[1] Wu X,Li M,Chen SQ,et al. Pin1 facilitates isoproterenolinduced cardiac fibrosis and collagen deposition by promoting oxidative stress and activating the MEK1/2ERK1/2 signal transduction pathway in rats.Int J Mol Med,2018, 41: 1573-1583.
[2] Zhao X,Xia C, Wang X,et al.Cyclophilin J PPIase Inhibitors Derived from 2, 3-Quinoxaline-6 Amine Exhibit Antitumor Activity. Front Pharmacol,2018, 9: 126-137.
[3] Obama K,Kato T,Hasegawa S,et al. Overexpression of peptidyl-prolyl isomerase-like 1 is associated with the growth of colon cancer cells. Clin Cancer Res, 2006, 12: 70-76.
[4] Stegmann CM,Lührmann R,Wahl MC. The crystal structure of PPIL1 bound to cyclosporine A suggests a binding mode for a linear epitope of the SKIP protein. PLoS One,2010, 5: e10013-e10022.
[5] Nakatsu Y,Mori K,Matsunaga Y,et al.The proly lisomerase Pin1 increases β-cell proliferation and enhances insulin secretion. J Biol Chem,2017,292: 11886-11895.
[6] Wang X,Zhang S,Zhang J,et al. A large intrinsically disordered region in SKIP and its disorder-order transition induced by PPIL1 binding revealed by NMR. J Biol Chem,2010, 285: 4951-4963.
[7] Simhadri VL,Hamasaki-Katagiri N,Lin BC, et al. Single synonymous mutation in factor IX alters protein properties and underlies haemophilia B. J Med Genet,2017, 54: 338-345.
[8] Chen CL,Zhao JW. Analysis of regulatory mechanism after ErbB4 gene mutation based on local modeling methodology.Genet Mol Res,2016, 15:gmr.15028647. |
