赫拉
生物
神经母细胞瘤RAS病毒癌基因同源物
错义突变
基因亚型
癌症研究
基因
分子肿瘤学
突变
癌症
癌变
细胞生物学
功能(生物学)
计算生物学
遗传学
突变体
选择性拼接
外显子
癌细胞
GTPase激活蛋白
克拉斯
信号转导
抗凋亡Ras信号级联
MAPK/ERK通路
作者
G. Aaron Hobbs,Channing J. Der,Kent L. Rossman
摘要
ABSTRACT RAS proteins (KRAS4A, KRAS4B, NRAS and HRAS) function as GDP–GTP-regulated binary on-off switches, which regulate cytoplasmic signaling networks that control diverse normal cellular processes. Gain-of-function missense mutations in RAS genes are found in ∼25% of human cancers, prompting interest in identifying anti-RAS therapeutic strategies for cancer treatment. However, despite more than three decades of intense effort, no anti-RAS therapies have reached clinical application. Contributing to this failure has been an underestimation of the complexities of RAS. First, there is now appreciation that the four human RAS proteins are not functionally identical. Second, with >130 different missense mutations found in cancer, there is an emerging view that there are mutation-specific consequences on RAS structure, biochemistry and biology, and mutation-selective therapeutic strategies are needed. In this Cell Science at a Glance article and accompanying poster, we provide a snapshot of the differences between RAS isoforms and mutations, as well as the current status of anti-RAS drug-discovery efforts.
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