Genetic interaction between <i>mck1</i> deletion and cyclin mutants.

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细胞周期调控

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https://figshare.com/articles/dataset/_Genetic_interaction_between_mck1_deletion_and_cyclin_mutants_/201165 数据链接链接失效反馈

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Genetic interaction between mck1 deletion and cyclin mutants.

创建时间：

2012-12-06

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

癌症分子机制

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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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The highest temperature that supports normal growth (°C) for haploid progeny of crosses between SPB remodeling candidate gene deletion strains and spc110 mutants.

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酵母表型分析

Results from Figures S1–S16 are compiled in this table: after mating each haploid spc110 mutant to each haploid deletion mutant, sporulating the diploids, and determining the genotypes of the resultin

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Arrest of G(1)-S Progression by the p53-Inducible Gene PC3 Is Rb Dependent and Relies on the Inhibition of Cyclin D1 Transcription

细胞周期调控

肿瘤抑制基因

The p53-inducible gene PC3 (TIS21, BTG2) is endowed with antiproliferative activity. Here we report that expression of PC3 in cycling cells induced accumulation of hypophosphorylated, growth-inhibitor

PubMed Central30

Crystal Structure of Mitotic Checkpoint Complex

蛋白质晶体

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Crystal Structure of Mitotic Checkpoint Complex Descriptor: MITOTIC SPINDLE CHECKPOINT COMPONENT MAD2, MITOTIC SPINDLE CHECKPOINT COMPONENT MAD3, WD REPEAT-CONTAINING PROTEIN SLP1 Authors: Kulkarni, K

Protein Data Bank Japan2023-12-20 更新20

Genetic interaction between <i>mck1</i> deletion and cyclin mutants.

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