The Creighton and Deneen labs recently developed a mouse model of glioblastoma involving in utero CRISPR/Cas9-mediated knockout of three known tumor suppressors Nf1, Trp53, and Pten (termed 3xCr).¹ Here, Yu et al. modified this mouse model to screen for driver mutations in phosphatidylinositol 3-kinases (PI3Ks). Phosphatidylinositol (3,4,5)-trisphosphate [PtdIns(3,4,5)P3] is produced in the inner leaflet of the plasma membrane when Class I PI3Ks phosphorylate the 3’-position hydroxyl group of the D-myo-inositol head group.² Proteins with plekstrin homology (PH) domains are recruited to the plasma membrane under such circumstances, such as PDK1 and AKT, and activate a number of cell signaling...

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文学亮点

Creighton和Deneen实验室最近开发了一种胶质母细胞瘤小鼠模型，涉及子宫内CRISPR / Cas9介导的敲除三种已知的肿瘤抑制因子Nf1，Trp53和Pten（称为3xCr）。¹这里，Yu等。修改了此小鼠模型，以筛选磷脂酰肌醇3-激酶（PI3Ks）中的驱动程序突变。当I类PI3Ks磷酸化D-myo-的3'-位羟基时，质膜内小叶会生成磷脂酰肌醇（3,4,5）-三磷酸[PtdIns（3,4,5）P 3]肌醇头组。在这种情况下，具有plekstrin同源性（PH）结构域的^2个蛋白被募集到质膜上，例如PDK1和AKT，并激活许多细胞信号传导...