CDH1降解
中文名称
通路描述
上皮 - 间质转化（EMT）的早期阶段可能涉及CDH1的翻译后下调，而晚期EMT则涉及CDH1的转录沉默（Janda et al. 2006）。据报道，两种E3泛素连接酶可报道泛素化CDH1并促进其降解。MDM2（HDM2）被报道通过蛋白酶体介导CDH1的泛素依赖性降解（Yang et al. 2006; Adhikary et al. 2014; Lu et al. 2015; Wang et al. 2020; Zhao et al. 2020），而CBLL1（Hakai）被报道介导CDH1的泛素依赖性溶酶体降解（Fujita et al. 2002; Shen et al. 2008; Chen et al. 2009; Hartsock and Nelson 2012; Smyth et al. 2012; Sako-Kubota et al. 2014; Lu et al. 2018; 综述 Zhang et al. 2023）。
英文描述
The CRY:PER:kinase complex represses transactivation by the BMAL:CLOCK (ARNTL:CLOCK) complex A complex containing Cryptochrome proteins CRY1, CRY2, Period proteins PER1, PER2, PER3, and kinases CSNK1D and/or CSNK1E binds a heterodimer containing phosphorylated CLOCK and phosphorylated, acetylated BMAL1 bound to E-boxes in the promoters of target genes (inferred from mouse homologs in Griffin et al. 1999, Langmesser et al. 2008, Ye et al. 2011, Ye et al. 2014, Aryal et al. 2017, Cao et al. 2021). This effectively delivers the kinases CSNK1D and/or CSNK1E to the proximity of CLOCK, resulting in further phosphorylation of CLOCK (inferred from mouse homologs in Cao et al. 2021). NPAS2, which acts redundantly with CLOCK, may be similarly phosphorylated. The phosphorylation of CLOCK causes the dissociation of the BMAL1:CLOCK heterodimer from DNA (inferred from mouse homologs in Ye et al. 2014, Chiou et al. 2016, Cao et al. 2021), terminating the diurnal activation of gene expression by BMAL1:CLOCK.
所含基因
12 个基因