CD95 _ Fas
- Known as:
- CD95 _ Fas
- Catalog number:
- 10-395-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- 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
- This study aimed to investigate the associations between the physical activity of hemodialysis (HD) patients and their informal caregivers and measures of their well-being and quality of life (QoL). - Source: PubMed
Publication date: 2026/09/03
Κougioumtzidou OuraniaMichou VasilikiIntzevidou EleniLamprou VasileiosKanaki AngelikiPapagianni AikateriniDeligiannis AsteriosKouidi Evangelia - SND1 is an oncoprotein found to be overexpressed in breast cancer, especially in triple-negative breast cancer(TNBC). In our previous study, a novel SND1-interacting peptide 4-2 was identified, exhibiting cytotoxicity to TNBC cells by inducing SND1 degradation. This study for the first time demonstrated the degradation of SND1 was proteasome-dependent. A series of peptide 4-2 derivatives were constructed using PROTAC technology. Among these, 4-2 VHL-recruiting PROTAC showed significantly increased SND1 degradation efficiency and higher anticancer activity to TNBC cells. The in vivo efficacy study suggested the D-isoform of 4-2VHL PROTAC suppressed the growth of TNBC cells in xenograft mouse model more effectively than peptide 4-2. Mechanistically, 4-2 VHL-recruiting PROTAC was demonstrated to induce pyroptosis of TNBC cells through Fas-mediated IL-17signaling. This study provides a new lead compound for the development of theSND1-targeted therapy via the proteolysis-targeting system. - Source: PubMed
Wang QiqiHuang QiufengOu HuipingHuang TingtingHe YunjiaoLi Peng - Ribosomal protein S3 (RPS3) is an essential structural component of the 40S ribosomal subunit, yet growing evidence highlights crucial extraribosomal roles in genome maintenance, cell-cycle control, and immune signaling. Dysregulation of RPS3 contributes to diverse human disorders, including cancer, inflammatory diseases, neurodegeneration, and resistance to antimicrobial and anticancer therapies. As a cofactor of NF-κB and a participant in DNA damage responses, RPS3 occupies a node that integrates stress signaling with transcriptional reprogramming, enabling both protective and pathological outcomes. The present review critically evaluates mechanistic insights into RPS3 biology, emphasizing recent findings that delineate its context-dependent effects, discrepancies across models, and remaining gaps that restrict translational applications. Understanding these complexities is essential to assess RPS3's potential as a biomarker and therapeutic target. - Source: PubMed
Dreik JoelineAl Ali MarwaDaher JalilNasr Zeina - Drosophila suzukii (Matsumura), known as spotted-wing drosophila, is an invasive fruit fly that lays their eggs in soft-skinned fruits with its serrated ovipositor. In this study, we evaluated the effects of oviposition and residence behavior of D. suzukii by two saturated fatty acids (FAs): palmitic acid (C16:0) and stearic acid (C18:0). Both FAs were identified from a novel D. suzukii attractant, Decoy Attract and Kill, using gas chromatography-mass spectrometry and liquid chromatography-high resolution mass spectrometry. The FAs were then tested for their potential to alter oviposition in laboratory trials on blueberry with different concentrations and ratios to determine the optimal behavioral effects. We examined whether exposure to these FAs increased post-contact residence time and altered oviposition behavior. Exposure to 6.62 mg/L C16:0 and 3.61 mg/L C18:0 showed the strongest contact-mediated arrestment, resulting in increased oviposition on FA-treated blueberries. Females exposed to a 2:1 ratio of C16:0:C18:0 showed the greatest contact-dependent arrestment, followed by the 1:1 ratio, C16:0, and C18:0 alone. Additionally, we confirmed that both FAs act in a contact-dependent manner, increasing oviposition behavior after landing. Both C16:0 and C18:0 are effective contact-based arrestants that have the potential to protect soft-skinned fruits from D. suzukii oviposition damage. - Source: PubMed
Yoon Ho JungKim-Fu Mitchell LLi XinyuField Jennifer AMermer SerhanWalton Vaughn M - Nucleic acid sensing by endolysosomal Toll-like receptors is critically involved in systemic lupus erythematosus (SLE) and related autoimmune diseases. Downstream of TLR7, TLR8, and TLR9, the SLE-associated SLC15A4-TASL complex selectively mediates IRF5 activation, while being dispensable for NF-κB and MAPK pathways. Here, we show that the SLC15A4-TASL signaling axis is broadly required for disease development and pathogenesis across three complementary genetic SLE models, reflecting different etiologies. Genetic ablation of () and its paralogue () ameliorated or fully prevented autoimmune manifestations resulting from loss of function, respectively. Furthermore, SLC15A4-TASL complex deficiency was sufficient to protect from disease, including splenomegaly, immune activation, and autoantibody formation, driven by the patient-derived gain-of-function mutation, even in the presence of functional NF-κB and MAPK responses. Last, splenocyte transfer into lymphopenic -deficient mice demonstrated that protection extends to DNA-driven autoimmunity, in which TLR7 and TLR9 act redundantly, strongly supporting a B cell-intrinsic role. Notably, SLC15A4-TASL complex deficiency blunted the generation of pathogenic age-associated B cells in all three autoimmune models as well as in aged animals. Collectively, these data demonstrate the central role of the SLC15A4-TASL complex in SLE, supporting its potential as therapeutic target. - Source: PubMed
Publication date: 2026/09/01
Drobek AlesDelacrétaz MaevaVasilakou AlikiMonguió-Tortajada MartaBernaleau LéaDubois MaximeSisirak VanjaRebsamen Manuele