MYD88 Polyclonal Antibody100 ug
- Known as:
- MYD88 Polyclonal Antibody100 ug
- Catalog number:
- 3244-100
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- MYD88 Polyclonal Antibody100
Related genes to: MYD88 Polyclonal Antibody100 ug
- 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 Polyclonal Antibody100 ug
Related articles to: MYD88 Polyclonal Antibody100 ug
- Polyneuropathy due to antibodies to myelin-associated glycoprotein (MAG) is a rare disease with an estimated prevalence of 1 per 100,000. Symptoms start in the sixth or seventh decade of life, presenting sensory polyneuropathy with sensory ataxia, paresthesia, mild motor deficit, and tremor of upper extremities. The neurophysiological features are compatible with length-dependent demyelination. It is caused by monoclonal gammopathy of the IgM type produced by clonal B cells. In recent years the monoclonal anti-CD20 antibody has become the preferred first-line treatment, but with limited efficacy. We identified a cohort of 42 patients diagnosed with anti-MAG polyneuropathy. Clinical data were collected retrospectively, and flow cytometry files and immune histochemistry slides were reassessed. We report that in most cases of anti-MAG polyneuropathy, the monoclonal IgM is kappa-restricted, the B-cell population shows lymphoplasmacytic differentiation, MYD88 mutation is a frequent finding, and the clonal B-cell population includes plasma cells. These findings most likely explain the low efficacy of rituximab monotherapy. We found the burden of symptoms to be high among patients with anti-MAG polyneuropathy as most of our patients had received intravenous immunoglobulin infusions and/or B-cell-directed treatment. We suggest that future treatment protocols for anti-MAG polyneuropathy should incorporate plasma cell-directed drugs. Furthermore, we found complement receptor 1 (CD35) to be down regulated on clonal B lymphocytes but not on normal B lymphocytes in these patients. We suggest that this may be a common feature of clonal B lymphocytes in chronic lymphoproliferative diseases. - Source: PubMed
Tjønnfjord Geir ErlandOsnes Liv Toril NSpetalen SigneHaave UllaPopperud Trine HManiaol Angelina HØstlie IngunnBajelan LiviaHamnvik Lars Henrik DMarvyin KristoMiskovic DraganaTjønnfjord Eirik BWinje KristofferMoksnes MagnusTvedt Tor Henrik AKvam Ann KristinMalecka Agnieszka - Neuroinflammation is a central pathological process in cerebral ischemia/reperfusion injury. Electroacupuncture has demonstrated neuroprotective potential in ischemic stroke; however, whether electroacupuncture engages a defined central cholinergic anti-inflammatory reflex to regulate microglial phenotype remains unknown. - Source: PubMed
Publication date: 2026/07/03
Niu Jing-YuanLuo XinLi Xian-DongZhang JianWu QiongPei Yi-FengWang Jia-QiZhao Qian-KunWang YueZhang GongChen Hui-Sheng - Exertional heat stroke (EHS) is a life‑threatening condition characterized by hyperthermia, systemic inflammation and central nervous system injury, particularly in desert dry‑heat environments. Excessive activation of inflammatory signaling pathways, notably the Toll‑like receptor (TLR)4/myeloid differentiation factor 88 (MyD88)/NF‑κB axis, critically contributes to brain damage and neuroendocrine dysfunction in EHS. Curcumin exhibits anti‑inflammatory and neuroprotective effects; however, poor bioavailability limits its clinical application. Notably, nanocrystal formulations may improve the therapeutic efficacy of curcumin. In the present study, network pharmacology and molecular docking were employed to identify the potential therapeutic targets of curcumin in EHS. A rat model of desert dry‑heat‑induced EHS was established and nanocurcumin was administered intravenously following heat exposure. Histopathological examination, ELISA analyses of neuroendocrine hormones and inflammatory cytokines, serum biochemical assays and western blotting were subsequently performed. These evaluations assessed brain injury, hypothalamic‑pituitary‑adrenal and hypothalamic‑pituitary‑thyroid axes functions, systemic inflammation, peripheral organ injury indicators and activation of the TLR4/MyD88/NF‑κB signaling pathway. Network analysis revealed 138 overlapping target genes between curcumin and EHS, identifying AKT1, TNF, EGFR, BCL2, STAT3, SRC and NFKB1 as key hub genes. Kyoto Encyclopedia of Genes and Genomes pathway analysis highlighted enrichment of the 'Toll‑like receptor signaling pathway' and 'NF‑κB signaling pathway'. Molecular docking indicated favorable binding affinities of curcumin to essential inflammatory proteins, including TLR4, MyD88 and NFKB1. In vivo experiments demonstrated that nanocurcumin reduced neuronal injury in the cerebral cortex and hypothalamus of rats. Furthermore, nanocurcumin significantly decreased serum concentrations of corticotropin‑releasing hormone, corticosterone, thyrotropin‑releasing hormone and thyroid‑stimulating hormone, and restored adrenocorticotropic hormone, total triiodothyronine and free triiodothyronine levels. Nanocurcumin also lowered serum TNF‑α, IL‑6 and IL‑1β levels, and improved biochemical markers of liver, kidney and tissue injury (alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, creatine kinase and lactate dehydrogenase). Within the 4‑h observation period, medium and high doses of nanocurcumin did not worsen biochemical markers compared with those in the EHS or saline groups. Additionally, nanocurcumin administration dose‑dependently inhibited TLR4, MyD88 and NF‑κB protein expression in brain tissues. In conclusion, nanocurcumin may alleviate brain injury, neuroendocrine dysfunction and systemic inflammation associated with desert dry‑heat‑induced EHS, and may improve biochemical indicators of peripheral organ damage; these effects likely involve suppression of the TLR4/MyD88/NF‑κB signaling pathway. These findings support the use of nanocurcumin as a promising adjunctive therapy for managing EHS. - Source: PubMed
Publication date: 2026/07/03
Su LisongQu JinquanLi JiajiaShi WenhuiSong LaiyangLiang FeixingLiu Jiangwei - Bone marrow metastasis from hormone receptor-positive breast cancer can be challenging to detect, especially in patients with concurrent hematologic malignancies, where isolated epithelial cells may be hidden by a dominant lymphoid infiltrate. This situation requires careful histopathologic and immunophenotypic evaluation to prevent misdiagnosis. - Source: PubMed
Publication date: 2026/07/02
Drittone DeniseMariniello MonicaEsposito LuisaNoccioli NiccolòMaiorana GianlucaLa Verde GiacintoMazzuca FedericaPisegna Simona - Approximately 5%-10% of patients with chronic lymphocytic leukemia (CLL) develop autoimmune hemolytic anemia (AIHA). However, its pathogenesis and prognostic significance remain heterogeneous and incompletely defined. This study investigated the clinical and molecular features of CLL-associated AIHA and aimed to clarify its prognostic impact. We retrospectively analyzed baseline characteristics, first-line treatments, and survival outcomes in 1,404 patients with CLL. The incidence of AIHA was 10.4%, with 69.2% of cases classified as warm-antibody AIHA (wAIHA). CLL patients with AIHA were characterized by male predominance, advanced disease stage, IGHV4-34 usage, and other adverse biological features. Among the tested genes, DNMT3A mutations were more frequent in patients with AIHA, while MYD88 mutations were enriched in cold-antibody AIHA (cAIHA). Although AIHA conferred a significantly adverse prognostic impact on CLL outcomes, this effect was markedly attenuated with targeted therapies. Unmutated IGHV status predicted inferior outcomes in the overall CLL cohort, but not among patients with AIHA. Our findings underscore the importance of routine AIHA screening in high-risk CLL and support consideration of targeted therapies to mitigate the adverse impact of AIHA on long-term survival. - Source: PubMed
Publication date: 2026/07/02
Yan YutingXia YongxinCui RuiChen WeihaoWang TingyuYu YingXiong WenjieAn GangZou DehuiQiu LuguiWang LiangYi Shuhua