2022年3月31日 · CDKN1A/p21(WAF1), RB1, ARID1A, FLG, and HRNR mutation patterns provide insights into urinary tract environmental exposure carcinogenesis and potential treatment strategies. Am J Cancer Res. 2021...

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....

Cyclin D-CDK4/6激酶磷酸化各种细胞靶点，最重要的是 视网膜母细胞瘤蛋白 (RB1)，以及相关的RBL1 (p107)和RBL2 (p130)。 在RB1未磷酸化的形式下，RB1结合 E2F转录因子 ，并使其功能被抑制。

这两种细胞周期蛋白都可以结合和激活CDK1。CDK1除了可以促进G2-M期转换，实际上还能通过与多个间期细胞周期蛋白关联调节G1进程和G1-S期转换。在kegg图中，主要描述CyclinA/B-CDK1的上游调节。但实际上其也调控大量下游基因。这里就将其参与的上下游调节一起描述。

Canonically, RB1 regulates cell cycle progression and represents the down-stream target for CDK4/6 inhibitors that are in clinical use. However, newly discovered features of the RB1-pathway suggest new therapeutic strategies to counter resistance and improve precision medicine.

2022年10月7日 · Here, using live-cell sensors for CDK4/6 and CDK2 activities, we propose that CDK4/6 initiates Rb inactivation and CDK2 activation, which coordinates the timing of cell-cycle commitment and...

Canonically, RB1 regulates cell cycle progression and represents the downstream target for cyclin-dependent kinase (CDK) 4/6 inhibitors that are in clinical use. However, newly discovered features of the RB1 pathway suggest new therapeutic strategies to counter resistance and improve precision medicine.

2023年3月28日 · Reconstitution of a p85β full-length protein but not a p85β Y464F mutant protein in p85β knockdown cells suppressed RB1 expression and increased CDC2 expression (Figure 5F), suggesting that nuclear p85β regulates RB1 expression. Furthermore, RB1 expression was suppressed by nuclear p85β at the transcriptional level (Figures 5G–5I).

RB1 and CDK1. Number of citations of the paper that reports this interaction (PubMedID 9885575) 139; Data Source: BioGRID (enzymatic study, enzymatic study, enzymatic study, enzymatic study, enzymatic study, enzymatic study, enzymatic study, enzymatic study) HPRD (in vivo) RB1 CDK1;

在 G1 末期被周期素依赖性激酶 (CDK) 磷酸化的 Rb 会诱使 Rb 分裂，并允许 E2F 介导的 S 期促进基因的转录。 作为对上游信号的反应，INK4 和 Kip/Cip 家族抑制剂会控制 CDK 活性，并防止其进入 S 期。 DNA 损伤会通过 ATM/ATR 和 Chk1/2 激酶激活反应通路来限制 CDK 活性，从而导致细胞周期停滞和 DNA 修复或细胞死亡。 G2/M 检查点可防止带有受损 DNA 的细胞进入有丝分裂 (M) 阶段。 与 cyclin B 结合的活化 CDK1 (cdc2) 可推动细胞进入有丝分裂阶段。