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- W2141926729 abstract "The liver is unique in its capacity to regenerate after injury, during which hepatocytes actively divide and establish cell-cell contacts through cell adhesion complexes. Here, we demonstrate that the loss of α-catenin, a well-established adhesion component, dramatically disrupts liver regeneration. Using a partial hepatectomy model, we show that regenerated livers from α-catenin knockdown mice are grossly larger than control regenerated livers, with an increase in cell size and proliferation. This increased proliferation correlated with increased YAP activation, implicating α-catenin in the Hippo/YAP pathway. Additionally, α-catenin knockdown mice exhibited a phenotype reminiscent of clinical cholestasis, with drastically altered bile canaliculi, elevated levels of bile components and signs of jaundice and inflammation. The disrupted regenerative capacity is a result of actin cytoskeletal disorganisation, leading to a loss of apical microvilli, dilated lumens in the bile canaliculi and leaky tight junctions. This study illuminates a novel, essential role for α-catenin in liver regeneration." @default.
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- W2141926729 date "2014-10-30" @default.
- W2141926729 modified "2023-10-18" @default.
- W2141926729 title "Loss of α-catenin elicits a cholestatic response and impairs liver regeneration" @default.
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- W2141926729 doi "https://doi.org/10.1038/srep06835" @default.
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