作者: Bo Chen , Zheng Xue , Guanghui Yang , Bingyang Shi , Ben Yang
DOI: 10.1371/JOURNAL.PONE.0064877
关键词: Phosphorylation 、 KLF4 、 Cell biology 、 PI3K/AKT/mTOR pathway 、 Cellular differentiation 、 AKT1 、 Molecular biology 、 Homeobox protein NANOG 、 SOX2 、 Biology 、 Protein kinase B 、 General Biochemistry, Genetics and Molecular Biology 、 General Agricultural and Biological Sciences 、 General Medicine
摘要: The mechanism by which Akt modulates stem cell homeostasis is still incompletely defined. Here we demonstrate that phosphorylates special AT-rich sequences binding protein 1 (SATB1) at serine 47 and protects SATB1 from apoptotic cleavage. Meanwhile, Oct4 threonine 228 Klf4 399, accelerates their degradation. Moreover, PI3K/Akt signaling enhances the of to Sox2, thereby probably impairing formation Oct4/Sox2 regulatory complexes. During retinoic acid (RA)-induced differentiation mouse F9 embryonal carcinoma cells (ECCs), activation profile as well its substrate spectrum strikingly correlated with down-regulation Oct4, Nanog, suggests coupled onset differentiation. Accordingly, Akt-mediated phosphorylation crucial for capability repress Nanog expression activate transcription Bcl2 Nestin genes. Taken together, conclude involved in ECCs through coordinated phosphorylations pluripotency/differentiation factors.