Loss of extracellular matrix-integrin signaling switches off YAP/TEAD and lets prostate adenocarcinoma organoids turn neuroendocrine; LATS inhibition reverses it, and combined YAP, NOTCH and AR inhibition fully reprograms them.

bioRxiv · Aug 23, 2026 · PreprintCancer Biology✦ In-depth digest

Role of YAP in early ectodermal specification anda Huntington's Disease model of human neurulation

Francesco M. Piccolo, Nathaniel R. Kastan, Tomomi Haremaki, Qingyun Tian, Tiago L. Laundos, Riccardo De Santis, Andrew J Beaudoin, Thomas S. Carroll, Ji‐Dung Luo, Ksenia Gnedeva, Fred Etoc, Albert James Hudspeth, Ali H. Brivanlou

This study investigates YAP's role in early ectodermal specification and its link to Huntington's Disease using human neuruloids, finding YAP activation influences ectodermal fate and that reducing YAP activity can partially rescue HD phenotypes.

eLife · Mar 23, 2022Peer-reviewedDevelopmental Biology

Small-molecule inhibition of Lats kinases promotes Yap-dependent proliferation in postmitotic mammalian tissues

Nathaniel R. Kastan, Ksenia Gnedeva, Theresa Alisch, Aleksandra A. Petelski, David J. Huggins, Jeanne Chiaravalli, Alla Aharanov, Avraham Shakked, Eldad Tzahor, Aaron Nagiel, Neil Segil, Albert James Hudspeth

The paper identifies a small-molecule inhibitor of Lats kinases that promotes Yap-dependent proliferation in postmitotic mammalian tissues, enabling hair cell regeneration in the inner ear.

Nature Communications · May 25, 2021Peer-reviewedDevelopmental Biology