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Loss of YAP1/TAZ expression in the pancreatic endocrine compartment is not a passive consequence of endocrine specification, rather, Hippo pathway-mediated inhibition of YAP1/TAZ in endocrine progenitors is a prerequisite for endocrine specification and differentiation.

The cell junction-associated protein Amotl2a controls tissue size in the zebrafish lateral line primordium by limiting the activity of the Hippo effector Yap1 and the Wnt effector Lef1.

Yap interacts with Rif1, a major DNA replication timing factor, and functions as a brake to control the DNA replication program in Xenopus early embryos and post-embryonic stem cells.

Alveolar type 2 stem cells are actively maintained by Hippo signaling and Taz promotes alveolar epithelial regeneration and the resolution of bleomycin induced pulmonary fibrosis upon inactivation of the Hippo pathway in Alveolar type 2 stem cells.

HIPPO signaling antagonizes the apical domain of polarized cells, driving cell internalization, regulated gene expression, and cell fate change during formation of pluripotent stem cell progenitors in the mouse embryo.

Local coordination between shear and hydrostatic stress regulates valve shape and size.

P-body is a new downstream effector of YAP/TAZ for tumorigenesis and tumor progression, suggesting disruption of P-bodies as a potential therapeutic strategy for tumors with active YAP.

Pharmacological and genetic blockade of β1-AR-Gαs signaling prolongs the cardiac regenerative window in juvenile mouse by activating YAP.

Mechanosensitive channels Piezo1/2 are required for osteoblast differentiation from progenitors by sensing fluid sheer stress and matrix rigidity and regulating NFATc1, YAP1 and ß-catenin activities through Ca²⁺ stimulated phosphatase calcineurin.

The LATS/YAP/TAZ cascade promotes SOX2+ pituitary stem cell fate and when over-activated, transforms normal stem cells into cancer stem cells.