作者: A.O. Awonuga , W. Zhong , M.E. Abdallah , J.A. Slater , S.C. Zhou
DOI: 10.1002/MRD.21342
关键词: Protein kinase A 、 Cell biology 、 Somatomammotropin 、 Biology 、 Eomesodermin 、 Stem cell 、 Trophoblast 、 Downregulation and upregulation 、 MAPK8 、 Molecular biology 、 Transcription factor 、 Developmental biology 、 Genetics
摘要: Eomesodermin (Eomes) is a transcription factor essential for trophoblast development. Stress stimuli activate stress-activated protein kinase (MAPK8/9) and modulate factors in stem cells (TSC). In this study, we test the hypothesis that stress-induced Eomes upregulation downstream development are MAPK8/9-dependent. Immunocytochemical immunoblot assays suggest induced by hyperosmolar stress dose- time-dependent manner. Two MAPK8/9 inhibitors work different mechanisms, LJNKl1 SP600125, block induction of stress. During normal TSC differentiation, heart neural crest derivatives expressed 1 (HAND1) dependent on Eomes, chorionic somatomammotropin hormone (CSH1) expression HAND1. Similar to HAND1 CSH1 MAPK8/9-dependent, nearly all stressed TSC. normally requires downregulation inhibitor differentiation 2 (ID2) as well upregulation. It was shown previously induces AMP-activated (PRKAA1/2)-dependent ID2 loss MAPK8/9-independent Inhibition PRKAA1/2 with compound C LJNKl1, more than alone, inhibits Taken together these data regulate Eomes/HAND1 ID2, respectively. Together network mediates Therefore, triggers proportional increase early event could be adaptive inducing CSH1. But flexibility undergo lead pathophysiological consequences if endured became unbalanced.