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A more recent version of this article appeared on July 1, 2003
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Submitted on February 1, 2003
Accepted on February 28, 2003
1 Department of Medicine, VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, CA 94304; the Digestive Disease Center, Stanford University School of Medicine
2 Department of Medicine, VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, CA 94304; the Digestive Disease Center, Stanford University School of Medicine; and the Cancer Research Center, Heidelberg, Germany
* Corresponding author. E-mail address: mbishr{at}stanford.edu.
Of the >20 epithelial keratins, keratin 20 (K20) has an unusual distribution and is poorly studied. We began to address K20 function, by expressing human wild-type and Arg80
His (R80H) genomic (18-kb) and cDNA K20 in cells and mice. Arg80 of K20 is conserved in most keratins, and its mutation in epidermal keratins causes several skin diseases. R80H but not wild-type K20 generates disrupted keratin filaments in transfected cells. Transgenic mice that overexpress K20 R80H have collapsed filaments in small intestinal villus regions, when expressed at moderate levels, while wild type K20-overexpressing mice have normal keratin networks. Overexpressed K20 maintains its normal distribution in several tissues, but not in the pancreas and stomach, without causing any tissue abnormalities. Hence, K20 pancreatic and gastric expression are regulated outside the 18-kb region. Cross-breeding of wild-type or R80H K20 mice with mice that overexpress wild-type K18 or K18 that is mutated at the conserved K20 Arg80-equivalent residue show that K20 plays an additive and compensatory role with K18 in maintaining keratin filament organization in the intestine. Our data suggest the presence of unique regulatory domains for pancreatic/gastric K20 expression, and support a significant role for K20 in maintaining keratin filaments in intestinal epithelia.
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