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Diverse Targets of ?-catenin during the Epithelial-Mesenchymal Transition Define Cancer Stem Cells and Predict Disease Relapse

ChEBI2015-04-04 更新2026-07-21 收录

癌细胞机制

上皮-间质转化靶标

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-67571 数据链接链接失效反馈

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Diverse Targets of ?-catenin during the Epithelial-Mesenchymal Transition Define Cancer Stem Cells and Predict Disease Relapse

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创建时间：

2015-04-04

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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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Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [RNA-Seq]. Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [RNA-Seq]

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Velcrin compounds kill cancer cells expressing high levels of phosphodiesterase 3A (PDE3A) and Schlafen family member 12 (SLFN12) by inducing complex formation between these two proteins, but the mech

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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

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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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Diverse Targets of ?-catenin during the Epithelial-Mesenchymal Transition Define Cancer Stem Cells and Predict Disease Relapse

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