During ES cell differentiation, Yap1 directly regulates apoptosis-related genes like Bcl-2 and Mcl-1 to attenuate apoptosis and promote cell survival to allow for successful cell fate changes.

Papillomavirus E7 proteins activate the YAP1 oncogene in basal epithelial cells by degrading PTPN14, in doing so promoting basal cell retention and contributing to carcinogenesis.

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.

Analysis of a double mutant in the Hippo pathway transcription factors Yap1 and Wwtr1 reveals novel roles for these factors in posterior body formation and epidermal morphogenesis in the vertebrate embryo.

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 and TAZ, the ultimate targets of the Hippo signaling pathway, are transcriptional co-activators of AP-1 proteins and STAT3 through which they are important for breast cellular transformation.

The C terminal fusion partners of TAZ-CAMTA1, YAP-TFE3 and potentially other TAZ/YAP fusion proteins in cancer recruit epigenetic modifiers that modulate a baseline TEAD-based transcriptional program.

Genetic studies reveal a role for Yap1 in lymphatic endothelial progenitor cell sprouting and proliferation during early zebrafish lymphatic vascular development.

Substrate rigidity modulates genomic stress in the epidermal basal cells of the developing zebrafish embryo and Yap1 and Wwtr1 are required for its survival.

The transcriptional regulator YAP directs the specification and differentiation of stem cells that give rise to salivary gland ductal epithelium.