MYD88
- Known as:
- MYD88
- Catalog number:
- Y213421
- Product Quantity:
- 200ul
- 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
- The fifth edition of the World Health Organization (WHO) classification defines cold agglutinin disease (CAD) as a clonal B-cell lymphoproliferative disorder occurring in the absence of overt lymphoma, whereas cases associated with lymphoma are classified as cold agglutinin syndrome (CAS). However, whether this distinction fully reflects the biological spectrum of cold agglutinin-associated disorders remains uncertain. - Source: PubMed
Publication date: 2026/06/17
Sato YukiKoyama DaisukeYamada ShokiSuzuki KengoFukatsu MasahikoOka YukaHashimoto YukoIkezoe Takayuki - STING bridges innate and adaptive immunity to exert potent antitumor effects, and its agonists play emerging roles in combination therapies with tyrosine kinase inhibitors (TKIs). However, the interaction between STING and receptor tyrosine kinases (RTKs) remains incompletely understood. Here, we identify VEGFR2 as a negative regulator of cGAMP-STING signaling. Upon cGAMP stimulation, both STING and VEGFR2 are activated. Activated VEGFR2 recruits and activates AKT1 to attenuate STING activation. Conversely, STING suppresses VEGFR2 phosphorylation, establishing a reciprocal inhibitory feedback loop. A cell-based screen reveals that the VEGFR2 inhibitor Ki8751 not only relieves VEGFR2-AKT1-mediated suppression but also activates MyD88-dependent NF-κB signaling to further amplify STING responses. Additionally, we show that Ki8751 synergizes with cGAMP to elicit robust, STING-dependent antitumor immunity in vivo. Our findings identify the VEGFR2-STING regulatory axis and provide a mechanistic rationale for co-targeting VEGFR2 and STING to improve cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/18
Han FangpingSun PengboWei YuanyuanHan JingWang YiKuai RuiZhang Conggang - Acute respiratory distress syndrome (ARDS) is characterized by robust inflammation in the lungs and systemic circulation. In this context, the Toll-like receptor (TLR) signaling pathway plays a major role, driving inflammation that promotes host defense but also causing pathological tissue damage. To limit excessive inflammation, TLR signaling must be tightly controlled. One mechanism that modulates TLR signaling is alternative splicing of TLR pathway pre-mRNAs, which balances production of positively acting inflammatory mediators with alternative splice forms that terminate inflammation. To determine whether altered TLR pathway splicing contributes to pathological inflammation in ARDS, we evaluated two central mediators of the TLR signaling pathway, the MyD88 signaling adapter and the IRAK1 signaling kinase, in leukocytes isolated from bronchoalveolar lavage (BAL) of ARDS patients. We found that gene expression was decreased in BAL immune cells while gene expression was increased. In parallel, we monitored long pro-inflammatory (MyD88-L and IRAK1) and shorter anti-inflammatory (MyD88-S and IRAK1c) splice forms and determined that IRAK1 splicing was shifted in a pro-inflammatory direction in ARDS patients. Lastly, we evaluated relationships between MyD88 isoform levels in BAL leukocytes and clinical outcomes. We conclude that pre-mRNA splicing of TLR pathway genes is altered in lung immune cells in patients with ARDS, that monitoring splicing of these genes may provide important prognostic information, and that manipulating splicing of these genes may be a useful novel therapeutic approach that needs further investigation. - Source: PubMed
Publication date: 2026/06/18
Janssen William JLapinig MatthewWynn ElizabethAguilar MartinMould Kara JHume Patrick SMcClendon JazalleLee Frank Fang-YaoMoore Camille MAlper Scott - Primary central nervous system large B-cell lymphoma (PCNS-LBCL) exhibits the worst prognosis among all extranodal LBCLs, with the enriched genetic mutations in MyD88, CD79B and PIM1. However, the upfront incorporation of targeted therapies remains an unmet need in newly diagnosed (ND) patients. In this study, we found that in the presence of MyD88 context, B-cell receptor downstream bruton's tyrosine kinase (BTK) was significantly overexpressed, which subsequently enhanced the stability of PIM1 oncoprotein. To evaluate the intracranial delivery of BTK inhibitor(BTKi), patient-derived PCNS-LBCL xenografted mice models were treated with highly-selective BTKi orelabrutinib, either monotherapeutically or in combining with methotrexate. Interestingly, orelabrutinib showed excellent efficiency crossing BBB with the functional BTK blockade and promoted PIM1 degradation, providing the molecular basis of incorporating BTKi into PCNS-LBCL therapy. Thus, we determined the efficacy and toxicity of orelabrutinib in combination with high-dose methotrexate in a prospective dose-escalating cohort and real-world practice. The patients being treated with orelabrutinib-included ORMD regimen showed better response and more prolonged survival compared to those with RMD regimen. We further investigated the genetic mutations of PCNS-LBCL across tumor tissue, cerebrospinal fluid (CSF) and plasma. The mutations in CSF circulating tumor DNA (ctDNA) rather than plasma-ctDNA were more consistent to those in tumor tissue, indicating that CSF-ctDNA is a useful tool for monitoring PCNS-LBCL. In summary, our data provided the molecular rationale as well as clinical evidences that incorporation of BTKi into frontline induction therapy is a promising strategy for ND PCNS-LBCL. - Source: PubMed
Publication date: 2026/06/17
Yuan YanDai BoZhong HaoshuZheng JiajunFan ZhenChen DiWang QianWu HaoLi YuanZhu PingDing TianlingWang ShuWu KunpengZhang YuWang ZhenhuaFeng RuiZhu FengpingZheng KangQin ZhiyongYang BojieChen HongLin XiaoleiYao YuZhuang DongxiaoShi ZhifengMao YingChen Tong - Opioid-induced delirium represents a major clinical challenge with substantial implications for patient safety and outcomes. An integrated evaluation combining pharmacovigilance and genetic evidence remains limited. This study aimed to systematically assess delirium risk across different opioids and to elucidate underlying molecular mechanisms by integrating real-world safety data with Mendelian randomization (MR) analysis. - Source: PubMed
Chen XuetaiLiu YutingZhu MingxuanChen XingmanLiu FengyunJin JiahaoJiang ZhiguoQian BinLi Feng