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Catenins: Keeping cells from getting their signals crossed

Journal

DEVELOPMENTAL CELL
Volume 11, Issue 5, Pages 601-612

Publisher

CELL PRESS
DOI: 10.1016/j.devcel.2006.10.010

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Funding

  1. NIAMS NIH HHS [R01 AR027883, AR27883, R01 AR027883-28, R37 AR027883] Funding Source: Medline

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Adherens junctions have been traditionally viewed as building blocks of tissue architecture. The foundations for this view began to change with the discovery that a central component of AJs, beta-catenin, can also function as a transcriptional cofactor in Wnt signaling. In recent years, conventional views have similarly been shaken about the other two major AJ catenins, a-catenin and p120-catenin. Catenins have emerged as molecular sensors that integrate cell-cell junctions and cytoskeletal dynamics with signaling pathways that govern morphogenesis, tissue homeostasis, and even intercellular communication between different cell types within a tissue. These findings reveal novel aspects of AJ function in normal tissues and offer insights into how changes in AJs and their associated proteins and cytoskeletal dynamics impact wound-repair and cancer.

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