Chapter category:

Decoding the Signaling Mechanism of Toll-Like Receptor 4 Pathways in Wild Type and Knockouts

This chapter appears in the following book:

E-Cell System: Basic Concepts
and Applications

Edited by: Satya Nanda Vel Arjunan, Pawan K. Dhar and Masaru Tomita
ISBN: TBA
» Get more information about this book at landesbioscience.com «

Chapter authors:
Kumar Selvarajoo

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The Myeloid Differentiation Primary‑Response Protein 88 (MyD88)‑dependent and—independent pathways induce proinflammatory cytokines when toll‑like receptor 4 (TLR4) is activated through lipopolysaccharide (LPS) stimulus. Recent studies have implicated a crosstalk mechanism between the two pathways. However, the exact location and nature of this interaction is poorly understood. Using my previous ordinary differential equations‑based computational model of the TLR4 pathway, I investigated the roles played by the various proposed crosstalk mechanisms by comparing in silico nuclear factor κB (NF‑κB) and Mitogen‑Activated Protein (MAP) kinases dynamic activity profiles with experimental results under various conditions in macrophages to LPS stimulus (MyD88 deficient, TRAF‑6 deficient etc.). The model that best represents the experimental findings suggests that the pathways interact at more than one location: i) TRIF to TRAF‑6, ii) TRIF‑RIP1‑IKK complex and iii) TRIF to cRel via TBK1.

Kumar Selvarajoo
Bioinformatics Institute, A*STAR, Biopolis, Singapore, Institute for Advanced Biosciences, Keio University, Tsuruoka Japan

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Chapter category:

Decoding the Signaling Mechanism of Toll-Like Receptor 4 Pathways in Wild Type and Knockouts

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