MyD88 (C-Terminus) Peptide
- Known as:
- MyD88 (C-Terminus) Peptide
- Catalog number:
- 2127P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- MyD88 (C-Terminus) Peptide
Related genes to: MyD88 (C-Terminus) Peptide
- 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 (C-Terminus) Peptide
Related articles to: MyD88 (C-Terminus) Peptide
- Chronic inflammation and oral dysbiosis are common features of oral squamous cell carcinoma (OSCC). The commensal streptococci, S. anginosus, is increased in oral diseases including OSCC. Our previous work revealed that S. anginosus promotes inflammatory responses from macrophage cell lines, however the molecular mechanism by which S. anginosus interacts with macrophages to instigate this response remains to be investigated. Here, we found S. anginosus activated primary bone marrow derived macrophages (BMMs), which presented increased NF-κB activation and downstream inflammatory cytokines TNF⍺, IL-6 and IL-1β at 24 hours post-infection. S. anginosus viability, TLR2, TLR4 and MyD88 were dispensable for NF-κB activation, but each promoted the induction of distinct downstream inflammatory mediators, with only MyD88 being necessary for NF-κB activation in response to heat-killed S. anginosus. S. anginosus replicated intracellularly within BMMs without causing cell death and induced expression of inflammasome sensors AIM2, NLRC4 and NLRP3. S. anginosus-infected BMMs lacking the inflammasome adapter protein ASC (Asc-/-) or Caspase-1 (Caspase1-/-) had significantly diminished IL-1β production compared to wild type BMMs, indicating that S. anginosus activated the inflammasome. S. anginosus primarily triggered the inflammasome through NLRP3 as S. anginosus-infected Nlrp3-/- BMMs and NLRP3 inhibitor (MCC950)-treated wild type BMMs displayed diminished IL-1β production compared to wild type controls. Lastly, S. anginosus-infected Asc-/- and to a lesser extent Nlrp3-/- mice displayed reduced weight loss, reduced inflammatory cytokines, and increased bacterial burden compared to C57BL/6 mice. These findings indicate that S. anginosus replicates within macrophages and promotes a proinflammatory response in part through activating the NLRP3 inflammasome. - Source: PubMed
Publication date: 2026/05/08
Arias Anika MReinartz Dakota MSairs ChloeKumar Sangeetha SenthilByrnes Harrison CWilson Justin E - The prevalence of type 2 diabetes mellitus (T2DM) has been rising in recent years, prompting interest in natural plant polysaccharides for their ability to mitigate the disease. To enhance its bioactivity, a degraded polysaccharide from sweet corn cob with ultrasonic-assisted enzymatic method (UE-DSCCP-A) was prepared, and its structure was also characterized. Furthermore, the significant alleviation effect of UE-DSCCP-A on T2DM has been explored and examined. - Source: PubMed
Publication date: 2026/05/07
Xiu WeiyeWang XinYu ShiyouNa ZhiguoLi ChenchenWang JingyangMa Yongqiang - Heavy metal pollution, particularly copper (Cu) and cadmium (Cd), poses a serious threat to aquatic ecosystems due to its toxicity and bioaccumulation potential. This study investigated the effects of individual and combined exposure to Cu and Cd on largemouth bass, focusing on the gut-liver axis and the TLR4/NF-κB pathway in hepatotoxicity. A total of 480 size-matched fish were randomly assigned to four groups (Control, Cu, Cd, and Cu + Cd) and exposed to sublethal concentrations of CuSO₄ (9.275 mg/L) and CdCl₂·2.5H₂O (1.15285 mg/L) for 14 days, followed by physiological, molecular, and omics analyses. Results showed that both single and combined exposures disrupted intestinal structure and barrier function, accompanied by downregulation of tight junction genes. Oxidative stress responses were tissue-specific, with increased reactive oxygen species (ROS) and MDA levels in the intestine but decreased levels in the liver, along with suppressed antioxidant enzyme activities. Inflammatory responses were activated, as indicated by elevated cytokine levels and upregulation of TLR4/MyD88/NF-κB signaling in the liver. Microbiota analysis revealed that Cd exposure increased gut microbial diversity, whereas Cu + Cd co-exposure reduced α-diversity and altered microbial composition, with increased Proteobacteria and decreased beneficial taxa such as Bacteroidota and Firmicutes. Untargeted metabolomics showed that hepatic metabolic profiles were altered, mainly affecting lipid, energy, and immune-related pathways. Overall, combined Cu + Cd exposure exerted stronger toxic effects than single exposures, inducing more severe intestinal damage, microbial dysbiosis, and metabolic disturbances. These findings highlight the critical role of the gut-liver axis in mediating heavy metal toxicity. - Source: PubMed
Publication date: 2026/05/05
Yang XiaofeiQiao MingyueDeng YanChen SongsongLi ChengShu YuankeJiang Li - To evaluate the individual and combined diagnostic performance of cytokine, molecular, and clonality biomarkers for primary vitreoretinal lymphoma (PVRL). - Source: PubMed
Publication date: 2026/05/05
Lou YuchenMa ChenxiaoZhang XiaodanZhang MengChai HongruiZhao YinlongLiu Xin - Parkinson's disease (PD) is the second most common neurodegenerative disorder, which is on the rise and poses an increasing burden on health care systems across the world. The essential factors of dopaminergic neurodegeneration in PD are neuroinflammation, α-synuclein (α-syn) aggregation, mitochondrial dysfunction, and gut microbiota dysbiosis. The toll-like receptor 4 (TLR4), one of the central elements of the innate immune system, has become one of the key controls of PD pathogenesis. Studies have shown that TLR4 is overexpressed in PD and mediates neuroinflammatory reactions through the activation of downstream signaling pathways, i.e., MyD88-dependent and TRIF-dependent pathways. TLR4 can also mediate context-dependent effects, such as its prolonged stimulation can worsen neuroinflammation and neuronal damage, whereas in the initial stages of the disease, it can be engaged in the process of clearing pathological α-syn aggregates. This review presents the recent evidence of clinical research, animal models, and in vitro research on the role of TLR4 in PD. The review also discusses the molecular pathways of neuron inflammation caused by TLR4 and its communication with α-syn aggregation, mitochondrial impairment, and the gut-brain axis. It also covers some of the newer therapeutic approaches that have been developed to address TLR4 signaling, such as natural compounds, drug repurposing strategies, and microbiota-based therapies. Taking into account these effects, TLR4 is regarded as a potential therapeutic target of PD. The comprehensive insight into its dual regulation capabilities can be employed to formulate more effective disease-modifying treatments. - Source: PubMed
Publication date: 2026/05/06
Dong ShuoLu JiayinWu LingfengWang SiyiGong YuboHu JinglinLiu YangChen Xinhua