MYD88 Antibody
- Known as:
- MYD88 Antibody
- Catalog number:
- 2127
- Product Quantity:
- 0.5 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- MYD88 Antibody
Related 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
- Triple-negative breast cancer (TNBC) is a specific subtype of breast cancer with limited treatment options and a generally poorer prognosis compared to other subtypes, making the exploration of effective therapeutic strategies for TNBC particularly important. Recorded in the traditional Chinese medicine (TCM) monograph of Qing Dynasty, the classical TCM formula Xihuang Pill (XHP) has been used to treat "mammary rock" (breast cancer). XHP is now widely employed in clinical practice for breast cancer treatment in China. Nonetheless, the efficacy of XHP in treating TNBC and its associated mechanisms remain unclear. - Source: PubMed
Publication date: 2026/05/17
Huang HuimingWang FeiWei XuejiaoQiu XinyuWang ZhuguoGao YufengZhang RuoxinXie WanyingWang XiaoxueSong YuelinTu PengfeiLi JunHu Zhongdong - Beyond their pivotal role in hemostasis and thrombosis, the function of platelets in inflammation and immune regulation is increasingly recognized. 8-oxo-7,8-dihydroguanosine (8-oxo-Guo) is an endogenous nucleic acid oxidation product. Unclear is whether 8-oxo-Guo possesses the capacity to modulate the inflammatory status of circulating blood and platelet function. The present study investigated the influence of 8-oxo-Guo on platelet activation responses. An intravenous injection of 8-oxo-Guo in C57BL/6J mice enhanced platelet activity and increased levels of plasma inflammatory factors. To elucidate the underlying mechanism, human purified platelets were used. The results showed that 8-oxo-Guo treatment increased the expression of Toll-like receptor 2 (TLR2) and TLR4 on platelets. Integrated proteomic and phosphoproteomic analysis, combined with Western blot, demonstrated that 8-oxo-Guo activated multiple inflammation-related signaling pathways, including TLR2/TLR4-MyD88-associated signaling. Surface plasmon resonance analysis further demonstrated direct interactions between 8-oxo-Guo and TLR4/TLR2 with micromolar-range affinities, and pharmacological inhibition of TLR2 or TLR4 attenuated 8-oxo-Guo-induced inflammatory signaling. Consistent results were obtained from both in vivo and in vitro experiments. Our findings suggest that 8-oxo-Guo promotes platelet inflammatory activation at least partly through TLR2/TLR4-associated signaling, thereby expanding our understanding of platelet functions in oxidative stress-related immune regulation and identifying a potential therapeutic target for inflammatory diseases. - Source: PubMed
Publication date: 2026/05/20
Pan Jia-XinLi JinLi RuiSheng GangZeng Lv-TaoGao Xu-FanHuan RanLiu Wen-SongBu Xiao-XiaoWang Quan-ErXi HuanQi Ruo-MeiCai Jian-Ping - Endometriosis is a chronic inflammatory disease characterized by immune microenvironment dysregulation, with the IL-33/ST2L signaling axis playing a crucial role in macrophage polarization and disease progression. Despite growing evidence of IL-33's involvement in endometriosis pathogenesis, the mechanisms underlying IL-33-induced macrophage polarization and the therapeutic potential of a natural immunomodulator luteolin remain incompletely understood. - Source: PubMed
Publication date: 2026/05/21
Wang WeiChen YanranWang WenxinJiang LinhongBai DandanYang YunjunWang HaixiaWang MengyuanSi HaipengLong JunYuan DongpingLi Jin - Sepsis frequently leads to profound neuromuscular dysfunction, in part driven by spinal neuroinflammation. The receptor tyrosine kinase Mer is a key regulator of immune homeostasis, yet its role in sepsis-induced neuromuscular impairment remains unclear. This study investigated the contribution of Mer signaling to spinal neuroinflammation and neuromuscular dysfunction in sepsis. Sepsis was induced in rats using the cecal ligation and puncture (CLP) model. Neuromuscular function was assessed by muscle mass analysis, compound muscle action potential (CMAP) recordings, and nerve conduction studies. Neuronal survival and neuromuscular junction (NMJ) integrity were evaluated histologically. Spinal inflammatory responses and signaling pathways were analyzed by measuring cytokine levels, microglial activation, and expression of TLR4/MyD88/NF-κB and STAT1/SOCS pathway components. To assess therapeutic potential, the Mer ligand Protein S (ProS) was administered intrathecally in both wild-type (WT) and Mer-deficient (Mer) rats. Mer deficiency significantly aggravated sepsis-induced muscle wasting, reduced CMAP amplitude, prolonged latency, impaired motor conduction velocity, increased neuronal loss, and exacerbated NMJ disintegration. These functional impairments were associated with elevated spinal IL-6 and TNF-α levels, enhanced microglia/macrophage activation, upregulated TLR4/MyD88/NF-κB signaling, and suppressed STAT1/SOCS pathway activation. Intrathecal ProS treatment markedly improved neuromuscular performance, attenuated spinal inflammatory responses, and restored neuronal integrity and NMJ structure in both WT and Mer CLP rats. ProS/Mer signaling plays a critical protective role in sepsis-induced neuromuscular dysfunction by suppressing pro-inflammatory pathways and activating anti-inflammatory STAT1/SOCS signaling in the spinal cord. Therapeutic targeting of the ProS/Mer axis may represent a promising strategy for the treatment of sepsis-associated neuromyopathy. - Source: PubMed
Wang ShijieYang YuSun JiaxinYan BinLi TiantianWen LiliZhang HongweiShu JinjunXie Fei - To investigate the characteristics and prognostic factors of primary breast diffuse large B-cell lymphoma (PB-DLBCL) . Clinical data on 60 patients with PB-DLBCL admitted to Ruijin Hospital, affiliated with Shanghai Jiao Tong University School of Medicine, from November 2013 to September 2022, were respectively collected, and survival and prognostic analyses were conducted. Among them, 44 patients underwent targeted sequencing (of 55 lymphoma-related genes) to assess the gene mutation status and its impact on survival outcomes. All 60 patients with PB-DLBCL were female. The median age was 56.5 years (49.0, 61.0). The overall 5-year progression-free survival (PFS) rate was 66.5% (95% : 51.0% -86.7% ), and the 5-year overall survival (OS) rate was 90.6% (95% : 80.5% -100.0% ). After one-line treatment, 96.7% (58 patients) achieved complete remission (CR). The results of univariate analysis showed that elevated LDH (=3.380, 95% : 1.160-9.791, =0.025) and nongerminal center B-cell (non-GCB) type (=3.560, 95% : 1.000-12.700, =0.049) were adverse prognostic factors for PFS in patients with PB-DLBCL, whereas elevated LDH (=6.212, 95% : 1.150-38.941, =0.034) was an adverse prognostic factor for OS. Multivariate analysis did not identify independent adverse prognostic factors for PFS in patients with PB-DLBCL. Targeted sequencing results showed that the mutation frequencies of PIM1, MYD88, KMT2D, CD79B, DTX1, and MPEG1 were >20%. Log-rank test revealed that patients with PIM1 mutations (=27) had a significantly lower 5-year PFS rate compared to those without mutations (=17) [59.8% (95% : 39.7% -90.0% ) 80.7% (95% : 58.3% -100% ), =0.019]. Regarding MPEG1, patients without mutations (=34) exhibited a significantly lower 5-year PFS rate than those with mutations (=10) [59.4% (95% : 41.0% -86.1% ) 100%, =0.048]. For DTX1, patients with mutations (=10) had a significantly lower 5-year OS rate than those without mutations (=34) [48.0% (95% : 18.8% -100% ) 100%, =0.004]. Similarly, patients with MYD88 mutations (=21) showed a significantly lower 5-year OS rate than those without mutations (=23) [75.4% (95% : 52.9% -100% ) 100%, =0.004]. The 5-year OS rate of PB-DLBCL is relatively high, whereas the PFS rate is relatively low. Elevated LDH levels and having the non-GCB type are adverse prognostic factors affecting patient survival. The mutation frequencies of PIM1, MYD88, KMT2D, CD79B, DTX1, and MPEG1 are higher in PB-DLBCL. Patients with mutations in PIM1, MYD88, and DTX1 have a poor prognosis, whereas those with MPEG1 mutations have a favorable prognosis. - Source: PubMed
Zhang H QHe J YChen S YZhang H LWang LXu P PZhao W L