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Rocaglamide selectively inhibits the G1-S-phase transition in cancer cells by activation of the ATM/ATR-mediated Chk1/2 cell cycle checkpoints

ChEBI2013-10-12 更新2026-07-21 收录

细胞周期调控

癌症治疗靶点

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-41072 数据链接链接失效反馈

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Rocaglamide selectively inhibits the G1-S-phase transition in cancer cells by activation of the ATM/ATR-mediated Chk1/2 cell cycle checkpoints

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创建时间：

2013-10-12

细胞周期调控

蛋白质降解机制

Legionella pneumophila, an environmental bacterium that parasitizes protozoa, is the causative pathogen of Legionnaires' disease. L. pneumophila adopts a distinct biphasic life cycle that allows it to

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Additional file 16 of STAU2 protein level is controlled by caspases and the CHK1 pathway and regulates cell cycle progression in the non-transformed hTERT-RPE1 cells

细胞周期调控

蛋白相互作用分析

Additional file 16: Table S9. Gene ontology (GO) of STAU2 interactors that show reduced proximity to STAU2 in hTERT-RPE1 cells treated with the CHK1 inhibitor PF47 compared to untreated cells. List of

Figshare2021-03-05 更新60

DataSheet4_PRR11 promotes cell proliferation by regulating PTTG1 through interacting with E2F1 transcription factor in pan-cancer.zip

癌症分子机制

细胞周期调控

The upregulated proline rich 11 (PRR11) plays a critical role in cancer progression. The relevant biological functions of PRR11 in pan-cancer development are not well understood. In the current study,

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In-phase oscillation of global regulons is orchestrated by a pole-specific organizer. Caulobacter vibrioides NA1000

细胞周期调控

极性发育分子机制

Cell fate determination in the asymmetric bacterium Caulobacter crescentus (Caulobacter) is triggered by the localization of the developmental regulator SpmX to the old (stalked) cell pole during the

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A kinase-phosphatase switch transduces environmental information into a bacterial cell cycle circuit. Caulobacter vibrioides

细胞周期调控

环境胁迫信号转导

The bacterial cell cycle has been extensively studied under standard growth conditions. How it is modulated in response to environmental changes remains poorly understood. Here, we demonstrate that th

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Rocaglamide selectively inhibits the G1-S-phase transition in cancer cells by activation of the ATM/ATR-mediated Chk1/2 cell cycle checkpoints

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