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      Loss of cooperative function of transforming growth factor-beta signaling proteins, smad3 with embryonic liver fodrin, a beta-spectrin, in primary biliary cirrhosis.

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          Abstract

          Modulation of fibrogenesis, epithelial, and mesenchymal cell fates are prominent effects of transforming growth factor-beta (TGF-beta) signaling by Smad proteins. We have previously shown that Smad2 and Smad3 insufficiency leads to a loss of bile ducts. In addition, Smad3/4 activity is mediated by embryonic liver fodrin (ELF), a beta-Spectrin. In mouse elf(-/-) mutants and in liver explant cultures, loss of ELF function results in T lymphocytic proliferation and absent intrahepatic bile ducts. A similar phenotype is seen in a number of cholestatic diseases with progressive loss of intrahepatic bile ducts and fibrosis. However, the expression patterns of Smads or role of ELF in cholestatic and fibrotic liver diseases are not yet known.

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          Author and article information

          Journal
          Liver Int.
          Liver international : official journal of the International Association for the Study of the Liver
          1478-3223
          1478-3223
          Dec 2004
          : 24
          : 6
          Affiliations
          [1 ] GI/Developmental Biology, Medicine, Surgical Sciences, Lombardi Cancer Center, Georgetown University & DVAMC, Washington, DC, USA.
          Article
          LIV958
          10.1111/j.1478-3231.2004.0958.x
          15566516
          dec90738-6cfd-4718-84df-444d742695e6
          History

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