MyD88 (Intermediate Domain) Peptide
- Known as:
- MyD88 (Intermediate Domain) Peptide
- Catalog number:
- 2125P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- MyD88 (Intermediate Domain) Peptide
Related genes to: MyD88 (Intermediate Domain) 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
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- Luteal phase defect (LPD) is a prevalent endocrine disorder contributing significantly to female infertility and early pregnancy loss. Nuangong Tiaojing Formula (NTF), a traditional Chinese medicine formula, has demonstrated clinical efficacy in treating LPD, yet its underlying mechanisms remain incompletely elucidated. - Source: PubMed
Publication date: 2026/04/17
Hao MingqianXue XiLi YinjiaWu XingchengGao YaqinCui YutingLi YunshuZhang MingtaoQin FeiLyu GaohongXu LiuZhou HuifangChen Zhipeng - Inflammation is closely linked to depression, and natural compounds show promise for treating inflammatory depression, though their mechanisms remain unclear. Eleutheroside B (EB), a key bioactive component of the classic Araliaceae plant Eleutherococcus senticosus with various central protective effects, but its antidepressant properties remain to be explored. - Source: PubMed
Publication date: 2026/04/26
Wu ShuoJiang YunhaoZhai CaiyuLi PeipeiYang HongyangXu ChiWang YujunLiu Jing-GenZhang Lesha - CX3CR1 is a chemokine receptor expressed on respiratory epithelial and immune cells and has been identified as a host factor important for infections with respiratory syncytial virus (RSV). In this review, we discuss the roles CX3CR1 plays in the pathogenesis of RSV infections as a viral entry receptor and regulator of immune cell trafficking. The conserved CX3C motif of the RSV G glycoprotein binds to CX3CR1 to mediate viral attachment and entry into respiratory epithelial cells. Furthermore, soluble G protein (sG) can bind to CX3CR1 and competitively interfere with cell signaling induced by the chemokine CX3CL1, resulting in inhibition of immune cell recruitment to the site of infection. In addition, sG engages TLR2 on epithelial cells, activating MyD88-NF-κB signaling and priming the NLRP3 inflammasome, which enhances viral dissemination through pyroptotic cell death. CX3CR1 signaling should be viewed as one of several overlapping host factors that-along with developmental changes in interferon and STAT3 signaling, airway anatomy, inflammasome activity, and tissue-resident memory responses-contribute to differential disease outcomes of RSV infection. A more complete molecular understanding of RSV-CX3CR1 interactions and downstream host responses may enable the development of improved prevention and treatment strategies. - Source: PubMed
Publication date: 2026/04/13
Meineke RobertLudlow MartinOsterhaus Albert D M ERimmelzwaan Guus F - : is an important bacterial pathogen in crucian carp and can cause serious disease outbreaks and substantial economic losses in aquaculture. : To evaluate how infection and its inactivated vaccine modulate immune responses in . : 270 juveniles were allocated into three groups: a saline-injected control group (Ctrl), a vaccination group receiving an inactivated vaccine (Vac), and an artificial infection group (AIG) subjected to stimulation. Liver, spleen, head kidney, gill, and intestine samples were collected from fish after anesthesia. The relative transcript levels of , , , , , , , and were quantified. For liver transcriptome analysis, the effective library concentration was determined. And the 16S rRNA gene resulting reads of fish gill symbiotic microbiota were processed for downstream bioinformatic analysis. : The results showed that the Vac achieved an RPS of 73.33%, and vaccination significantly upregulated multiple immune-related genes in different fish organs. With transcription across organs emerging as a robust sentinel readout. The Pearson correlation coefficient () of BAFF between other genes were all ≥0.8. GO and KEGG enrichment analyses indicated that AIG had more DEGs than Vac (5885 vs. 4008) and Ctrl (6910 vs. 6178), respectively. Some genes in AIG revealed significant over-representation of immune pathways, such as , , and . The fish gill microbiota comprised a diverse set of low-abundance taxa, the phylum level was dominated by Proteobacteria and Fusobacteriota across all groups; whereas, the Vac group remained broadly closer to the Ctrl group in overall composition. : These results indicated marked post-challenge immune-metabolic coupling in the liver, and suggested coordinated immunophysiological interplay between the liver and the spleen. Gill microecology of symbiotic bacteria was affected by vaccination or challenge reactions, which in turn affects the health of the gills or the organism itself. - Source: PubMed
Publication date: 2026/03/29
Wang JunboHuang ShiyongLai YingtiaoWang PingWang FeifeiPan DahuiZhao FeiGong Hua - Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment but are associated with serious immune-related cardiac toxicities. In this study, AC16 human cardiomyocytes were exposed to nivolumab alone or in combination with ipilimumab. The expression of apoptosis- and inflammation-associated proteins and key components of the TLR4-MyD88-NF-B signaling pathway was examined by Western blotting. Apoptotic responses were evaluated using flow cytometry and immunofluorescence assays. BALB/c mice were administered nivolumab or nivolumab plus ipilimumab intraperitoneally for 4 weeks followed by histopathological assessment of cardiac tissue and measurement of myocardial injury biomarkers. Network pharmacology, protein-protein interaction analysis, GO/KEGG enrichment, and molecular docking were applied to identify active constituents of and their potential targets in immune-related cardiac injury. Combined treatment with nivolumab and ipilimumab markedly increased cardiomyocyte apoptosis and elevated the expression of NLRP3 and ASC. Increased phosphorylation of IKK and NF-B p65 indicated activation of the TLR4-MyD88-NF-B signaling cascade. Knockdown of either TLR4 or NLRP3 significantly mitigated apoptosis and reduced inflammatory protein expression. In vivo, combined ICI therapy led to higher levels of myocardial injury markers and proinflammatory mediators. Network pharmacology analysis identified six major compounds from , with sinomenine showing strong predicted binding to TLR4 (binding energies ranging from -9.6 to -5.7 kcal/mol). These findings demonstrate that under the present experimental conditions, combined nivolumab and ipilimumab treatment was associated with greater activation of the TLR4-MyD88-NF-B-NLRP3 axis and greater cardiomyocyte injury than nivolumab alone. However, because the combination group received a higher total antibody dose, the current study does not distinguish whether this difference reflects increased total drug exposure, additivity, or the specific contribution of CTLA-4 blockade. Bioactive constituents of , particularly sinomenine, may represent potential cardioprotective modulators against ICI-induced cardiac injury. - Source: PubMed
Publication date: 2026/04/23
Gao MengjiaoLiu XinyaWu LiJiang YunYu JianZhang Yuanming