Cooperation of PDCL (PhLP1) and TRiC/CCT in G-protein beta folding
中文名称
通路描述
TRiC/CCT 是 G 蛋白 beta 亚基（WGS1-5）正确折叠所必需的。TRiC/CCT 与 Phosducin-like 蛋白 PDCL（也称为 PhLP 或 PhLP1）协同作用，该蛋白与 G 蛋白 beta 亚基 1-5（GNB1, GNB2, GNB3, GNB4, GNB5）相互作用。PDCL 通过 TRiC/CCT 完成 G 蛋白 beta 亚基的折叠，促进折叠后的 G 蛋白 beta 亚基 1-4（GNB1, GNB2, GNB3, GNB4）从复合物中释放，并促进 G 蛋白 beta 亚基 1-4 与 G 蛋白 gamma 亚基 1-12 形成异二聚体 G 蛋白 beta:gamma 复合物。在 G 蛋白 beta 5（GNB5）的情况下，PDCL 稳定 GNB5 与 TRiC/CCT 的相互作用并促进 GNB5 折叠，从而正面向 RGS 家族蛋白的 GNB5 二聚体形成。然而，PDCL 的过表达会干扰 GNB5:RGS 二聚体的形成，因为 PDCL 和 RGS 蛋白结合到 GNB5 蛋白的相同区域。
英文描述
RUNX1 and FOXP3 control the development of regulatory T lymphocytes (Tregs) The complex of CBFB and RUNX1 (AML1) controls transcription of the FOXP3 gene. FOXP3 is a transcription factor that acts as a key regulator of development and function of regulatory T lymphocytes (Tregs). Tregs are CD25+CD4+ T lymphocytes involved in suppression of aberrant immune responses seen in autoimmune diseases and allergies. FOXP3 can bind to RUNX1 and control transcriptional activity of the RUNX1:CBFB complex. RUNX1 stimulates transcription of IL2 and IFNG1 (IFN-gamma), and the expression of these two genes is repressed upon binding of FOXP3 to RUNX1. The complex of FOXP3 and RUNX1, on the other hand, stimulates transcription of cell surface markers of Tregs, such as CD25, CTLA-4 and GITR. In the absence of FOXP3, RUNX1 represses transcription of these genes (Shevach 2000, Maloy and Powrie 2001, Sakaguchi 2004, Ono et al. 2007, Kitoh et al. 2009).
The RUNX1:CBFB complex directly stimulates transcription of the CR1 gene, encoding Complement receptor type 1 (CD35) (Kim et al. 1999, Rho et al. 2002). Expression of CR1 on the surface of activated T cells contributes to generation of Tregs (Torok et al. 2015).
The RUNX1:CBFB complex directly stimulates transcription of the CR1 gene, encoding Complement receptor type 1 (CD35) (Kim et al. 1999, Rho et al. 2002). Expression of CR1 on the surface of activated T cells contributes to generation of Tregs (Torok et al. 2015).
所含基因
10 个基因