17-DMAG FDA In the predicted network NSC GN2, tmem59 is regu lated directly by cd59a, myrip and sncg. Meanwhile, four pathways were found in NSC GN2 to Inhibitors,Modulators,Libraries regulate the expression of tmem59 from pou6f1. Tmem59 is located downstream in all the pathways, indicating that tmem59 is probably regulated by all the other genes. These con clusions are in accordance with observations from ear lier studies. Our study suggests that the 36 genes probably act on the differentiation of NSCs and have similar function with tmem59. suggests that the influence of pou6f1 on mouse telence phalon development is originated from the effect on NSCs during the mouse embryonic development. This study provides further insights into the role of the dif ferentiation of NSCs. Thirdly, our study suggests that TMEM59 has similar localization with most of its regulators.

Recently, TMEM59 was reported to be a Golgi localized protein, which is crucial in modulated complex glycosylation, cell surface expression and secretion of amyloid precursor protein. As known, proteins in the cell plasma are synthesized directly in free ribosome, while some Inhibitors,Modulators,Libraries other membrane proteins which transfer to the nucleus, are synthesized in rough endoplasmic reticulum. The second type of protein will be transported to subcellular location secreted by Golgi complex. Among the 27 annotated genes in the predicted network NSC GN2, more than 85% were identified to be nonplasmic localized. This sug gests that 85% of the 27 proteins are Golgi localized in maturation and has similar localization with TMEM59.

Furthermore, our study suggests that the tmem59 related gene regulatory network is probably AD related. As the Inhibitors,Modulators,Libraries precursor of b amyloid protein, b amyloid precursor protein is addressed to be the first genetic mutation. The deposition of Ab in pla ques of brain is already identified to be the cause of AD. As been reported, TMEM59 is Golgi localized in Hek293 Inhibitors,Modulators,Libraries cell line, and modulate the complex glycosyla tion, cell surface expression and secretion of APP. The study indicates that TMEM59 may be associated with AD. In our predicted mouse NSCs related network NSC GN2, three genes which regulate Tmem59 directly are identified as sncg, cd59a and myrip. Sncg has been identified to be correlated to dementia hippocampus of AD and pathology of Parkinsons dis ease. Deficiency of complement regulator cd59a is the cause of neurodegeneration in AD.

And Rab27 binding protein MYRIP is involved in insu lin exocytosis, impaired which is the pathogenesis of AD. Besides, there are nearly 50% of all the genes in NSC GN2 have been reported to be directly or indir ectly related to AD. Therefore, tmem59, which directly regulated Inhibitors,Modulators,Libraries by cd59a, myrip and sncgis, is suggested inhibitor expert to be associated with AD, and the unreported genes in NSC GN2 are probably related to AD either.