Results 81 to 90 of about 76,910 (294)
Unresponsiveness of MyD88-Deficient Mice to Endotoxin [PDF]
Immunity, 1999 MyD88 is a general adaptor protein that plays an important role in the Toll/IL-1 receptor family signalings. Recently, Toll-like receptors 2 and 4 (TLR2 and TLR4) have been suggested to be the signaling receptors for lipopolysaccharide (LPS). In this study, we demonstrate that MyD88 knockout mice lack the ability to respond to LPS as measured by shock ...
Kawai, Taro +4 more
openaire +2 more sources
Advanced Science, EarlyView.In an invasive beetle–fungus complex, the mutualist Leptographium procerum induces host HSP83 and modulates Toll‐dependent antifungal immunity. HSP83 mediates two‐tiered control by associating with selected fungal recognition receptors and restraining Dorsal‐driven antimicrobial peptide transcription.
Qingtai Yang +8 more
wiley +1 more source
MyD88 signaling in dendritic cells and the intestinal epithelium controls immunity against intestinal infection with C. rodentium. [PDF]
PLoS Pathogens, 2017 MyD88-mediated signaling downstream of Toll-like receptors and the IL-1 receptor family is critically involved in the induction of protective host responses upon infections.
Christin Friedrich +8 more
doaj +1 more source
, 2015 A) MyD88-specific inhibitor peptide reduces reporter gene expression compared to control peptide. MyD88 activity was inhibited in BMDMs by increasing concentration of a specific peptide inhibitor (MyD88-Inh Pep) prior to infection (MCMV-gLuc).
Elena Isern (719578) +7 more
core +1 more source
Advanced Science, EarlyView.D4F‐functionalized ceria nanozyme–CasRx nanoparticles preferentially target renal macrophages through SR‐B1‐mediated uptake in ischemia–reperfusion injury. Ceria scavenges excessive ROS, while CasRx silences STING signaling, shifting macrophages toward a less inflammatory, pro‐resolving state and increasing the proportion of regulatory T cells.
Weibo Chen +11 more
wiley +1 more source
Advanced Science, EarlyView.During pancreatitis, IL‐1α is released from necrotic acinar cells. In response to IL‐1α, pancreatic fibroblasts release chemokines and cytokines that regulate the recruitment of immune cells to the damaged organ. Furthermore, IL‐1α primes fibroblasts, resulting in increased tissue fibrosis during chronic pancreatitis.
Hala Mazloum +13 more
wiley +1 more source
Journal of Physiological InvestigationThis study investigates the mechanism by which a compound mixture of Chuanxiong and Baizhi (CMCB) modulates the TLR4/MyD88/nuclear factor kappa B (NF-κB) pathway to alleviate neuroinflammation in nitroglycerin (NTG)-induced chronic migraine (CM) rat ...
Xin Li +5 more
doaj +1 more source
Advanced Science, EarlyView.Sepsis‑induced pediatric acute respiratory distress syndrome suppresses FOXF1 in lung endothelial cells which causes life‐threatening lung damage. To counter this, researchers developed nanoparticles that specifically target these cells and deliver FOXF1 mRNA.
Zicheng Deng +14 more
wiley +1 more source
Ac‐SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes
Animal Models and Experimental Medicine, EarlyView.Schematic diagram of Ac‐SDKP regulating the FAS/FASL and mitochondrial apoptosis pathways via HSP27. Ac‐SDKP inhibits HSP27 expression, activates the FAS/FASL pathway and Caspase‐3 signaling, increases Caspase‐8 and Caspase‐3 expression, and induces cell apoptosis.
Wenxin Guo +13 more
wiley +1 more source
, 2014 (A–B) M2-2 forms a complex with MyD88 in the overexpression system. 293 cells were transfected with plasmids encoding HA-tagged MyD88 and V5-tagged M2-2 or their control vectors as indicated.
Guanping Zhang (533405) +5 more
core +1 more source