Virus-inducible IGFALS facilitates innate immune responses by mediating IRAK1 and TRAF6 activation
暂无分享,去创建一个
Ying Zhu | Gang Xu | Shi Liu | Chuanjin Luo | W. Cao | Lin Liu | Zhikui Cheng | Qi Zuo | Chen Yu | Feiyan Deng | Kaiwen Dou
[1] Fengna Chu,et al. Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis , 2020, Frontiers in Molecular Neuroscience.
[2] T. Dainichi,et al. Immune Control by TRAF6-Mediated Pathways of Epithelial Cells in the EIME (Epithelial Immune Microenvironment) , 2019, Front. Immunol..
[3] P. Cohen,et al. The role of hybrid ubiquitin chains in the MyD88 and other innate immune signalling pathways , 2017, Cell Death and Differentiation.
[4] Sky W. Brubaker,et al. Innate immune pattern recognition: a cell biological perspective. , 2015, Annual review of immunology.
[5] R. Baxter,et al. D440N mutation in the acid-labile subunit of insulin-like growth factor complexes inhibits secretion and complex formation. , 2011, Molecular endocrinology.
[6] M. Kempers,et al. Homozygous and heterozygous expression of a novel mutation of the acid-labile subunit. , 2008, European journal of endocrinology.
[7] G. Ooi,et al. The acid-labile subunit (ALS) of the 150 kDa IGF-binding protein complex: an important but forgotten component of the circulating IGF system. , 2001, The Journal of endocrinology.