Both YAP1-MAML2 and constitutively active YAP1 drive the formation of tumors that resemble NF2 mutant meningiomas in mice [human]. Both YAP1-MAML2 and constitutively active YAP1 drive the formation of tumors that resemble NF2 mutant meningiomas in mice [human]

We analyzed the expression profiles of human and mouse meningiomas (driven by NF2 loss, YAP1-MAML2, TRAF7/KLF4/SMO1/AKT1, or constitutively active non-fusion YAP1). We found that YAP1-MAML2 meningiomas resemble NF2mutant tumors and constitutively exert de-regulated YAP1 activity that is dependent on the interaction with TEADs. Overall design: HEK 293 cells were grown in 48 well plates, transfected with indicated RCAS plasmids and total RNA was isolated 48 hours post-transfection

本研究分析了由NF2缺失、YAP1-MAML2融合、TRAF7/KLF4/SMO1/AKT1突变，或组成型激活的非融合型YAP1驱动的人及小鼠脑膜瘤（meningiomas）的表达谱。研究发现，YAP1-MAML2型脑膜瘤与NF2突变型肿瘤表型相似，且组成性呈现失调的YAP1活性，该活性依赖于与TEADs的相互作用。实验设计概述：将HEK 293细胞接种于48孔板中，转染指定的RCAS质粒，于转染后48小时提取总RNA。