MyD88 Antibody
- Known as:
- MyD88 Antibody
- Catalog number:
- 3244R-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biovis
- 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
- Global anthropogenic climate change is restructuring the thermohygric parameters that govern Aspergillus flavus and Aspergillus parasiticus ecology, expanding the geographic range and contamination intensity of aflatoxin in staple food crops worldwide. Aflatoxin B1, a Group 1 IARC carcinogen and the most potent naturally occurring hepatocarcinogen, undergoes CYP3A4/CYP1A2-mediated bioactivation to the exo-8,9-epoxide, which alkylates N7-guanine residues in DNA, generating AFB1-N7-guanine adducts that produce G → T transversions culminating in the TP53 R249S gain-of-function mutation, a molecular fingerprint of aflatoxin-driven hepatocellular carcinoma. Beyond direct genotoxicity, AFB1 drives mitochondrial dysfunction through oxidative phosphorylation impairment, glutathione depletion, cardiolipin peroxidation, and mitochondrial membrane potential collapse. It activates NF-κB, STAT3, and TGF-β inflammatory signaling; and engages hepatic stellate cells in fibrogenesis culminating in cirrhosis. Critically, AFB1 also disrupts the gut microbiome, depleting butyrateproducing Ruminococcaceae, Faecalibacterium prausnitzii, and Akkermansia muciniphila while expanding pro-inflammatory Proteobacteria and Enterobacteriaceae. These dysbiotic changes compromise tight junction integrity, increase intestinal permeability, elevate portal LPS, and activate hepatic TLR4/MyD88/NF-κB and NLRP3 inflammasome cascades that amplify the carcinogenic consequences of direct AFB1 genotoxicity. This review integrates mechanistic evidence from molecular toxicology, microbiome biology, immunometabolism, and systems oncology to establish a unified framework positioning gut dysbiosis as a modifiable intermediate pathway in climate-sensitive aflatoxin-driven carcinogenesis. - Source: PubMed
Publication date: 2026/09/28
Oyedokun Precious AdeoyeOwolabi Victor PelumiOyedokun Marvelous DasolaNdako James AjigasokoaAdegbola Peter IfeoluwaOyedokun Nicodemus Adeyemi - Spinal cord injury (SCI) causes persistent neurological deficits that extend beyond motor impairment, with sensory dysfunction and neuropathic pain substantially compromising quality of life. Stem cell-derived exosomes have emerged as promising cell-free therapeutic agents because they deliver diverse bioactive molecules, including proteins, microRNAs, and long non-coding RNAs, while retaining many of the paracrine benefits of stem cells. This review summarizes recent advances in the application of stem cell-derived exosomes for sensory restoration and neuropathic pain relief after SCI, with particular emphasis on their underlying mechanisms and emerging delivery strategies. We first discuss exosome biogenesis, molecular composition, intercellular communication, and engineering approaches. We then summarize their established roles in motor recovery through neuroprotection, immunomodulation, axonal regeneration and myelin repair. Importantly, we highlight emerging evidence that stem cell-derived exosomes may restore sensory function by promoting axonal regeneration, synaptic remodeling, neural differentiation, and glial metabolic reprogramming. In parallel, exosomes alleviate neuropathic pain by suppressing microglial and astrocytic activation, modulating TLR/MyD88/NF-κB signaling, reducing neuroinflammation and pathological nociceptive signaling, and promoting remyelination and tissue repair. Exosomes also preserve blood-spinal cord barrier integrity through regulation of endothelial cells, pericytes, matrix metalloproteinases, and vascular signaling, for both motor and sensory recovery. Finally, we discuss challenges related to exosome heterogeneity, manufacturing standardization, delivery, safety, and limited sensory-specific evidence, and highlight engineering and biomaterial-based strategies for future clinical translation. Overall, stem cell-derived exosomes represent a multifunctional therapeutic platform with potential to move SCI treatment beyond motor recovery toward comprehensive sensory restoration and pain management. - Source: PubMed
Publication date: 2026/09/26
Mithu Md MiftahulSahiduzzaman Roy Shirsendu NarayanMathew John JacobHaraveer Devunipalli KarthikThongbam BasundhariKumar Kancharllapalli PrasannaDey SourovArifuzzaman Md - Sepsis-induced endothelial dysfunction contributes to systemic inflammation and multiple organ injury. Non-muscle myosin heavy chain IIA (NMMHC IIA) has emerged as a potential therapeutic target for sepsis. However, effective interventions remain limited. This study investigated whether ruscogenin (RUS) alleviates sepsis-induced multiple organ injury by regulating NMMHC IIA. Sepsis was induced in mice via cecal ligation and puncture. Endothelium-specific NMMHC IIA-knockdown (MYH9) mice were created using the Cre-loxP system. Histopathology, Western blotting, immunofluorescence, Evans blue (EB) leakage, enzyme-linked immunosorbent assay, and biochemical assays were performed to evaluate organ injury, inflammation, and vascular permeability. An in vitro lipopolysaccharide (LPS)-induced endothelial injury model was established in human umbilical vein endothelial cells, and endothelial integrity was evaluated using transendothelial electrical resistance and EB-albumin permeability assays. NMMHC IIA expression markedly increased in multiple organs during sepsis. MYH9 alleviated sepsis-induced multiple organ injury, including lung, intestine, liver, and kidney damage. RUS markedly improved survival, reduced vascular hyperpermeability, and alleviated inflammatory and organ injury responses in septic mice and LPS-stimulated endothelial cells, which was associated with TLR4/MyD88/NF-κB signaling pathway suppression. However, RUS provided no additional benefit after NMMHC IIA silencing, supporting an endothelial NMMHC IIA-dependent mechanism. Endothelial NMMHC IIA is a key mediator of sepsis-induced multiple organ injury. RUS exerts protective effects against sepsis by targeting NMMHC IIA. These findings provide new insights into the treatment of sepsis-associated multiple organ injuries and warrant further investigation for potential clinical applications. - Source: PubMed
Publication date: 2026/09/26
Tang JiahuiChen HaiyuXu MengchenZhang ShengpengYu BoyangGong ShuaishuaiZhang YuanyuanKou Junping - Musk has traditionally been used for cardiovascular disorders, but its active constituents and mechanisms of action in acute myocardial infarction (AMI) remain unclear. - Source: PubMed
Lu FengWang QinyuWang DanDuan HuxinyueHe YacongWu Chunjie - The concurrent presence of acute myeloid leukemia (AML) and a Waldenström macroglobulinemia (WM)-related compartment within the same bone marrow is uncommon. Conventional diagnostics can establish coexistence but cannot completely resolve the cellular architecture and shared immune context of collision marrows. - Source: PubMed
Publication date: 2026/09/11
Cao XinLu WeiHuang Hongming