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Protein kinase a‐dependent pSer675‐β‐catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis
Conclusion: These data show that in fibrocystin‐defective cholangiocytes, cAMP/PKA signaling stimulates pSer675‐phosphorylation of β‐catenin and Rac‐1 activity. In the presence of activated Rac‐1, pSer675‐β‐catenin is translocated to the nucleus, becomes transcriptionally active, and is responsible for increased motility of Pkhd1del4/del4 cholangiocytes. β‐Catenin‐dependent changes in cell motility may be central to the pathogenesis of the disease and represent a potential therapeutic target. (Hepatology 2013)
Source: Hepatology - September 30, 2013 Category: Internal Medicine Authors: Carlo Spirli, Luigi Locatelli, Carola M. Morell, Romina Fiorotto, Stuart D. Morton, Massimiliano Cadamuro, Luca Fabris, Mario Strazzabosco Tags: Autoimmune, Cholestatic and Biliary Disease Source Type: research

PKA dependent p‐Ser‐675β‐catenin, a novel signaling defect in a mouse model of Congenital Hepatic Fibrosis
Conclusions: These data show that in fibrocystin‐defective cholangiocytes, cAMP/PKA signaling stimulates pSer‐675phosphorylation of β‐catenin and Rac‐1 activity. In the presence of activated Rac‐1, pSer‐675‐β‐catenin is translocated to the nucleus, becomes transcriptionally active, and is responsible for increased motility of Pkhd1del4/del4 cholangiocytes. β‐catenin dependent changes in cell motility may be central to the pathogenesis of the disease and represent a potential therapeutic target.. (HEPATOLOGY 2013.)
Source: Hepatology - June 6, 2013 Category: Internal Medicine Authors: Carlo Spirli, Luigi Locatelli, Carola M. Morell, Romina Fiorotto, Stuart D. Morton, Massimiliano Cadamuro, Luca Fabris, Mario Strazzabosco Tags: Autoimmune, Cholestatic and Biliary Disease Source Type: research