FADD pSer191 antibody Ab
- Known as:
- FADD pSer191 (anti-) Antibody
- Catalog number:
- 1488297
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- FADD pSer191 antibody
Related genes to: FADD pSer191 antibody Ab
- Gene:
- FADD NIH gene
- Name:
- Fas associated via death domain
- Previous symbol:
- -
- Synonyms:
- MORT1, GIG3
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2019-04-23
Related products to: FADD pSer191 antibody Ab
Related articles to: FADD pSer191 antibody Ab
- Liver fibrosis is a common pathological stage in the progression of various chronic liver diseases. Current interventions primarily focus on anti-inflammatory and antioxidant effects, lacking safe and universally applicable strategies for reversal. This work aimed to clarify the chemical basis and the potential mechanism of the ethyl acetate fraction of Prismatomeris tetrandra(HG). The constituents of HG were characterized by liquid chromatography-mass spectrometry(LC-MS). Transcriptomic dataset was analyzed for differential expression, which was followed by weighted gene co-expression network analysis(WGCNA). Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analyses were performed to build a "constituent-target-pathway" network for key pathway screening. A mouse liver fibrosis model was induced by carbon tetrachloride(CCl_4). After mice were administered continuously for 4 weeks, serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), malondialdehyde(MDA), hyaluronic acid(HA), laminin(LN), procollagen type Ⅲ(PCⅢ), and type Ⅳ collagen(COL4) were detected. Hematoxylin and eosin(HE) and Masson staining were performed to assess histological changes, and Western blot was employed to detect the expression of alpha-smooth muscle actin(α-SMA) and the proteins related to death receptor pathway(Fas, Fas ligand [FasL], and Fas-associated death domain protein [FADD]). The results showed that the fraction was rich in coumarins and flavonoids. Bioinformatics analysis indicated that the signaling primarily acted on apoptosis-related pathways. In vivo, HG ameliorated liver injury and oxidative stress, reduced serum fibrosis markers, alleviated collagen deposition, and suppressed hepatic stellate cell(HSC) activation, with an overall dose-dependent trend. Network pharmacology results indicated that HG may reduce extracellular matrix(ECM) deposition by rebalancing inflammatory receptor-kinase signaling and promoting death receptor-mediated programmed cell death. Collectively, HG exhibits a clear anti-fibrotic effect in hepatic fibrosis models, potentially through mobilization of the extrinsic apoptotic pathway, which provides a basis for further validation of key monomers and causal mechanisms. - Source: PubMed
Wu Ming-MinLuo KeSu Jing-KangYang Zeng-Yan - Parkinson's disease (PD) is a progressive neurodegenerative disorder with limited disease-modifying therapies. PANoptosis, an integrated form of programmed cell death involving apoptosis, pyroptosis, and necroptosis, has been implicated in neuroinflammation-related neurodegeneration. However, the roles of PANoptosis-related genes in PD remain unclear. - Source: PubMed
Publication date: 2026/06/30
Li ZhouYang RongFeng HaoSun MouLiu Hongjun - Zinc oxide nanoparticles (ZnONPs) are widely used in sunscreens and cosmetics; however, increasing evidence suggests their potential to induce skin toxicity, particularly under conditions of skin function disruption. Here, we investigated the mechanisms underlying allergic skin inflammation triggered by repeated ZnONPs exposure following UVR damage using an in vivo hairless mouse model and in vitro Adverse Outcome Pathway (AOP)-based new approach methodologies (NAMs). Co-exposure to ZnONPs and UVR caused persistent barrier dysfunction, epidermal hyperplasia, mast cell degranulation, elevated serum IgE levels, and increased expression of Th2-associated cytokines (IL-4, IL-13, and IL-17A), indicating enhanced allergic skin inflammation. KeratinoSens and h-CLAT assays demonstrated that UVR augmented ZnONPs-induced keratinocyte activation (key event 2) and dendritic cell activation (key event 3). Mechanistically, ZnONPs combined with UVR induced mitochondrial dysfunction, oxidative stress, and canonical NLRP3 inflammasome activation in keratinocytes, leading to pyroptotic cell death. Instead, dendritic cells activated an alternative TLR4-RIPK1-FADD-caspase-8 inflammasome pathway independent of pyroptosis. Collectively, these findings demonstrate that ZnONPs can function as sensitizers under barrier-compromised conditions through different inflammasome pathways, highlighting the need to adapt current skin sensitization testing strategies for nanomaterials and to incorporate mechanistic endpoints into future risk assessment frameworks. - Source: PubMed
Publication date: 2026/06/30
Chen Yu-YingWang Bour-JrCheng Yung-HsuanCheng Hsien-JenChen Rong-JaneWang Ying-Jan - Deltamethrin (DLM) along with its main metabolite 3-phenoxybenzoic acid (3-PBA) are increasingly detected in environmental media. They both have the ability to accumulate on human by food chains with potential neurotoxicity. However, at present, there are relatively few studies on the neurotoxic effects of DLM and 3-PBA. This study investigated the neurotoxicity and mechanism in HT22 hippocampal neurons by DLM (5, 25, 50, 100, and 150 μM) and 3-PBA (100, 500, 1000, 1500, and 2000 μM). Cytotoxicity assays revealed that both DLM and 3-PBA dose-dependently inhibited HT22 cell viability. Notably, DLM exhibited higher potency than 3-PBA, as evidenced by its lower IC value. Enzyme-linked immunoassay showed that exposure to DLM and 3-PBA interfered with the secretion of neurotransmitters (Ach, DA, GABA) and disrupted the transmission of signaling molecules (NO). Biochemical analysis revealed that both compounds reduced intracellular antioxidants (SOD and GSH-Px), and surged ROS production. This oxidative imbalance led to mitochondrial dysfunction and subsequent apoptosis. Oxidative damage mechanism study showed that DLM and 3-PBA exposure reduced the expression levels of Nrf2, HO-1, and AKT proteins, as well as the transcription of Nrf2, HO-1, and Akt genes in the Nrf2/HO-1 antioxidant pathway, reducing the antioxidant capacity of HT22 cells. Apoptotic mechanism showed that DLM and 3-PBA reduced the expression levels of Bcl-2, Bcl-xL proteins and genes. They also increased the expression levels of JNK, BAX, Cyto c, Caspase-9 proteins, alongside the upregulation of JNK, BAX, Cyto c, and Caspase-9 genes in the endogenous apoptotic signaling pathway. Meanwhile, DLM and 3-PBA exposure also increased the expression levels of FasL, FADD, Caspase-8, Caspase-3 proteins, as well as FasL, FADD, Caspase-8, and Caspase-3 genes in the exogenous apoptotic signaling pathway, thereby inducing apoptosis. These findings highlight the potential neurotoxicity and molecular mechanisms of DLM and 3-PBA, emphasizing the need for further research to assess and mitigate the health risks associated with pesticide exposure. - Source: PubMed
Publication date: 2026/06/30
Liang YihuiShi TianliZhang RuikeMao GuanghuaFeng WeiweiLi QianChen YaoChen NaWu Xiangyang - Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a curative therapy for high-risk hematologic malignancies, yet its efficacy is limited by the onset of graft-versus-host disease (GVHD). Acute GVHD (aGVHD) primarily affects epithelial cells of the gastrointestinal tract, skin, and liver by the involvement of alloreactive T-cells and pro-inflammatory cytokines. The barrier-protective role of hypoxia-inducible factor (HIF), regulated by prolyl hydroxylase, has been significantly implicated in hypoxic inflammatory conditions. In this study, Roxadustat, a prolyl hydroxylase inhibitor, was tested in a murine model of aGVHD (C57BL/6J → BALB/cJ) to decrease hypoxia-mediated early gastrointestinal injury. Recipients were treated with roxadustat or vehicle intraperitoneally daily for the first week post-transplant, and then twice a week till day 42. Roxadustat significantly improves survival by day + 42 with reduced clinical GVHD symptoms. Reduced gut pathology with significant reduction of serum IFN- γ and TNF-α levels, suggesting a decreased systemic inflammation. Roxadustat significantly decreased T-cell infiltration and prevented TNF-α-induced intestinal epithelial cell apoptosis through HIF-1α-dependent repression of Fas-associated death domain protein (FADD) and cleaved caspase 3. In vitro, roxadustat suppressed TNF-α production by peritoneal macrophages and mixed lymphocyte reaction. These results suggest that roxadustat attenuates early gut injury, offering an alternative strategy for acute GVHD following allo-HSCT. - Source: PubMed
Publication date: 2026/06/27
Raguraman VasantharajaMohiyuddin ShanidPlank TylerBenge CatherineBanker LinneaHammer Richard DPalaniyandi SenthilnathanHildebrandt Gerhard C