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
- Current therapies for diabetic kidney disease (DKD) slow progression but fail to halt irreversible renal fibrosis, largely because early pathogenic drivers are overlooked. While endothelial glycocalyx disruption is recognized as an initiator of albuminuria, existing literature lacks a unified model connecting this initial barrier loss to the full fibrotic cascade. This review systematically integrates the molecular networks driving glycocalyx degradation, specifically detailing the synergistic interplay among oxidative stress, sheddase activation, and the AGEs/RAGE/NF-κB axis. Unlike previous reviews, we explicitly map how the shedding of core components-such as Syndecans and Glypicans-triggers downstream leukocyte adhesion via the intracellular MyD88/NF-κB pathway, actively propagating renal inflammation and exacerbating the progression of renal fibrosis. By redefining glycocalyx damage as a critical pathological amplifier that actively drives glomerular filtration barrier disruption and subsequent inflammatory and fibrotic cascades, rather than a passive structural consequence of hyperglycemia, we expose critical gaps in standard DKD management. We further critically evaluate the clinical viability of emerging glycocalyx-targeted strategies, highlighting specific applications for early diagnostic biomarkers and addressing current challenges in targeted drug delivery, ultimately providing a precise roadmap for preventing DKD progression. - Source: PubMed
Publication date: 2026/10/07
Li MeixuanSun GuiboWang Min - Tumor necrosis factor receptor-associated factors (TRAFs) are key signaling proteins involved in cellular innate immune pathways. However, knowledge of TRAF genes in echinoderms remains limited. We cloned a novel TRAF gene (SiTRAF) from the sea urchin Strongylocentrotus intermedius. The full-length open reading frame of SiTRAF was 1,731 bp, encoding 576 amino acids. Domain prediction analysis showed that SiTRAF possessed domains conserved in the TRAF protein family. Phylogenetic analysis revealed that SiTRAF clustered with TRAF proteins from S. purpuratus, forming a relatively independent evolutionary branch within the echinoderm TRAF homologs. SiTRAF mRNA was detected in all tested sea urchin tissues, with the highest expression level in the intestine. Transcriptional expression of SiTRAF was significantly induced following stimulation with lipopolysaccharide and polyinosinic-polycytidylic acid. Additionally, RNA interference targeting SiTRAF suppressed the expression of IRFs, Rel, IL-17, and several strongylocin genes following lipopolysaccharide stimulation. Co-immunoprecipitation assays indicated a physical protein association between SiTRAF and SiMyD88, a key adaptor of the Toll-like receptor signaling pathway. Dual-luciferase reporter gene assays indicated that SiTRAF overexpression significantly inhibited the activity of a series of immune-related reporter genes and dose-dependently suppressed the SiMyD88-mediated activation of IL-6, AP-1, and NF-κB. Additionally, SiTRAF regulated the phosphorylation levels of MAPKs, such as P38, JNK, and Erk1/2. These findings suggest that SiTRAF participates in the innate immune regulatory processes of sea urchins. This study provides new insights into TRAF-mediated immune signaling in invertebrates and lays a theoretical foundation for the future selective breeding of disease-resistant sea urchin strains. - Source: PubMed
Publication date: 2026/10/07
Liu FengchenLiu TongChu XiaolongLiu ChenZhao KaixinZhang XuekaiHan YijingLiu YaqiongThiyagarajan VengatesenHuang BaoyuWang Xiaotong - ObjectiveAtopic dermatitis (AD) involves complex immune dysregulation, with the IL-18 BP/IL-18 axis emerging as a critical yet underexplored regulator of pathological inflammation. While α-boswellic acid (α-BA) has shown therapeutic promise in AD, its role in regulating the IL-18 BP/IL-18 axis under the inflammatory microenvironment is unclear. This study aimed to elucidate whether α-BA could restore IL-18 BP/IL-18 homeostasis and thus suppress inflammation while preserving immune defense.MethodsA two-sample Mendelian randomization (MR) analysis using summary-level genome-wide association data was conducted to evaluate the potential causal contribution of circulating IL-18 levels to AD susceptibility. DNFB-induced AD mouse model and TNF-α/IFN-γ-stimulated HaCaT cells were used to evaluate α-BA's effects on barrier function, cytokine profiles, and IL-18 BP/IL-18 axis modulation. RNA sequencing (RNA-seq) was employed to identify the critical mediator of α-BA.ResultsMR analysis showed a statistically significant but modest association between genetically predicted circulating IL-18 levels and AD risk (OR=1.003, <0.05). α-BA restored epidermal barrier integrity in AD mice and normalized serum IgE and IL-13 levels. In HaCaT cells, α-BA treatment rebalanced the IL-18 BP/IL-18 axis and reduced pro-inflammatory cytokines. In addition, α-BA inhibited MyD88/NF-κB signaling, whereas blocking the IL-18 BP/IL-18 axis abolished this effect. RNA-seq identified metalloendopeptidase (MME) as a candidate molecule associated with α-BA treatment, and pharmacological inhibition of MME attenuated the effects of α-BA on the IL-18 BP/IL-18 axis.Conclusionsα-BA may alleviate AD by modulating the IL-18 BP/IL-18 axis and downstream MyD88/NF-κB signaling pathways. MME may contribute to α-BA-mediated regulation of the IL-18 BP/IL-18 axis. - Source: PubMed
Publication date: 2026/10/07
Pan JianliWang LuhaoJing RongrongChen ZhichaoZhou YinlingWang Lusheng - Innate immune receptors are central to host resistance against Trypanosoma cruzi infection, yet how parasite genetic diversity is associated with these responses remains poorly understood. Here, we characterized acute infection outcomes and myocardial innate immune transcriptional profiles in mice subjected to single and mixed infections with genetically distinct T. cruzi parasites (DTUs TcII, TcIII, and TcVI). Swiss mice were infected with RN2, RN23, Y, or CL-Brener individually or in combination, and parasitemia, survival, and cardiac gene expression were assessed. The Y strain, CL-Brener clone, and RN2 + RN23 + CL-Brener condition exhibited a high-severity profile, with marked parasitemia (8000-28,000 trypomastigotes/5 μL), mortality of 74%-100%, reduced myocardial transcription of Tlr2, Tlr4, Tlr9, Trif, and Myd88, and increased transcription of Nlrp3, Casp1, Il1β, and Tnfα. In contrast, RN2 and RN23 single infections exhibited low-severity profiles and higher transcription of innate immune mediators associated with parasite control. Mixed-infection groups displayed transcriptional and infection profiles differing from the corresponding single-infection groups under a standardized total inoculum. Together, these findings identify distinct myocardial innate immune transcriptional profiles across single and mixed T. cruzi infection conditions and support further investigation of the contributions of parasite population composition and dose to acute infection outcomes. - Source: PubMed
Sampaio George Harisson FelintoBarbosa-Silva Andressa Noronhado Nascimento Brito Carlos RamonBatista Lucas Abrantesde Negreiros Christiane Carlos Araújode Medeiros Brito Ramayana MoraisMartins Rand RandallNascimento Manuela Sales Limada Câmara Antonia Claudia Jácomeda Matta Guedes Paulo Marcosda Cunha Galvão Lúcia Maria - Cisplatin-induced acute kidney injury (Cis-AKI) is a common and severe dose-limiting complication of cisplatin-based chemotherapy, and effective preventive or therapeutic strategies remain limited. Pterostilbene (PTE), a naturally occurring polyphenolic compound, exhibits potent anti-inflammatory and antioxidant properties; however, its protective effects and underlying mechanisms in Cis-AKI are not fully understood. In this study, we investigated the renoprotective effects of PTE in cisplatin-induced injury using HK-2 cells and a mouse model of Cis-AKI. In vitro, PTE significantly alleviated cisplatin-induced cytotoxicity, improved cell viability, and attenuated tubular epithelial cell injury. In addition, PTE reduced oxidative stress, suppressed pro-inflammatory cytokine production, and inhibited apoptosis in cisplatin-treated HK-2 cells. In vivo, PTE improved renal function, alleviated tubular histopathological injury, and preserved renal tubular mitochondrial ultrastructure in cisplatin-treated mice. Exploratory transcriptomic screening highlighted TLR4/NF-κB-related signaling as a candidate pathway for further validation. Mechanistically, PTE inhibited TLR4/MyD88/NF-κB activation, whereas both pharmacological activation of TLR4 with Kdo2-Lipid A (KLA) and genetic restoration of TLR4 expression partially reversed the protective effects of PTE against cisplatin-induced inflammation, oxidative stress, apoptosis, and tubular epithelial damage. Collectively, these findings indicate that PTE protects against Cis-AKI, at least in part, through suppression of the TLR4/MyD88/NF-κB signaling cascade, thereby mitigating inflammation, oxidative stress, and apoptosis. These results suggest that PTE represents a promising therapeutic candidate for the prevention and treatment of Cis-AKI. - Source: PubMed
Publication date: 2026/10/06
Shen HaoyuWang ZhishuoZhang ChengSong ZongmianHeng ChongShi PeipeiZhang JianjiangHan Hao