationic trypsinogen mutants. |
| Q37793725 | The acinar-ductal tango in the pathogenesis of acute pancreatitis. |
| Q42155388 | Trypsinogen activation in acute and chronic pancreatitis: is it a prerequisite? |
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