scholarly journals Inflammation and the Emerging Role of the Toll-Like Receptor System in Acute Brain Ischemia

Stroke ◽  
2008 ◽  
Vol 40 (3, Supplement 1) ◽  
pp. S34-S37 ◽  
Author(s):  
B. J. Marsh ◽  
S. L. Stevens ◽  
B. Hunter ◽  
M. P. Stenzel-Poore
Keyword(s):  
Brain Ischemia ◽  
Toll Like Receptor ◽  
Receptor System ◽  
Acute Brain Ischemia

Role of Toll-like receptor 1, 2 and 4 on thromboxane B2 production by different microbial products

2018 ◽  
Vol 56 (08) ◽  
pp. e254-e255
Author(s):  
J Zhang ◽  
A Wieser ◽  
H Li ◽  
I Liß ◽  
AL Gerbes ◽  
...  
Keyword(s):  
Thromboxane B2 ◽  
Toll Like Receptor ◽  
Microbial Products

scholarly journals Role of toll like receptor-9 (1237 T/C) gene polymorphism in patients with type 2 diabetes and diabetic foot ulcer

2021 ◽  
Vol 1879 (2) ◽  
pp. 022012
Author(s):  
Furqan Naeem Al-Karawi ◽  
Naji Al-Hasnawiand Abeer Thaher ◽  
Thekra Abd Jebur Al-Kashwan
Keyword(s):  
Type 2 Diabetes ◽  
Gene Polymorphism ◽  
Diabetic Foot ◽  
Foot Ulcer ◽  
Diabetic Foot Ulcer ◽  
Toll Like Receptor

scholarly journals Essential role of IRAK-4 protein and its kinase activity in Toll-like receptor–mediated immune responses but not in TCR signaling

2007 ◽  
Vol 204 (5) ◽  
pp. 1013-1024 ◽  
Author(s):  
Tatsukata Kawagoe ◽  
Shintaro Sato ◽  
Andreas Jung ◽  
Masahiro Yamamoto ◽  
Kosuke Matsui ◽  
...  
Keyword(s):  
Immune Responses ◽  
Kinase Activity ◽  
Interleukin 1 ◽  
Cell Receptor ◽  
Nuclear Factor Κb ◽  
Toll Like Receptor ◽  
Tcr Signaling ◽  
Mitogen Activated Protein

Interleukin-1 receptor–associated kinase 4 (IRAK-4) was reported to be essential for the Toll-like receptor (TLR)– and T cell receptor (TCR)–mediated signaling leading to the activation of nuclear factor κB (NF-κB). However, the importance of kinase activity of IRAK family members is unclear. In this study, we investigated the functional role of IRAK-4 activity in vivo by generating mice carrying a knockin mutation (KK213AA) that abrogates its kinase activity. IRAK-4KN/KN mice were highly resistant to TLR-induced shock response. The cytokine production in response to TLR ligands was severely impaired in IRAK-4KN/KN as well as IRAK-4−/− macrophages. The IRAK-4 activity was essential for the activation of signaling pathways leading to mitogen-activated protein kinases. TLR-induced IRAK-4/IRAK-1–dependent and –independent pathways were involved in early induction of NF-κB–regulated genes in response to TLR ligands such as tumor necrosis factor α and IκBζ. In contrast to a previous paper (Suzuki, N., S. Suzuki, D.G. Millar, M. Unno, H. Hara, T. Calzascia, S. Yamasaki, T. Yokosuka, N.J. Chen, A.R. Elford, et al. 2006. Science. 311:1927–1932), the TCR signaling was not impaired in IRAK-4−/− and IRAK-4KN/KN mice. Thus, the kinase activity of IRAK-4 is essential for the regulation of TLR-mediated innate immune responses.

scholarly journals Key Role of CD36 in Toll-Like Receptor 2 Signaling in Cerebral Ischemia

Stroke ◽  
2010 ◽  
Vol 41 (5) ◽  
pp. 898-904 ◽  
Author(s):  
Takato Abe ◽  
Munehisa Shimamura ◽  
Katherine Jackman ◽  
Hitomi Kurinami ◽  
Josef Anrather ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Detrimental Role of Heat Shock Protein 60&70 and Toll-like Receptor 4 in Skeletal Muscle Ischaemia In Vitro

2013 ◽  
Vol 57 (5) ◽  
pp. 77S
Author(s):  
Ali Navi ◽  
Rebekah Yu ◽  
Xu Shi-Wen ◽  
Sidney Shaw ◽  
George Hamilton ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Muscle Ischaemia

scholarly journals Dual Role of the Tyrosine Kinase Syk in Regulation of Toll-Like Receptor Signaling in Plasmacytoid Dendritic Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0156063 ◽  
Author(s):  
Besma Aouar ◽  
Denisa Kovarova ◽  
Sebastien Letard ◽  
Albert Font-Haro ◽  
Jonathan Florentin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tyrosine Kinase ◽  
Plasmacytoid Dendritic Cells ◽  
Dual Role ◽  
Receptor Signaling ◽  
Toll Like Receptor
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