CD95 _ FAS
- Known as:
- CD95 _ Fas Cell Surface Death Receptor
- Catalog number:
- AM03061FC-N
- Product Quantity:
- 100 Tests
- 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
- Preoperative risk assessment in vascular surgery relies on clinical scores and lipids that do not capture atherosclerotic disease activity. Circulating fatty acid synthase (cFAS) is a liver-derived enzyme whose concentration correlates with arterial plaque FAS content independent of LDL. The 5-item modified frailty index (mFI-5) is a validated predictor of postoperative mortality. Whether cFAS predicts outcomes after vascular surgery, and whether combining it with the mFI-5 improves risk discrimination, have not been examined. - Source: PubMed
Publication date: 2026/08/12
Zaghloul MohamedCatlett RyanKoklu BeraElahi AbdullahSoltan OmarYacoub JadIbrahim DinaAbu-Amer WahidGao FengZayed Mohamed A - Successful oogenesis requires the precise coordination of nutrient uptake, storage, and utilization to meet the high metabolic demands of egg production. In mammals, fatty acid (FA) metabolism has emerged as a key driver of oocyte maturation; however, the mechanisms by which follicles regulate FA trafficking and utilization remain poorly understood across all systems. To address these issues, we leverage the genetic tractability of oogenesis. We found that nurse cell mitochondria are metabolically active and catabolize FA in a stage-dependent manner, with fatty acid oxidation (FAO) peaking during mid-oogenesis. By exposing explanted follicles to fluorescently labeled FAs, we monitored FA trafficking and found massive enrichment in lipid droplets. Mutants for the triglyceride lipase ATGL exhibited a reduction in both mitochondrial membrane potential and FAO, suggesting that mitochondria utilize FA from triglycerides stored in LDs. To determine the significance of this transient FA storage in LDs, we prevented the formation of nurse cell LDs with mutations in the triglyceride synthase DGAT1. The mutant follicles display excess accumulation of FAs in mitochondria, mitochondrial stress, and developmental arrest. We find that this mitochondrial dysfunction and follicle arrest are consequences of FA toxicity to mitochondria: limiting FA influx into follicles or FA import into mitochondria alleviates these defects. Our findings demonstrate that LD-derived FAs are actively mobilized to fuel the energy demands of oogenesis while LDs buffer against lipotoxicity, revealing a critical balance between FA storage and oxidation. These findings highlight LDs as central hubs regulating energy homeostasis and developmental progression in the follicle. - Source: PubMed
Publication date: 2026/08/12
White Roger PKilwein Marcus DWelte Michael A - Chirality has emerged as a new mechanism for inducing spin and Berry-curvature phenomena in quantum materials and molecular chemistry. Collinear antiferromagnets (AFMs) are promising for spintronics and topological magnetism, yet realizing large Berry curvature and spin-split bands remains challenging. Here we report a chiral-superlattice route to spin-split topological phenomena from collinear antiferromagnetism. We study the collinear AFM UOTe, in which we show a spontaneous chiral superlattice arising from frozen chiral phonons at a finite wave vector. Without the superlattice, the pristine collinear AFM in UOTe has neither Berry curvature nor spin-split bands. When electrons move through the chiral superlattice, their orbital Bloch wavefunction and quantum geometry are modulated by the strong chiral superlattice potential, generating large Berry curvature, which we detect by the nonlinear Hall effect. At 150 K, the chiral-superlattice-induced Berry curvature couples to the collinear AFM order, leading to an anomalous Hall angle of about 0.14 abruptly near the Néel temperature T which is among the largest in bulk magnets. Moreover, our spin Hanle precession measurement shows that the chiral superlattice also generates spin-polarized current from the collinear AFM, a long-standing goal in spintronics. We shed light on the supermodulation formation mechanism based on chemical ion size and physical interlayer-intralayer energy competitions, which we use to propose a design principle to discover similar bond-mismatch superlattices, providing a chiral superlattice pathway through real-space engineering of quantum geometry. - Source: PubMed
Publication date: 2026/10/07
Dinh ThaoLiu MengkeQiu Jian-XiangMardanya SougataSung Suk HyunLe Xuan HoangBroyles ChristopherZhu ChengfengXu QiaozhiChen HaotianRehfuss ZackLiu Yu-FeiZeng XiaoyuLi HouchenGuo PengLiu JinchenHuang TianyeShi JingtianSmith MichaelBlawat Joanna MSingleton JohnMcDonald RossArvizo Iván ECui DongtaoZheng Shao-LiangWatanabe KenjiTaniguchi TakashiSharma Vineet KumarGhorai SudipGhosh BarunLin HsinLim Ting YongChang Tay-RongBansil ArunMartin IvarVishwanath AshvinXie WeiweiFelser ClaudiaSinova JairoGao AnyuanLukin Mikhail DHoffman Jennifer EChowdhury SugataMa QiongSun KaiBaggari Ismail ElRan ShengGhiasi Talieh SPark HongkunKim PhilipXu Su-Yang - Identifying robust predictive biomarkers for immune checkpoint blockade (ICB) remains a challenge. While alternative splicing (AS) shapes tumor immunity, the lack of large-scale, consensus-based datasets constrains the characterization of ICB-specific splicing landscapes. - Source: PubMed
Publication date: 2026/10/07
Zhang YihaoGuo YunzhiWang HaitaoXiong YiChen MinjunCai YingLi XinWu JunHao JiaqiJin Su-HanZhang WeiDai LuohuanLiu HongweiLi JianfengZhang JiahuiHecht MarkusFrey BenjaminGaipl Udo SChen XinLi XuejunWang ShixiangMa HuZhou Jian-Guo - Mycobacterium tuberculosis relies on the fatty acid synthase II (FAS II) pathway for the biosynthesis of mycolic acids, which are essential components of its lipid-rich cell envelope and major contributors to intrinsic drug resistance. The HadAB dehydratase complex catalyzes a critical dehydration step during early meromycolate chain elongation; however, the structural basis governing substrate accommodation and inhibitor recognition has remained unclear. Here, we report the first substrate-bound crystal structure of M. tuberculosis HadAB in complex with Palmitoyl-CoA at 1.69 Å resolution, revealing the architecture and dynamic remodeling of the acyl housing tunnel. The structure reveals that the tunnel is formed at the HadA-HadB interface, with HadA contributing primarily to substrate accommodation and HadB providing the catalytic machinery. Comparison with the previously determined apo-structure reveals substrate-induced displacement of the α4 hot-dog helix of HadA, resulting in elongation and reshaping of the tunnel to accommodate fatty acyl intermediates. The structure further reveals the positioning of Cys61, at the distal end of the acyl housing tunnel, and Cys105, which mediate covalent inhibition by thiourea-derived compounds. Biochemical analyses demonstrate selective activation of Thioacetazone and SPA0355 by mycobacterial Baeyer-Villiger monooxygenases, EthA and MymA, leading to cysteine-dependent modification and inhibition of HadAB. A cell viability assay against Mycobacterium smegmatis demonstrated promising antimycobacterial activity for SPA0355, similar to Thioacetazone. Furthermore, modelling of HadAB-AcpM provided insights into the interaction between HadAB and its physiological acyl carrier protein AcpM. Together, these findings establish the molecular basis of substrate recognition, tunnel plasticity, and prodrug-mediated inhibition of HadAB, providing a framework for structure-guided development of therapeutics that target mycobacterial lipid biosynthesis. - Source: PubMed
Publication date: 2026/10/07
Ganguly Soumya SarathiSaha RituparnaSingh Bina KumariDe SoumyaDas Amit Kumar