PI5P 调节 TP53 乙酰化
中文名称
通路描述
在细胞应激条件下，磷脂酰肌醇-5-磷酸（PI5P）的核水平增加，并通过与 ING2 相互作用导致 ING2 的核滞留/积累。ING2 结合 TP53（p53）并招募组蛋白乙酰转移酶 EP300（p300）到 TP53，导致 TP53 乙酰化。核内 PI5P 水平增加正调节 TP53 乙酰化（Ciruela et al. 2000, Gozani et al. 2003, Jones et al. 2006, Zou et al. 2007, Bultsma et al. 2010）。
英文描述
Cooperation of PDCL (PhLP1) and TRiC/CCT in G-protein beta folding The chaperonin complex TRiC/CCT is needed for the proper folding of all five G-protein beta subunits (Wells et al. 2006). TRiC/CCT cooperates with the phosducin-like protein PDCL (commonly known as PhLP or PhLP1), which interacts with both TRiC/CCT and G-protein beta subunits 1-5 (GNB1, GNB2, GNB3, GNB4, GNB5) (Dupre et al. 2007, Howlett et al. 2009). PDCL enables completion of G-protein beta folding by TRiC/CCT, promotes release of folded G-protein beta subunits 1-4 (GNB1, GNB2, GNB3, GNB4) from the chaperonin complex, and facilitates the formation of the heterodimeric G-protein beta:gamma complex between G-protein beta subunits 1-4 and G-protein gamma subunits 1-12 (Lukov et al. 2005, Lukov et al. 2006, Howlett et al. 2009, Lai et al. 2013, Plimpton et al. 2015, Xie et al. 2015). In the case of G-protein beta 5 (GNB5), PDCL stabilizes the interaction of GNB5 with the TRiC/CCT and promotes GNB5 folding, thus positively affecting formation of GNB5 dimers with RGS family proteins (Howlett et al. 2009, Lai et al. 2013, Tracy et al. 2015). However, over-expression of PDCL interferes with formation of GNB5:RGS dimers as PDCL and RGS proteins bind to the same regions of the GNB5 protein (Howlett et al. 2009).
所含基因
38 个基因