CD95 _ FAS
- Known as:
- CD95 _ Fas Cell Surface Death Receptor
- Catalog number:
- GTX13549
- Product Quantity:
- 50 µg
- 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
- Cancer progression following an initial response to immunotherapy (secondary resistance; 2°R) is a major and poorly understood problem. We treated mice bearing B16 melanoma with a combination of a regulatory T cell (Treg) depleting, non-IL-2 blocking antibody (anti-CD25NIB) and an autologous cancer cell vaccine (GVAX). The regimen yielded initial tumor shrinkage followed by 2°R; lethal progression occurred in ~90% of partially responsive (PR) tumors by days 35-50. Cell lines derived from 2°R tumors retained treatment sensitivity upon re-implantation into naïve mice, suggesting resistance was related to a loss of immune control over time. Profiling PR and 2°R tumors by flow cytometry and single-cell RNA/TCR sequencing, we found that activated CD8⁺ T cells with tumor-reactive features declined in abundance, whereas non-activated T cells and Tregs increased. Activated CD8⁺ cells showed heightened TCR stimulation, clonal expansion, and expression of apoptotic signatures and death receptors, including Fas. Their loss was not explained by lymph node accumulation or differentiation to non-activated states. These findings were validated in a clinically relevant MC38 colon carcinoma model treated with anti-PD-L1 checkpoint blockade, confirming that depletion of activated, tumor-reactive clones is a shared mechanism of 2°R across therapeutic modalities. Fas ligand (FasL) blockade reversed this loss and prolonged survival. Longitudinal transcriptional and tissue staining data from human checkpoint blockade studies similarly indicated that activated T cells decline in abundance over time and at 2°R. These findings implicate death of activated T cells as a mechanism of 2°R and suggest Fas-FasL blockade may extend response durability. - Source: PubMed
Publication date: 2026/09/15
Qing ChenGhorani EhsanFoster Kane AUddin ImranBeattie GordonCostoya CristobalGalvez-Cancino FelipeWalczak HenningAmann MariaPeggs Karl SQuezada Sergio A - Microsatellite-stable (MSS) colorectal cancer (CRC) shows limited responsiveness to immune checkpoint inhibitors, often in the context of a fibrotic and immunosuppressive tumor microenvironment. Cancer-associated fibroblasts (CAFs) are central to extracellular matrix (ECM) remodeling, yet the underlying regulatory mechanisms remain unclear. Here, we identify Fas apoptotic inhibitory molecule 2 (FAIM2) as a stromal regulator that is downregulated in MSS CRC and associated with immune infiltration and patient prognosis. Single-cell RNA sequencing localizes FAIM2 predominantly to CAFs, where it inversely correlates with collagen production. Functional studies in L-929 cells and primary CAFs show that FAIM2 overexpression suppresses endoplasmic reticulum (ER) stress signaling and reduces collagen I and matrix metalloproteinase 2 (MMP2) expression; these effects are attenuated by the ER stress inducer Tunicamycin. Conversely, FAIM2 knockdown enhances ER stress and collagen synthesis, which are mitigated by the ER stress inhibitor tauroursodeoxycholic acid (TUDCA). Mechanistically, carboxylesterase 1 (CES1) is identified as a downstream effector negatively regulated by FAIM2, mediating ER stress and ECM remodeling. In vivo, FAIM2 overexpression restrains tumor growth, reduces collagen deposition, and promotes tertiary lymphoid structure (TLS) formation, whereas CES1 co-overexpression counteracts these effects. Together, these findings reveal a potential FAIM2-CES1-ER stress axis in CAFs associated with ECM remodeling and immune contexture in MSS CRC, providing a rationale for future studies exploring its therapeutic potential in immunotherapy. - Source: PubMed
Publication date: 2026/09/15
Tang RenWan HongtaoZhong MenglanYan KangpengXu BinXiong Jianyong - ObjectiveTo evaluate the radiographic outcomes, clinical effectiveness, and safety of lateral calcaneocuboid guided growth using a tension-band plate (8-plate) for the correction of residual forefoot adduction in children with idiopathic clubfoot.MethodsWe evaluated children presenting with residual forefoot adduction following previous clubfoot treatment. All patients underwent lateral calcaneocuboid-guided growth using an 8-plate. Radiographic assessment included preoperative and postoperative measurements of the talo-first metatarsal angle (T1MA), calcaneo-fifth metatarsal angle (C5MA), and the medial-to-lateral (M/L) column length ratio.ResultsFifteen feet (median age: 5 years) were analyzed. The M/L ratio showed a statistically significant improvement across the entire cohort (P < .05). While T1MA and C5MA demonstrated numerical improvement, statistical significance was primarily reached in simple deformities. Notably, a strong positive correlation was found between increasing age and improvement in the M/L ratio. Younger patients experienced a higher incidence of screw loosening and lower correction rates, likely due to softer bone density, whereas older children showed superior stability and more predictable outcomes. No major adverse events or permanent growth arrests were reported.ConclusionLateral calcaneocuboid guided growth is a safe, minimally invasive technique for managing residual forefoot adduction. However, clinical success is highly dependent on hardware stability.Levels of Evidence:Level IV: Case Series. - Source: PubMed
Publication date: 2026/09/15
Hassan Mohamed Sobhy AliEl Barbary Hassan MagdyArafa Amr SaidYassen Ahmed MohamedAbdelghany Ahmed Abdelmohsen - Early-life vascular risk factors are increasingly linked to midlife cognitive decline, though critical risk periods remain unclear. These factors also relate to structural brain changes, yet midlife alterations tied to cognitive decline are poorly defined. We leveraged data from the CARDIA study (Coronary Artery Risk Development in Young Adults) to identify critical periods and factors associated with midlife cognition and neuroimaging signatures. - Source: PubMed
Publication date: 2026/09/15
Yaghoobi ShahinSalboukh FatemehLlyod-Jones DonaldAllen NorrinaJacobs David RLauner Lenore JYaffe KristineMesulam M MarselGorelick Philip BBryan R NickNasrallah Ilya MSorond Farzaneh A - Accumulating evidence underscores the profound impact of the gastrointestinal ecosystem on skeletal muscle lipid dynamics. - Source: PubMed
Publication date: 2026/08/31
Zhaxi DaoziYu ChunlinWang JiayanYang DongmeiWang ZiYang WenqiZhang YudingYang ChaowuLi Zhixiong