看到Principles of Neural Science 上一系列蛋白激酶的示意图，觉得和太极阴阳图好像啊。例如cAMP-dependentprotein kinase A ，如同剑入剑鞘。当cAMP 结合调控亚基后，催化亚基才被释放出来。 在PDB protein data bank里的 PKA分子结构 所示：而非催化状态PKA 的分子结构还真的很像太极图。http://www.rcsb.org/pdb/101/motm.do?momID=57 图中红色为催化亚基（阳），被蓝色的调节亚基（阴）所结合。当cAMP 结合蓝色的调节亚基之后，催化亚基宝剑出鞘，行使催化功能。
STK33 plays an important positive role in the development of human large cell lung cancers with variable metastatic potential Ping Wang, Hongzhong Cheng, Jianqiang Wu, Anrun Yan and Libin Zhang Acta Biochim Biophys Sin 2015, 47: 214–223; doi: 10.1093/abbs/gmu136 Department of Thoracic Surgery, First People's Hospital of Yunnan Province, Kunming 650031, China Serine/threonine kinase 33 (STK33) is a novel protein that has attracted considerable interest in recent years. Previous research has revealed that STK33 expression plays a special role in cancer cell proliferation. However, the mechanisms of STK33 induction of cancer cells remain largely unknown. In this study, it is demonstrated that STK33 expression varies in NL9980 and L9981 cells which are homogeneous cell lines with similar genetic backgrounds. STK33 can promote cell migration and invasion and suppress p53 gene expression in the NL9980 and L9981 cells. In addition, this protein also promotes epithelial–mesenchymal transition (EMT). Moreover, STK33 knockdown decreases tumor-related gene expression and inhibits cell migration, invasion, and EMT, suggesting that STK33 may be a mediator of signaling pathways that are involved in cancer. In conclusion, our results suggest that STK33 may be an important prognostic marker and a therapeutic target for the metastatic progression of human lung cancer. 图例: STK33诱导Snail、Slug、Twist、FoxC2基因的表达 全文: http://abbs.oxfordjournals.org/content/47/3/214.full.pdf+html
http://onlinelibrary.wiley.com/doi/10.1111/acel.12218/full 文章阅读： A novel kinase regulates dietary restriction-mediated longevity in Caenorhabditis elegans Article first published online: 21 MAR 2014 AGING CELL DOI: 10.1111/acel.12218 Highlights： 1,RNAi knockdown of mekk-2 initiates a DR-like status,triggering a metabolic and physiological reprogramming which leads to healthy lifespan extension. 2,Metabolic shift to beta-oxidation,instead of RNAi treatment, is repsonsbile for increased xenobiotic detoxification in lipid oxidation. 3,Lifespan extension by mekk-2 RNAi is independent of DAF-16,but requires PHA-4 and partially depends on the activity of SKN-1. 4,MEKK-2 regulates lifespan in a tissue nonautonomous manner, in which hypodermis and muscle, instead of intestine-where most of aging genes functions plays an important role. 5,MEKK-2 functions as a negative regulator in aging process and may constitute a sensory module for nutrient sensing pathway, like AMPK.
标签: kinase
