Kim L, Kimmel A R
Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-2715, USA.
Curr Opin Genet Dev. 2000 Oct;10(5):508-14. doi: 10.1016/s0959-437x(00)00120-9.
Until recently, protein kinase GSK3 (glycogen synthase kinase 3), an essential component for cell-fate specification, had been considered a constitutively activated enzyme subject to developmentally regulated inhibition through hierarchical, linear signaling paths. Data from various systems now indicate more complex scenarios involving activating as well as inhibiting circuits, and the differential formation of multi-protein complexes that antagonistically affect GSK3 function.
直到最近，蛋白激酶GSK3（糖原合酶激酶3），一种细胞命运决定的关键成分，一直被认为是一种持续激活的酶，通过分级的线性信号通路受到发育调控的抑制。来自各种系统的数据现在表明存在更复杂的情况，涉及激活和抑制回路，以及多蛋白复合物的差异形成，这些复合物会拮抗地影响GSK3的功能。
