cyclin e-cdk2负责完成rb1的磷酸化，通过释放更多的e2f，促进细胞进入s期所需的蛋白质的合成。在g1期的发展过程中，一些e2f转录生成的蛋白在dna复制起点聚集并形成 复制前复合体 ，由orc1-6、cdc6、cdt1和mcm2-7 dna解旋酶组成。在s期开始时，dbf4-cdc7和cyclin e-cdk2的一 ...

2021年9月1日 · Key findings revealed that RB loss in advanced disease redirected E2F1 to serve as a critical regulator of glutathione synthesis, as evident through cistrome, transcriptome, and metabolome profiling.

2022年3月31日 · Among the RB-E2F target genes, a large number code for key cell cycle regulators. Their transcriptional repression by the RB-E2F complex is released through phosphorylation of RB, leading to...

2024年8月18日 · Rb通过两种相互作用抑制了E2F的活性：一是Rb pocket domain (RbP)与E2F的转录激活结构域（TD）结合；二是Rb羧基端结构域（RbC）与E2F的marked box (MB)结构域以及E2F二聚体结合蛋白DP的MB结构域结合。

2023年12月7日 · In the present study, we designed a series of small-molecule Thiazole-based HDACis, among which HR488B bound to HDAC1 with a high affinity and exerted effective anti-CRC activity both in vitro and...

2016年2月29日 · Mutations of the retinoblastoma tumor-suppressor gene (RB1) or components regulating the CDK-RB-E2F pathway have been identified in nearly every human malignancy. Re-establishing cell cycle...

Here, isogenic modeling of RB loss identified disease stage-specific rewiring of E2F1 function, providing the first-in-field mapping of the E2F1 cistrome and transcriptome after RB loss across disease progression.

2018年12月7日 · 未磷酸化或低磷酸化的rb与e2f转录因子相互作用并抑制e2f靶基因表达和g1 / s细胞周期转变。 然而，在有丝分裂原刺激或G1晚期，RB在多个位点通过细胞周期蛋白/ CDK复合物如CYCLIN D / CDK4 / 6过度磷酸化，导致E2F因子从RB隔离和细胞周期的进展中释放。

2023年5月15日 · Here, we showed that RB1 loss/E2F activation sensitized cancer cells to ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation, by upregulating expression of ACSL4 and enriching ACSL4-dependent arachidonic acid-containing phospholipids, which are key components of ferroptosis execution.

2023年11月28日 · Here, we show that breast cancer cells develop CDK4/6i resistance via a sequential two-step process of E2F activation. This process entails retinoblastoma (Rb)-protein degradation, followed by c-Myc-mediated amplification of E2F transcriptional activity.