Protein kinase A-dependent pSer(675) -beta-catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis
Protein kinase A-dependent pSer(675) -beta-catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis
These data show that in fibrocystin-defective cholangiocytes, cAMP/PKA signaling stimulates pSer(675) -phosphorylation of ?-catenin and Rac-1 activity. In the presence of activated Rac-1, pSer(675) -?-catenin is translocated to the nucleus, becomes transcriptionally active, and is responsible for increased motility of Pkhd1(del4/del4) cholangiocytes. ?-Catenin-dependent changes in cell motility may be central to the pathogenesis of the disease and represent a potential therapeutic target
1713-1723
Spirli, Carlo
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Locatelli, Luigi
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Morell, Carola M.
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Fiorotto, Romina
a3fb15a8-d882-4406-8d0e-6eeb95c98059
Morton, Stuart D.
7545cf7d-15a6-43cc-9949-41ece1749fef
Cadamuro, Massimiliano
eee3861c-58b8-43a4-99d2-24f488b45eae
Fabris, Luca
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Strazzabosco, Mario
18e0c674-2971-4029-8c9f-7770f14ea564
November 2013
Spirli, Carlo
a71a179c-0648-4d86-aad3-978470660acd
Locatelli, Luigi
15a4bfcd-ad79-45cd-a34d-a9ae7f3ed306
Morell, Carola M.
ec9ab184-0ea5-49d6-b044-5fa520e56d0a
Fiorotto, Romina
a3fb15a8-d882-4406-8d0e-6eeb95c98059
Morton, Stuart D.
7545cf7d-15a6-43cc-9949-41ece1749fef
Cadamuro, Massimiliano
eee3861c-58b8-43a4-99d2-24f488b45eae
Fabris, Luca
7ab16fef-75b0-4131-a451-86fc97903b92
Strazzabosco, Mario
18e0c674-2971-4029-8c9f-7770f14ea564
Spirli, Carlo, Locatelli, Luigi, Morell, Carola M., Fiorotto, Romina, Morton, Stuart D., Cadamuro, Massimiliano, Fabris, Luca and Strazzabosco, Mario
(2013)
Protein kinase A-dependent pSer(675) -beta-catenin, a novel signaling defect in a mouse model of congenital hepatic fibrosis.
Hepatology, 58 (5), .
(doi:10.1002/hep.26554).
Abstract
These data show that in fibrocystin-defective cholangiocytes, cAMP/PKA signaling stimulates pSer(675) -phosphorylation of ?-catenin and Rac-1 activity. In the presence of activated Rac-1, pSer(675) -?-catenin is translocated to the nucleus, becomes transcriptionally active, and is responsible for increased motility of Pkhd1(del4/del4) cholangiocytes. ?-Catenin-dependent changes in cell motility may be central to the pathogenesis of the disease and represent a potential therapeutic target
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Accepted/In Press date: 24 May 2013
Published date: November 2013
Organisations:
Medical Education
Identifiers
Local EPrints ID: 382373
URI: http://eprints.soton.ac.uk/id/eprint/382373
ISSN: 0270-9139
PURE UUID: 1463f0b3-31ab-4fde-8119-d203e92121f0
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Date deposited: 30 Oct 2015 09:48
Last modified: 15 Mar 2024 03:53
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Author:
Carlo Spirli
Author:
Luigi Locatelli
Author:
Carola M. Morell
Author:
Romina Fiorotto
Author:
Massimiliano Cadamuro
Author:
Luca Fabris
Author:
Mario Strazzabosco
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