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Hippo-Independent Regulation of Yki/Yap/Taz: A Non-canonical View

Authors
  • Cho, Yong Suk1
  • Jiang, Jin1, 2
  • 1 Department of Molecular Biology, UT Southwestern Medical Center, Dallas, TX , (United States)
  • 2 Department of Pharmacology, UT Southwestern Medical Center, Dallas, TX , (United States)
Type
Published Article
Journal
Frontiers in Cell and Developmental Biology
Publisher
Frontiers Media SA
Publication Date
Apr 01, 2021
Volume
9
Identifiers
DOI: 10.3389/fcell.2021.658481
Source
Frontiers
Keywords
Disciplines
  • Cell and Developmental Biology
  • Review
License
Green

Abstract

Initially identified in Drosophila, the Hippo signaling pathway has emerged as an evolutionarily conserved tumor suppressor pathway that controls tissue growth and organ size by simultaneously inhibiting cell proliferation and promoting cell death. Deregulation of Hippo pathway activity has been implicated in a wide range of human cancers. The core Hippo pathway consists of a kinase cascade: an upstream kinase Hippo (Hpo)/MST1/2 phosphorylates and activates a downstream kinase Warts (Wts)/Lats1/2, leading to phosphorylation and inactivation of a transcriptional coactivator Yki/YAP/Taz. Many upstream signals, including cell adhesion, polarity, mechanical stress, and soluble factors, regulate Hippo signaling through the kinase cascade, leading to change in the cytoplasmic/nuclear localization of Yki/YAP/Taz. However, recent studies have uncovered other mechanisms that regulate Yki/YAP/Taz subcellular localization, stability, and activity independent of the Hpo kinase cascade. These mechanisms provide additional layers of pathway regulation, nodes for pathway crosstalk, and opportunities for pathway intervention in cancer treatment and regenerative medicine.

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