WP45 - G1 to S cell cycle control - Homo sapiens

In the G1 phase there are two types of DNA damage responses, the p53-dependent and the p53-independent pathways. The p53-dependent responses inhibit CDKs through the up-regulation of genes encoding CKIs mediated by the p53 protein, whereas the p53-independent mechanisms inhibit CDKs through the inhibitory T14Y15 phosphorylation of Cdk2. Failure of DNA damage checkpoints in G1 leads to mutagenic replication of damaged templates and other replication defects. Source: Reactome
Protein phosphorylation sites were added based on information from PhosphoSitePlus (R), www.phosphosite.org.
Proteins on this pathway have targeted assays available via the [CPTAC Assay Portal](https://assays.cancer.gov/available_assays?wp_id=WP45).

在细胞周期G1期，存在两类DNA损伤应答通路，分别为p53依赖型通路与p53非依赖型通路。p53依赖型应答通过p53蛋白介导的、编码细胞周期蛋白依赖性激酶抑制剂（Cyclin-dependent kinase inhibitors，CKIs）的基因上调，以抑制细胞周期蛋白依赖性激酶（Cyclin-dependent kinases，CDKs）；而p53非依赖型机制则通过对Cdk2的T14、Y15位点实施抑制性磷酸化来抑制CDKs。G1期DNA损伤检查点功能失常，会引发受损DNA模板的致突变性复制以及其他复制相关缺陷。数据来源：Reactome
本通路的蛋白质磷酸化位点信息基于PhosphoSitePlus（R）数据库（www.phosphosite.org）的公开数据整理得到。
可通过[CPTAC检测门户](https://assays.cancer.gov/available_assays?wp_id=WP45)获取本通路相关蛋白质的靶向检测服务。