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Culture of MPP from find more which we and others have observed (Santagata et?al., 2014). Older MPP needed to be stressed with extraphysiologically stiff substrata to reveal their YAP/TAZ-dependent bias toward LEP, which was consistent with our observation in?vivo that YAP tended to be located in LEP with increased age. In younger women, YAP was in the nuclei of K14-expressing MEP, as well as the apical snouts of LEP. We previously demonstrated that postmenopausal LEP tend to express some K14, as well as other markers associated with MEP, and these new data suggest that age-dependent changes in YAP/TAZ activity may underlie that phenotype of aging. Radiographic density of breast tissue tends to decrease with age suggesting that the mechanical environment is also altered (Benz, 2008), but mechanical forces do not exclusively govern YAP/TAZ regulation. Our experimental approach took advantage of tuned Ceritinib in vitro mechanical perturbations of matrix to functionally probe the HMEC, but more broadly these results revealed that aging fundamentally alters Hippo pathway?regulation. The role of cell-cell contact in Hippo pathway regulation should be further investigated in the context of chronological age. Both Wnt/beta-catenin and NF2 are known to regulate YAP/TAZ in?vivo (Cockburn et?al., 2013?and?Imajo et?al., 2012), Ceftiofur and changes to both pathways have been implicated in different age-related cancers (Evans et?al., 2005?and?Seidler et?al., 2004). Little is known about whether YAP/TAZ play a role in other phenotypes of aging. Deficiency in C.?elegans yap-1 resulted in overall healthier aging relative to controls ( Iwasa et?al., 2013). Disrupted Hippo signaling in human and mouse ovarian follicles, which caused YAP activation, promoted growth and oocyte maturation, which are processes typically defective with age ( Kawamura et?al., 2013). Indirect evidence suggests mesenchymal stem cells also have dampened modulus-dependent differentiation responses with age. Bone is magnitudes stiffer than adipose tissue and the osteogenic potential of mesenchymal stem cells decreases and a bias toward adipogenesis increases with age ( Moerman et?al.