CD95
- Known as:
- CD95
- Catalog number:
- 6L95
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Hytest
- Gene target:
- CD95
Ask about this productRelated genes to: CD95
- 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
Related articles to: CD95
- Cotransplantation of allogeneic islets with microgels coated with streptavidin fused with Fas ligand and protease-resistant CXCL12 results in robust and sustained diabetes reversal for over 6 months in streptozotocin-induced diabetic mice and induces local immunomodulation, enhances Treg recruitment within the graft, and improves graft vascularization. This study addresses a critical challenge in cell transplantation, namely the need to develop technologies that enable local immunoprotection of the graft while eliminating the need for systemic immunosuppression. This combination microgel technology could offer a more favorable risk-benefit profile by reducing infection risks, organ toxicity, and tumorgenicity associated with the use of systemic immunosuppression. This novel combinatory immune modulatory approach is feasible and achieves anatomic site-specific immune protection while supporting long-term islet graft function without systemic immune suppression. - Source: PubMed
Publication date: 2026/09/29
Dogan FatmaEl Babsiri AssiaOzkan EsinYe SitongLu KatieArora AaruniKawai KentoOtsuka RyoBrauns Timothy AReeves Patrick MSluder Ann EPoznansky Mark C - Haloperidol is a widely used first-generation antipsychotic for the management of schizophrenia and acute neurocognitive disorders. However, its potential immunotoxic effects remain poorly understood. This study aimed to investigate the cytotoxic and genotoxic mechanisms of haloperidol in RAW264.7 macrophages, focusing on oxidative stress, mitochondrial dysfunction, and apoptosis. - Source: PubMed
Publication date: 2026/08/12
Lee Yen-JuChen Yen-PoHsu Wan-YunShay Serena-HainingTsai Ping-KunSu Chun-HungChen Shih-PinWu Sheng-WenChiang Chen-YuKuan Yu-Hsiang - KM-819, a first-in-class inhibitor of Fas-associated factor 1 (FAF1), was investigated in a Phase 2 clinical trial in Korean patients with multiple system atrophy (MSA). Among 34 KM-819-treated patients, 11 met the case definition for suspected DILI, and 9 of these (26%) were adjudicated by an independent hepatic adjudication committee (HAC) as KM-819-related DILI; no cases occurred among the 34 patients receiving placebo. Blood samples for genetic analysis were available from only 6 of the 9 adjudicated DILI cases; therefore, an exploratory comparative genetic analysis was performed using DNA samples from a total of 16 patients treated with KM-819, including the 6 available DILI cases and 10 patients without DILI. Whole-genome sequencing (WGS) identified the HLA-DPB1*05:01:01:01 allele in all 6 patients with DILI, compared to only 1 of the 10 patients without DILI (p = 0.0009), suggesting a potential association between HLA-DPB1*05:01:01:01 and DILI due to KM-819. In this discovery cohort, HLA-DPB1*05:01:01:01 showed 100% sensitivity, 90.0% specificity, a positive predictive value (PPV) of 85.7%, and a negative predictive value (NPV) of 100% for DILI due to KM-819, albeit with wide confidence intervals reflecting the small sample size. Given the small sample size, exploratory nature of the analysis, and use of the same cohort for both discovery and performance estimation, these findings should be considered hypothesis-generating. Therefore, HLA-DPB1*05:01:01:01 should be regarded as a candidate risk marker specific to this Korean cohort, requiring validation in larger, independent, and ethnically diverse cohorts before its application in clinical risk stratification. - Source: PubMed
Publication date: 2026/09/28
Han Jeong-HoonAndrade Raúl JBjörnsson Einar StefánLewis James HendricksLucena M IsabelGo SuyoungStankeviciute SimonaAithal Guruprasad PKim KyuchanLee Chong SikBarlow CarroleeKim Eunhee - Most inhibitors of lipid peroxidation (LPO) and associated ferroptosis are small molecules that trap LPO-propagating radicals. Among the handful of other inhibitors are select fatty acids: monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids substituted with deuterium atoms at their reactive bis-allylic positions (D-PUFAs), which render them significantly less reactive to LPO-propagating radicals. To probe whether the simple replacement of oxidizable PUFAs with non-oxidizable FAs is a general strategy for ferroptosis suppression, we prepared derivatives of representative PUFAs-linoleic acid (LA) and arachidonic acid (AA)-with cyclopropane rings in place of their unsaturations (CP-PUFAs). Cyclopropanation was predicted to boost the strength of the neighboring C-H bonds by ∼20 kcal/mol and increase the barrier to reaction with peroxyl radicals by ∼104-fold while preserving their cis geometry. CP-PUFAs suppressed ferroptosis induced by erastin2 in HT-1080 cells and RSL3 in HEK-293 cells, similarly to D-PUFAs and MUFAs. Palmitate, a representative endogenous saturated FA, did not suppress ferroptosis. Whereas d6-AA was more effective than d2-LA, the opposite was true of the CP-PUFAs, with CP4-AA possessing only modest activity while CP2-LA was comparable to the D-PUFAs. Lipidomics provides evidence for more extensive lipid remodeling upon treatment with CP2-LA relative to CP4-AA, with PUFAs being enriched in triacylglycerols at the expense of the diacylglycerols used for phospholipid synthesis. Overall, these results suggest that replacement of oxidizable PUFAs with non-oxidizable FAs is a general strategy to suppress ferroptosis-provided that the non-oxidizable FA can be utilized by the biosynthetic machinery and is not lipotoxic at concentrations necessary for protection. - Source: PubMed
Publication date: 2026/09/29
Mallais MelodieSzylo KrystinaMagtanong LeslieShchepinov Mikhail SDixon Scott JPratt Derek A - Type 2 diabetes mellitus (T2D) is the leading cause of end stage renal disease. Screening for chronic kidney disease is recommended for early diagnosis and intervention. This requires assessment of renal function by computing for estimated glomerular filtration rate (eGFR) and urine albumin-creatine ratio. Several formulas have been proposed for computation of eGFR. The European Renal Function Consortium (EKFC) equation, obtained by combining the full age spectrum (FAS) and Chronic Kidney Disease - Epidemiology Collaboration 2021 (CKD-EPI) equations, has been proposed as a more universal formula for eGFR. It has the advantage of eliminating correction for ethnicity and covers a wide age range. The aim of this study is to compare the EKFC and CKD-EPI 2021 equations to assess eGFR among Algerian population with T2D. - Source: PubMed
Publication date: 2026/08/29
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