CD95 _ FAS
- Known as:
- CD95 _ Fas Cell Surface Death Receptor
- Catalog number:
- BM2047
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD95 _ FAS
Related genes to: CD95 _ FAS
- Gene:
- FAS NIH gene
- Name:
- Fas cell surface death receptor
- Previous symbol:
- FAS1, APT1, TNFRSF6
- Synonyms:
- CD95, APO-1
- Chromosome:
- 10q23.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-25
- Date modifiied:
- 2019-04-23
Related products to: CD95 _ FAS
Related articles to: CD95 _ FAS
- Although the regulatory crosstalk between autophagy and apoptosis in response to stress has been well documented in higher multicellular eukaryotes, its functional significance in marine microalgae exposed to persistent organic pollutants (POPs) remains largely unclear. Here, we investigated the coordinated responses of these two pathways in the marine microalga Isochrysis galbana exposed to 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), a widespread coastal environmental contaminant. Exposure to BDE-47 (50-150 μg/L, 48 h) induced dose-dependent oxidative stress, characterized by excessive reactive oxygen species (ROS) accumulation, a decreased glutathione (GSH)/glutathione disulfide (GSSG) ratio, and increased malondialdehyde (MDA) content. Simultaneously, BDE-47 activated both the intrinsic apoptotic pathway, characterized by mitochondrial membrane potential (MMP) depolarization and elevated caspase-9 and caspase-3 activities, and the extrinsic pathway, reflected by the upregulation of Fas-associated death domain (FADD) and increased caspase-8 activity. Enhanced autophagic fluorescence intensity, autophagosomes formation, and upregulation of autophagy-related genes (ATGs) and proteins further confirmed that autophagy was also induced. Pharmacological inhibition assays revealed that the ROS scavenger N-acetylcysteine (NAC) markedly attenuated both autophagy and apoptosis, identifying ROS as a common upstream trigger for both processes. Inhibition of autophagy by 3-methyladenine (3-MA) exacerbated apoptotic damage, whereas blockade of apoptosis by Z-VAD-FMK promoted autophagic activity, indicating an antagonistic crosstalk in which autophagy suppresses apoptosis and vice versa. These findings demonstrate that the ROS-autophagy-apoptosis axis is functionally conserved in a marine microalga, and provide new insight into the cellular response of marine phytoplankton to organic pollutant stress. - Source: PubMed
Publication date: 2026/08/31
Bai LinsenLi YuanyuanDong LankunWang YouYang Yingying - Diabetic foot ulcers (DFUs) are debilitating complications of diabetes, leading to severe health outcomes and high healthcare costs. Understanding the molecular mechanisms is crucial for better management. This study aims to explore the roles of fatty acid metabolism (FAM) and the immune landscape in DFUs to identify potential diagnostic biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/08/25
Hu BoZhao JinghuiChai ShengnanZhang Long - Poor sleep quality and fatigue are common complications in hemodialysis patients. Although Sama Vritti pranayama breathing exercise as a yogic breathing is prescribed to improve sleep quality, its efficacy in this group of patients is not well established. The present study was conducted to examine the effects of Sama Vritti Pranayama applied to hemodialysis patients on sleep disturbance and fatigue. - Source: PubMed
Publication date: 2026/03/10
Heydarian FaribaMohammadi SepidehShamsalinia AbbasArzani Afsaneh - - Source: PubMed
Publication date: 2026/08/28
Moura Priscila AQuek Swee-PeckCardoso Márcio ZKronforst Marcus R - No therapies directly block apoptosis in tissue injury or the many diseases driven by cell loss. The BCL-2 family protein BAX is a central mediator of this pathway and C126 resides within a key regulatory region where physiologic or pharmacologic ligands can activate or inhibit its function. Here, we report enantioselective covalent BAX inhibitors that site-specifically react with C126 and confer cytoprotection across multiple cell types. These ligands constrain BAX conformation and suppress apoptosis in a strictly BAX-dependent manner. Medicinal chemistry optimization yielded covalent BAX inhibitor 3 (CBI-3), an analog with pharmacokinetics suitable for in vivo studies. In a murine model of Fas-induced fulminant hepatic failure, CBI-3 reduced hepatocyte apoptosis and preserved liver histology and survival. CBI-3 also conferred cytoprotection of motor neurons derived from human induced pluripotent stem cells of healthy and amyotrophic lateral sclerosis donors. These findings establish covalent BAX inhibition as a therapeutic strategy to directly block pathologic cell death. - Source: PubMed
Publication date: 2026/08/28
Shi PeiwenMelillo BrunoMcHenry Matthew WCamara Christina MYang KaNjomen EvertGodes MarinaPazyra-Murphy Maria FBranch Mary RoseTesar BethanySegal Rosalind ARubin Lee LCameron Michael DBird Gregory HWales Thomas EGygi Steven PCravatt Benjamin FWalensky Loren D