Journal
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA
Volume 35, Issue 2, Pages 303-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.ecl.2006.02.002
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Funding
- NIDDK NIH HHS [DK58088, R01 DK058088] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK058088] Funding Source: NIH RePORTER
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The past decade has witnessed remarkable progress in the genetics of chronic pancreatitis. Despite these accomplishments, the understanding of the molecular mechanisms through which PRSS1 and SPINK1 mutations cause chronic pancreatitis, has remained sketchy Pancreatitis-associated gene mutations are believed to result in uncontrolled trypsin activity in the pancreas. Experimental identification of the disease-relevant functional alterations caused by PRSS1 or SPINK1 mutations proved to be challenging, however, because results of biochemical analyses lent themselves to different interpretations. This article focuses on PRSS1 mutations and summarizes the salient biochemical findings in the context of the mechanistic models that explain the connection between mutations and hereditary pancreatitis.
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