Qki deficiency maintains stemness of glioma stem cells in suboptimal environment by downregulating endolysosomal degradation

被引:0
|
作者
Takashi Shingu
Allen L Ho
Liang Yuan
Xin Zhou
Congxin Dai
Siyuan Zheng
Qianghu Wang
Yi Zhong
Qing Chang
James W Horner
Brandon D Liebelt
Yu Yao
Baoli Hu
Yiwen Chen
Gregory N Fuller
Roeland G W Verhaak
Amy B Heimberger
Jian Hu
机构
[1] University of Texas MD Anderson Cancer Center,Department of Cancer Biology
[2] Stanford University,Department of Neurosurgery
[3] University of Texas MD Anderson Cancer Center,Department of Genomic Medicine
[4] University of Texas MD Anderson Cancer Center,Department of Bioinformatics and Computational Biology
[5] University of Texas MD Anderson Cancer Center,Department of Epigenetics and Molecular Carcinogenesis
[6] Institute for Applied Cancer Science,Department of Neurosurgery
[7] University of Texas MD Anderson Cancer Center,Department of Neurosurgery
[8] University of Texas MD Anderson Cancer Center,Department of Neurosurgery
[9] Houston Methodist Neurological Institute,Department of Pathology
[10] Fudan University Huashan Hospital,undefined
[11] University of Texas MD Anderson Cancer Center,undefined
来源
Nature Genetics | 2017年 / 49卷
关键词
D O I
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中图分类号
学科分类号
摘要
Jian Hu and colleagues use mouse models to show that Qki deficiency promotes gliomagenesis by allowing neural stem cells to maintain their stemness outside the subventricular zone. Mechanistically, they show that Qki deficiency decreases endolysosome-mediated degradation of receptors that are essential for maintaining self-renewal, allowing cells to cope with low ligand levels outside of their niche.
引用
收藏
页码:75 / 86
页数:11
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