CD95 _ FAS (inducing)
- Known as:
- CD95 _ Fas Cell Surface Death Receptor (inducing)
- Catalog number:
- BM2616
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD95 _ FAS (inducing)
Ask about this productRelated genes to: CD95 _ FAS (inducing)
- 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 (inducing)
(Asn5)-Delta-Sleep Inducing Peptide
(Asn5)-Delta-Sleep Inducing Peptide (rabbit), (Asn5)-DSIP (rabbit) 98% C35H49N11O14 CAS: 80064-67-1(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(b_Asp5)_Delta_Sleep Inducing Peptide Salt Trifluoroacetate Binding _ Synonym (b_Asp5)_Delta_Sleep Inducing Peptide (rabbit), (b_Asp5)_DSIP (rabbit) SumFormula C35H48N10O15(b_Asp5)_Delta_Sleep Inducing Peptide Salt Trifluoroacetate Binding _ Synonym (b_Asp5)_Delta_Sleep Inducing Peptide (rabbit), (b_Asp5)_DSIP (rabbit) SumFormula C35H48N10O15(Tyr1)-Delta-Sleep Inducing Peptide
(Tyr1)-Delta-Sleep Inducing Peptide (rabbit), (Tyr1)-DSIP (rabbit) 98% C33H47N9O16 CAS:(Tyr1)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Tyr1)_Delta_Sleep Inducing Peptide (rabbit), (Tyr1)_DSIP (rabbit) SumFormula C33H47N9O16(Tyr1)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Tyr1)_Delta_Sleep Inducing Peptide (rabbit), (Tyr1)_DSIP (rabbit) SumFormula C33H47N9O16(β-Asp5)-Delta-Sleep Inducing Peptide
(β-Asp5)-Delta-Sleep Inducing Peptide (rabbit), (β-Asp5)-DSIP (rabbit) 98% C35H48N10O15 CAS: 82602-88-81A13B,Cell migration-inducing gene 19 protein,Homo sapiens,Human,KIAA0049,M17S2,Membrane component chromosome 17 surface marker 2,MIG19,NBR1,Neighbor of BRCA1 gene 1 protein,Next to BRCA1 gene 1 prote20 kDa nuclear cap-binding protein,CBP20,CBP20,Cell proliferation-inducing gene 55 protein,Homo sapiens,Human,NCBP 20 kDa subunit,NCBP2,NCBP-interacting protein 1,NIP1,Nuclear cap-binding protein subu2B4,CD244,h2B4,Homo sapiens,Human,NAIL,Natural killer cell receptor 2B4,NK cell activation-inducing ligand,NK cell type I receptor protein 2B4,NKR2B42C101 Fas Ligand2R2 Fas3.22 Fas- FITC labeled Related articles to: CD95 _ FAS (inducing)
- Previous research indicated that physicians possess limited knowledge of the diagnosis and treatment of invasive fungal disease (IFD). - Source: PubMed
Chen YijianHuang XiaojunQiu HaiboCheng LinlingYu YunsongMa XiaochunFeng SizhouLi QiWu DepeiHuang WenxiangChen DechangLv XiaojuHu JiandaWang JingboLi JiabinYang WenjieZhan QingyuanSun BingWang Minggui - Sulfated galactan (SG) isolated from has demonstrated promise for cancer therapy and prevention through inhibition of cancer cell proliferation and migration. However, its structure‑activity relationship remains to be elucidated. The present study evaluated the microstructural characteristics and anticancer activity, particularly immunogenic cell death (ICD)‑inducing potential, of SG and its degraded derivative (DSG) in triple‑negative breast cancer cells. SG and DSG were prepared and structurally characterized using gel permeation chromatography, nuclear magnetic resonance, Fourier‑transform infrared and scanning electron microscopy coupled with energy‑dispersive X‑ray spectroscopy. ICD induction was assessed in human MDA‑MB‑231 breast cancer cells using an MTT assay, phase‑contrast microscopy, Hoechst/propidium iodide dual staining, intracellular reactive oxygen species (ROS) generation assay, and transmission electron microscopy (TEM). In addition, western blot analysis, immunofluorescence staining, and reverse transcription‑quantitative PCR were performed. Structural analyses revealed that SG and DSG share similar backbone structures but differ markedly in sulfate content and molecular weight. Both compounds were non‑toxic to normal breast epithelial MCF‑10A cells and exhibited mild cytotoxicity toward MDA‑MB‑231 cells. DSG treatment induced notable morphological changes in cancer cells, with reduced cell numbers, increased membrane permeability and elevated intracellular ROS levels. TEM revealed DSG‑induced ultrastructural changes consistent with cellular stress and cytotoxicity. DSG also markedly upregulated ICD‑associated proteins [calreticulin (CRT) and Fas receptor (Fas‑R)] and endoplasmic reticulum stress‑related genes (protein kinase RNA‑like endoplasmic reticulum kinase, inositol‑requiring enzyme 1, activating transcription factor (ATF)6, ATF4, eukaryotic initiation factor 2 α subunit, CRT and Fas‑R), with effects similar to the positive control doxorubicin. Therefore, these findings indicated that DSG enhances ICD in triple‑negative breast cancer cells and may potentially serve as a promising ICD‑inducing adjuvant for cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/19
Rudtanatip TawutPolsan YadaSakaew WarapornSomintara SomsudaPhanphak JenjiralaiEl-Abid JamalWongprasert KanokpanPariwatthanakun Choowadee - Topological materials have been reported as active and selective electrochemical catalysts for a variety of small-molecule energy-conversion reactions. The exceptional activity and selectivity of these materials have been attributed to their topologically non-trivial surface states, which support chiral spin currents and boast high carrier mobilities. For the topological semimetal PtGa, we find that these states are not robust under practical electrochemical conditions. During electrochemical operation, Ga rapidly corrodes from the surface, yielding a nanoporous, Pt-rich layer. Inductively coupled plasma mass spectrometry and scanning transmission electron microscopy imaging independently confirm Ga corrosion. Hydrogen evolution reaction activity measurements demonstrate that the electrocatalytic performance of PtGa is correlated with the number of Pt active sites, and first-principle calculations further show that introducing Ga vacancies into the PtGa crystal structure disrupts the topologically non-trivial surface states. These observations suggest that previous reports detailing the high electrochemical activity of PtGa might be better explained by an enrichment in Pt active sites following corrosion, rather than by a genuine increase in the intrinsic reaction rate mediated by PtGa's topological surface states. These results urge caution in attributing enhanced catalytic activity to topological surface states without verifying surface composition and electronic structure. They also highlight the distinct meaning of robustness in physics and chemistry. - Source: PubMed
Publication date: 2026/06/11
Johnston BrandonChen Meng-FuZhu MingxuanGuo PengXu Su-YangLee JoonhoNocera Daniel G - STAR0602 is a selective bifunctional T cell agonist targeting Vβ6/Vβ10 T-cell receptors fused to interleukin-2, with emerging clinical activity in anti-PDL1-resistant tumors. Its murine surrogate, mSTAR1302, expands Vβ13 T cells and mediates antitumor activity. Docetaxel, beyond its cytotoxic effects, induces immunogenic modulation of tumor cells. We hypothesized that docetaxel-driven tumor sensitization would enhance susceptibility to immune-mediated killing, while mSTAR1302 would expand functional T cell subsets, resulting in coordinated antitumor responses. - Source: PubMed
Publication date: 2026/06/03
Lee Jonelle KFabian Kellsye PSantiago-Sanchez Ginette SRosato FrancescaPadget Michelle RLee CailynSu ZhenMoisan JacquesKatragadda MadanSchlom JeffreyGulley James LBayliffe AndrewHodge James W - Methyltransferase-like protein 7A (METTL7A), an mA RNA methyltransferase and thiol methyltransferase enriched in hepatocytes, has been implicated in cancer biology, yet its role in hepatic lipid metabolism and nonalcoholic fatty liver disease (MASLD/NAFLD) remains unknown. Hepatic steatosis was induced in HepG2 and Huh7 cells using oleic acid (OA). The role of METTL7A was examined through shRNA-mediated knockdown, RNA sequencing, lipid metabolic assays, and rescue experiments. Protein interactions were assessed via mass spectrometry and co-immunoprecipitation. An AAV-shMETTL7A mouse MASLD/NAFLD model was used to validate in vivo relevance. METTL7A expression was significantly upregulated in OA-induced steatotic hepatocytes. METTL7A silencing mitigated lipid accumulation, improved cell viability, reduced LDL-C, TC, and TG levels, and restored HDL-C. Transcriptomic profiling identified PLIN5 as a key downstream target reduced upon METTL7A depletion. Mechanistically, METTL7A knockdown inhibited PI3K/AKT activation and suppressed PLIN5 expression. Mass spectrometry revealed SAPCD2 as a METTL7A-interacting protein, and SAPCD2 overexpression restored lipid accumulation, PI3K/AKT activation, and PLIN5 levels in METTL7A-deficient cells. In vivo, AAV-mediated METTL7A knockdown alleviated hepatic steatosis, normalized serum lipid profiles and liver injury markers, and reduced SAPCD2, PLIN5, FAS, and ACC while increasing HSL expression. METTL7A is a previously unrecognized regulator of hepatic lipid homeostasis that promotes steatosis by sustaining SAPCD2 expression and activating the PI3K/AKT pathway and PLIN5 expression. Targeting METTL7A may represent a promising therapeutic strategy for MASLD/NAFLD. - Source: PubMed
Publication date: 2026/06/18
Chen FengsuiYao LijiaYang LingLi XinbiaoZhou JunweiLi DongliangWu ZhixianChen Pin