Ask about this productRelated genes to: MYD88 antibody
- Gene:
- MYD88 NIH gene
- Name:
- MYD88 innate immune signal transduction adaptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-23
- Date modifiied:
- 2019-04-23
Related products to: MYD88 antibody
Related articles to: MYD88 antibody
- Breast cancer (BC) is a serious health issue, representing one of the most frequently occurring cancers among women. BC treatment and prevention are challenging due to its complex pathophysiology and variety of clinical signs. Therefore, we aimed to study the role of the TLR4/MYD88 signaling pathway in BC. - Source: PubMed
Publication date: 2026/09/11
Alshaban Sulaiman MohammedElkhadrary TawfikElnahhas WalidAwadalla AmiraEl-Khawaga Omali Y - This study aimed to evaluate the therapeutic efficacy of chelidonic acid (CA) in ()-induced keratitis and to elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/08/27
Liu WentingXu QiangLiu ZhenSun JintaoSun XiaoyanWan XiaomeiXue ShashaChe ChengyeTian Shaoqi - As global temperatures continue to rise, heat stress (HS) has emerged as a major health threat of growing concern. HS triggers systemic inflammation and multi-organ damage, but so far its molecular mechanisms remain unclear. In this study, we explored the potential mechanism by which the gut microbial alterations amplify HS-associated inflammatory responses. - Source: PubMed
Publication date: 2026/08/30
Ye XianxiCai QingpengPan YangjieXu MinxuanLi YulongYou MinjieYang JiayiChen SiyuanHe HuachengHong GuangliangZheng Hong - Sepsis is a systemic inflammatory response triggered by pathogenic infections, often accompanied by bacterial endotoxin release, accumulation of cell-free DNA (cfDNA), and excessive inflammatory reactions, leading to organ failure. Conventional antibiotic therapies are often inadequate in effectively eliminating pathogens and their toxic components, and fail to suppress the cfDNA-mediated inflammatory cascade. In this study, we developed a multifunctional nanotherapeutic platform based on hollow Prussian blue nanoparticles (HPB-NPs) loaded with polymyxin E (PME) and surface-modified with polyethylenimine (PEI). This versatile nanosystem (HPB-NPs@PME@PEI) exhibits potent antimicrobial activity against Gram-negative bacteria and specifically neutralizes lipopolysaccharides (LPS); PEI captures elevated levels of LPS and cfDNA in septic blood via electrostatic adsorption, thereby blocking its activation of the TLR4/MyD88 pathway and mitigating the cytokine storm; meanwhile, HPB scavenges reactive oxygen species (ROS), alleviating oxidative stress damage. Experimental results demonstrate that HPB-NPs@PME@PEI significantly reduces plasma cfDNA levels, suppresses the release of pro-inflammatory cytokines, and improves survival rates in a murine sepsis model. HPB-NPs@PME@PEI directly suppress LPS-induced inflammatory activation and NETosis in innate immune cells. Furthermore, by scavenging ROS and blocking the TLR4/MyD88/NF-κB pathway, HPB-NPs@PME@PEI effectively protects lung and renal epithelial cells from LPS injury. Thus, the nano-system operates via a synergistic mechanism, concurrently neutralizing LPS, clearing ROS, and inhibiting a major inflammatory signaling cascade. - Source: PubMed
Publication date: 2026/08/28
Song YangYu XueWu MingzheLiu JingWen ZhifengDong DaosongYe FangdieZhang Shijie - Acute respiratory distress syndrome (ARDS) is a severe inflammatory lung syndrome associated with high mortality and morbidity. Toll-like receptors (TLRs), key pattern-recognition receptors of innate immunity, mediate inflammatory responses to both infectious and sterile lung injury. Although TLR signaling has been increasingly implicated in ARDS pathogenesis, significant developmental and translational gaps remain, particularly in pediatric ARDS (PARDS). This review summarizes current evidence on TLR-mediated mechanisms in ARDS and PARDS, with emphasis on developmental regulation and translational relevance. - Source: PubMed
Publication date: 2026/08/13
Foo Clare Wei TianTan Herng LeeLeong Jing YaoYeo Joo GuanAlbani SalvatoreWong Judith Ju Ming