Andrea Geisz-Fremy
Boston University, MA·Biochemistry
Pancreatitis, a painful inflammation of the pancreas, often begins when a digestive enzyme switches on too early, inside the pancreas instead of in the gut. That enzyme is trypsin, which is made in an inactive form called trypsinogen.
- Fields
Biochemistry
Physiology
Medicine & Clinical Research
- Topics
pancreatitis
trypsin
autoactivation
- Grants
- 1 known grant, through Jan 2028
What they work on
- Test whether cathepsin B causes significant trypsin activation inside the pancreas without affecting pancreatitis severity in mice lacking autoactivation-boosting trypsinogen mutations.
- Determine whether pancreatitis severity depends on cathepsin B–mediated trypsinogen activation in mouse models with mutations that moderately increase trypsinogen autoactivation.
- Test whether cathepsin B activity sets the age of onset and severity of spontaneous pancreatitis in mice carrying a trypsinogen mutation that causes strong autoactivation.
More about the research
One of the earliest steps in the disease is trypsinogen becoming active trypsin within the pancreas. How this happens is debated: animal studies point to activation by another enzyme, cathepsin B, while human genetic studies point to autoactivation, where trypsin activates more trypsinogen. How much each route contributes to disease onset is unknown.
Why it matters
Pancreatitis has few targeted treatments because the first trigger, early trypsin activation, is poorly understood. Clarifying whether cathepsin B or trypsin autoactivation drives disease could point to new therapeutic and preventive approaches for patients with pancreatitis, including those with inherited trypsinogen mutations.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Taylor Triolo
University of Colorado Denver/Anschutz Medical Campus, CO·Medicine & Clinical Research·Early-career
Analyze whether baseline markers of beta cell function and stress predict C-peptide preservation during the partial remission, or "honeymoon," period in patients newly diagnosed with type 1 diabetes.
Seung K Kim
Stanford University, CA·Medicine & Clinical Research
Map gene regulation and measure electrical activity in individual islet cells from living subjects with chronic pancreatitis, with and without prediabetes, to find the earliest changes preceding type 3c diabetes.
Bernd Schnabl
University of California-San Diego, CA·Medicine & Clinical Research
Test whether the sugar-adding enzyme Fucosyltransferase 2 (Fut2) on intestinal lining cells limits colonization and translocation of the gut bacterium Enterococcus faecalis and thereby reduces liver disease, using mouse models of ethanol feeding.
The school
Boston University: 26 labs on PI Pages, $784M a year on research, 630 research doctorates a year.
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