Discovering differential activation machinery of the Toll-like receptor 4 signaling pathways in MyD88 knockouts.
To understand differential time activation of nuclear factor kappaB (NF-kappaB) and the temporal features of the downstream pro-inflammatory cytokines' [tumour-necrosis-factor-alpha (TNF-alpha) and IP-10] mRNA levels in myeloid differentiation primary-response protein 88 (MyD88) knockouts (KOs), I developed a computational model of the TLR4 pathway. The result suggests that the late phase expression of NF-kappaB activity observed in MyD88 KOs is possibly due to a number of novel intermediates acting along the MyD88-independent pathway. I also simulate that the TNF-alpha levels will increase at a longer time in MyD88 KOs, not previously mentioned.
Selvarajoo
Kumar
K
Cell Interaction Group, Bioinformatics Institute, 138671, Singapore. kumars@bii.a-star.edu.sg
D048868:Adaptor Proteins, Signal Transducing / Q000172:deficiency*; D000818:Animals; D030801:Animals, Genetically Modified; D003198:Computer Simulation; D007700:Kinetics; D008954:Models, Biological; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B / Q000378:metabolism; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D048868:Adaptor Proteins, Signal Transducing; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha