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Defective K-Ras Oncoproteins Initiate Cancer In Vivo and Evolve to Overcome Impaired Effector Binding

ChEBI2011-09-30 更新2026-07-21 收录

肿瘤癌蛋白功能

癌细胞机制

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-28687 数据链接链接失效反馈

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资源简介：

Defective K-Ras Oncoproteins Initiate Cancer In Vivo and Evolve to Overcome Impaired Effector Binding

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创建时间：

2011-09-30

癌细胞机制

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Data_Sheet_2_A Covalent Calmodulin Inhibitor as a Tool to Study Cellular Mechanisms of K-Ras-Driven Stemness.PDF

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Recently, the highly mutated oncoprotein K-Ras4B (hereafter K-Ras) was shown to drive cancer cell stemness in conjunction with calmodulin (CaM). We previously showed that the covalent CaM inhibitor op

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CD95L mRNA is toxic to cells [SmallRNA_CD95L.50hrs.Drosha_ko]

RNA干扰治疗

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>80% of a large number of tested siRNAs and shRNAs targeting CD95 or CD95 ligand (CD95L) induce a form of cell death that is characterized by the simultaneous activation of multiple death pathways and

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Type I IFNs promote cancer cell stemness by triggering the epigenetic regulator KDM1B. Type I IFNs promote cancer cell stemness by triggering the epigenetic regulator KDM1B

癌细胞机制

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Cancer stem cells (CSCs) are immature, immortal cells within tumors, adept at resisting therapeutic pressure and responsible for local and distant disease recurrence. Non-genetic mechanisms of acquire

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Defective K-Ras Oncoproteins Initiate Cancer In Vivo and Evolve to Overcome Impaired Effector Binding

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