Myd88
- Known as:
- Myd88
- Catalog number:
- 000371A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Myd88
Related genes to: Myd88
- 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
*Please allow 3-5 days for delivery time.* In mammals, TIR domain adapters, including Myd88, TIRAP, TICAM-1 (also called TRIF), and TRAM, act in Toll-like receptor (TLR) signaling pathway. The last meAdaptor protein Wyatt,Homo sapiens,Human,MAL,MyD88 adapter-like protein,TIR domain-containing adapter protein,TIRAP,Toll_interleukin-1 receptor domain-containing adapter proteinAdaptor protein Wyatt,Mal,Mouse,Mus musculus,MyD88 adapter-like protein,TIR domain-containing adapter protein,Tirap,Toll_interleukin-1 receptor domain-containing adapter proteinAnti-Human MyD88 Purified 10 ugAnti-Human MyD88 Purified 50 ugAnti-Human_Mouse MyD88 Purified 10 ugAnti-Human_Mouse MyD88 Purified 50 uganti-MYD88anti-MYD88anti-MYD88anti-MYD88anti-MYD88anti-MYD88anti-MYD88anti-MYD88 Related articles to: Myd88
- Metabolic dysfunction-associated steatotic liver disease (MASLD) and its inflammatory-fibrotic phenotype (MASH) exhibit pronounced immunometabolic coupling. This review synthesizes evidence along the gut-liver axis, from epithelial tight-junction and gut vascular barrier (GVB) failure to TLR4-MyD88/TRIF-NF-κB amplification and NLRP3 inflammasome activation and outlines the logic of the gut-derived exposure spectrum-lipopolysaccharide (LPS), endogenous ethanol, bile acids (BAs), short-chain fatty acids (SCFAs), and trimethylamine N-oxide (TMAO). We position BA-FXR/TGR5, SCFAs-GPR41/43, and AMPK/Nrf2 as upstream/downstream modulators that reset inflammatory thresholds and confer stage-dependent druggability. Based on node-to-pathway mapping, we summarize mechanisms and translational signals for berberine (BBR), Qushihuayu (QSHY), Da-Chai-Hu Decoction (DCHD), and polysaccharides (e.g., Astragalus, Ganoderma), emphasizing pharmacokinetic and site-of-exposure constraints that support "gut-first" actions. We propose a minimal companion biomarker set-LBP/sCD14, BA profiles with FGF19-C4 dynamics, and IL-1β/GSDMD-N-paired with hierarchical imaging gates (≥30% relative MRI-PDFF decline; MRE/ELF) to underpin response typing and go/no-go decisions. Finally, we highlight critical gaps (direct human GVB readouts; longitudinal multi-omics bridged to clinical outcomes) and outline a biomarker-driven multi-arm multi-stage (MAMS) pathway for adaptive, stratified development of multi-target traditional medicine interventions in MASLD/MASH. - Source: PubMed
Publication date: 2026/04/17
Ren LianjieHe QinHu ZhuyuanJin JinjinTao Feibao - This study investigated the effects of chronic heat stress (HS) on brain injury in broilers and the associated molecular changes. A chronic HS model was established by exposing broilers to 35 °C from 08:00 to 20:00 daily from 21 to 42 days of age, and samples were collected at 28, 35, and 42 days of age. Chronic HS significantly impaired growth performance and was associated with histopathological and ultrastructural alterations in brain tissue. Serum antioxidant enzyme activities and the total antioxidant capacity were significantly reduced, whereas malondialdehyde levels were significantly increased, indicating sustained oxidative stress (OS). Blood-brain barrier (BBB) permeability, assessed by Evans blue extravasation, was significantly higher in HS birds and was accompanied by reduced mRNA expression of the tight junction-related genes ZO-1 and Claudin-5. In addition, chronic HS was associated with increased mRNA expression in genes related to cellular stress, oxidative stress, and inflammation, including key components of the TLR4/MyD88/NF-κB/NLRP3 pathway, as well as decreased expression of IL-4. These findings suggest that chronic HS is associated with enhanced OS, altered neuroinflammatory gene expression, and BBB impairment in the broiler brain. Overall, this study provides evidence that chronic HS is associated with brain injury in broilers and highlights a potential link among OS, inflammation-related transcriptional changes, and BBB dysfunction, thereby offering a basis for further mechanistic and interventional studies. - Source: PubMed
Publication date: 2026/04/20
Feng SiliangZhou ChenyangTie YajinZhao ZhanqinLi MengyunSi Lifang - Weaning stress is frequently associated with intestinal oxidative stress, inflammatory activation, and epithelial apoptosis in piglets. This study investigated whether dietary supplementation with Chinese yam ( L., YAM) alleviates weaning-induced intestinal injury by modulating the oxidative stress-inflammation-apoptosis axis. 48 weaned piglets were assigned to a control diet or diets supplemented with low (1%)/high (2%) doses of YAM. Intestinal morphology, antioxidant capacity, inflammatory signaling, and apoptosis-related markers were assessed, and jejunal transcriptomic profiling was also performed. Supplementing with YAM improved villus architecture and enhanced intestinal antioxidant properties, manifested as increased total antioxidant capacity and reduced malondialdehyde levels. At the molecular level, YAM activated the Keap-1/Nrf2/HO-1 pathway and upregulated the expression of antioxidant-related genes, including superoxide dismutase 2 (SOD2), catalase (CAT), and NAD(P)H quinone dehydrogenase 1 (NQO1), and suppressed NF-κB signaling by reducing Myd88 and p-p65 protein levels. In addition, YAM modulated mitochondrial apoptosis by upregulating Bcl-2 and reducing the expression of Bax and Cleaved caspase-3. Transcriptomic analysis identified 1227 differentially expressed genes between the control and high-dose groups (784 upregulated and 443 downregulated). Mechanism-oriented module analysis further confirmed coordinated enhancement of antioxidant pathways alongside suppression of inflammatory and apoptotic gene signatures. These findings demonstrate that dietary YAM supplementation attenuates weaning-associated intestinal injury by rebalancing oxidative stress, inflammatory signaling, and apoptosis-related pathways, thereby supporting its potential application as a functional feed additive in swine production. - Source: PubMed
Publication date: 2026/04/08
Shi XiongweiGe ShaoguangWang HaiminChen XiaowangPan XiangyiLiu ChenQiu ZhengyingZou WenshuCao HaoLiu YujiaBai QiyuXin Ruihua - Activating PIK3CA mutations occur in approximately 40% of hormone receptor-positive (HR+)/HER2-negative breast cancers and represent a major driver of endocrine resistance. The PI3Kα-selective inhibitor alpelisib, in combination with fulvestrant, significantly improves progression-free survival in patients with PIK3CA-mutant disease, as demonstrated in the SOLAR-1 trial. However, this therapeutic strategy is frequently complicated by treatment-induced hyperglycemia, a metabolic disturbance that promotes oxidative stress, mitochondrial dysfunction, and inflammatory signaling, thereby increasing cardiovascular vulnerability. Sodium-glucose cotransporter-2 (SGLT2) inhibitors have emerged as cardiometabolic modulators with benefits extending beyond glucose lowering. In this study, we used a human cardiomyocyte in vitro model designed to recapitulate the hyperglycemic metabolic milieu observed in breast cancer patients receiving PI3Kα-targeted therapy, to investigate whether the SGLT2 inhibitor dapagliflozin directly protects cardiomyocytes from alpelisib- and fulvestrant-induced injury. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were cultured under hyperglycemic conditions (25 mM glucose) to mimic the metabolic environment associated with PI3Kα inhibitor-induced dysglycemia. Cells were exposed to alpelisib (100 nM) and fulvestrant (100 nM), alone or in combination, in the absence or presence of dapagliflozin (1 μM). Cardiomyocyte viability was assessed using the MTS assay, mitochondrial function by TMRM-based mitochondrial membrane potential (ΔΨm) measurements, and apoptosis by caspase-3 quantification. Cardiomyocyte injury was evaluated by release of cardiac troponin I and heart-type fatty acid binding protein (H-FABP). Lipid peroxidation markers (MDA and 4-HNE) were measured to assess oxidative membrane damage. Intracellular inflammasome-related signaling (NLRP3 and MyD88) and secreted inflammatory mediators (IL-1β, IL-18, IL-6, TNF-α, and CCL2) were quantified by ELISA. Exposure to alpelisib, particularly in combination with fulvestrant, significantly reduced cardiomyocyte viability, induced mitochondrial depolarization, and increased caspase-3-mediated apoptotic signaling. These alterations were accompanied by elevated lipid peroxidation (MDA and 4-HNE) and increased release of cardiac injury biomarkers (troponin I and H-FABP). Alpelisib-based treatments also activated inflammasome-related signaling, as indicated by increased intracellular NLRP3 and MyD88 levels and enhanced secretion of pro-inflammatory mediators (IL-1β, IL-18, IL-6, TNF-α, and CCL2). Co-treatment with dapagliflozin significantly attenuated these alterations, preserving mitochondrial membrane potential, reducing apoptotic signaling, limiting oxidative membrane damage, and suppressing inflammatory cytokine release. This study provides evidence that alpelisib-based therapy under hyperglycemic conditions is associated with oxidative, mitochondrial, and inflammatory stress responses in human cardiomyocytes, recapitulating key features of cardiometabolic stress relevant to PI3Kα-targeted therapy. Importantly, dapagliflozin markedly attenuated these alterations, supporting a potential cardioprotective role that may extend beyond glycemic control. These findings provide a mechanistic rationale for further investigation of SGLT2 inhibition as a cardiometabolic protective strategy in patients receiving PI3Kα inhibitor-based cancer therapy. - Source: PubMed
Publication date: 2026/04/17
Quagliariello VincenzoBerretta MassimilianoBarbato MatteoMaurea FabrizioCanale Maria LauraPaccone AndreaBisceglia IrmaTedeschi AndreaScherillo MarinoSantagata JacopoOliva StefanoDessalvi Christian CadedduForte PietroD'Ambrosio CristianaMatola Tiziana DiParmentola ReginaGabrielli DomenicoMaurea Nicola - 5-Fluorouracil (5-FU) is a first-line chemotherapeutic agent for solid tumors, but its clinical application is severely limited by dose-dependent intestinal injury that impairs patient quality of life and compromises therapeutic efficacy. Natural polysaccharides, especially marine-derived ones, have become safe and multi-targeted gut-protective candidates due to their excellent biocompatibility and prebiotic-like activities. swim bladder is a characteristic marine biological resource, and its polysaccharides (CIPs) have shown potential bioactivities, yet their protective mechanism against 5-FU-induced intestinal injury remains unclear. Our study explored the protective effects of swim bladder polysaccharides (CIPs) against 5-FU-induced intestinal injury in mice. Following 14-day preventive administration, CIPs alleviated 5-FU-induced body weight loss, diarrhea, colonic shortening, and mucosal injury, and restored goblet cell function. Mechanistically, CIPs enhanced intestinal barrier integrity by upregulating ZO-1, Occludin, and MUC2, suppressed the MyD88/NF-κB pathway to balance inflammatory cytokines, and ameliorated oxidative stress by regulating MDA, GSH, SOD, and CAT. CIPs also restored gut microbial diversity and the Firmicutes/Bacteroidota ratio, and modulated retinol and arginine metabolism. In vitro, CIPs reduced inflammation and oxidative damage in Caco-2 cells and promoted M2 macrophage polarization. Thus, CIPs alleviate 5-FU-induced intestinal injury via multi-targeted regulation of the gut-metabolic axis, showing great potential as a dietary intervention and gut health support agent in food science and oncology nutrition, and boosting the high-value utilization of marine resources. - Source: PubMed
Publication date: 2026/04/19
Zhao ShouhaoZhao RuixueSui DonglinLi YixuanLi HuanLi ShugangAi ChunqingBai XuetingSha YilinYan JingxianWang WudengRen Xiaomeng