期刊
INTERNATIONAL JOURNAL OF MEDICAL SCIENCES
卷 19, 期 2, 页码 274-285出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijms.67436
关键词
ZFP91; RIP1; E3 ligase; Ubiquitination; AML; Proteasome degradation
资金
- National Natural Science Foundation of China [81772280]
The research reveals that ZFP91 enhances AML cell proliferation and inhibits apoptosis by interacting with RIP1 and inhibiting its K48-linked ubiquitination. These findings provide evidence that targeted inhibition of ZFP91 could be a potential approach to treat AML.
Acute myeloid leukemia (AML) is a quickly progressive and devastated hematological malignancy with large rate of relapse and the appearance of chemotherapy resistance. Therefore, the identification of new therapeutic targets is urgent. ZFP91 is a hidden oncogene. Nevertheless, how ZFP91 takes part in regulating AML is less clear. Our research aims at investigating the molecular mechanisms and uncovering the effects of ZFP91 on AML. This research demonstrates that ZFP91 boosts AML cell proliferation and stops AML cell apoptosis. Mechanistically, experimental results showed the interaction between ZFP91 and RIP1 and inhibitory effect of ZFP91 on the K48-linked ubiquitination of endogenous RIP1, which is an important molecule in AML. Taken together, our results provide the evidence that targeted inhibition of ZFP91 could be a hopeful measure to treat AML.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据