Fitzgerald Katherine A, Chen Zhijian J
Division of Infectious Disease and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Cell. 2006 Jun 2;125(5):834-6. doi: 10.1016/j.cell.2006.05.014.
Upon recognition of microbial products, Toll-like receptors (TLRs) recruit distinct combinations of adaptors to induce TLR-specific gene expression. In this issue, Kagan and Medzhitov (2006) demonstrate that the adaptor TIRAP/Mal localizes to the plasma membrane by binding to phosphatidylinositol 4,5-bisphosphate (PIP2). This binding recruits a key adaptor MyD88 to TLR4, suggesting that there is crosstalk between the TLR signaling pathway and phospholipid metabolism.
一旦识别出微生物产物,Toll样受体(TLRs)就会募集不同的衔接蛋白组合,以诱导TLR特异性基因表达。在本期杂志中,卡根和梅德齐托夫(2006年)证明,衔接蛋白TIRAP/Mal通过与磷脂酰肌醇4,5-二磷酸(PIP2)结合而定位于质膜。这种结合将关键衔接蛋白髓样分化因子88(MyD88)募集到TLR4,这表明TLR信号通路与磷脂代谢之间存在相互作用。