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Discovering differential activation machinery of the Toll‐like receptor 4 signaling pathways in MyD88 knockouts
Author(s) -
Selvarajoo Kumar
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.01.046
Subject(s) - tlr4 , gene knockout , signal transduction , microbiology and biotechnology , tumor necrosis factor alpha , toll like receptor , receptor , alpha (finance) , chemistry , biology , gene , immunology , innate immune system , biochemistry , medicine , construct validity , nursing , patient satisfaction
To understand differential time activation of nuclear factor κB (NF‐κB) and the temporal features of the downstream pro‐inflammatory cytokines’ [tumour‐necrosis‐factor‐α (TNF‐α) 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‐κB 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‐α levels will increase at a longer time in MyD88 KOs, not previously mentioned.