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. HEK 293 cells were grown in 48 well plates, transfected with indicated RCAS plasmids and total RNA was isolated 48 hours post-transfection

我们分析了由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驱动的人源及小鼠脑膜瘤的表达谱。研究发现，YAP1-MAML2融合驱动的脑膜瘤与NF2突变型肿瘤表型高度相似，且持续呈现失调的YAP1活性，该活性依赖于其与TEADs的相互作用。将HEK 293细胞接种于48孔板中，转染指定的RCAS质粒，并于转染48小时后提取总RNA。