CD178 _ Fas Ligand (103_281)
- Known as:
- CD178 _ Fas Ligand (103_281)
- Catalog number:
- FL101
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD178 _ Fas Ligand (103_281)
Related genes to: CD178 _ Fas Ligand (103_281)
- Gene:
- FASLG NIH gene
- Name:
- Fas ligand
- Previous symbol:
- APT1LG1, TNFSF6
- Synonyms:
- FasL, CD178
- Chromosome:
- 1q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-09
- Date modifiied:
- 2019-04-23
Related products to: CD178 _ Fas Ligand (103_281)
&_945;2&_946;1 Integrin Ligand Peptide(1R,2R)_(+)_1,2_Diaminocyclohexane_N, min. 94%rost ligand (na(1S,2S)_(+)_1,2_Cyclohexanediamino_N, (S,S)_Jacobsen ligand(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N min. 94% rost ligand (n(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N Rost ligand(2-Bromoethyl)benzene CAS: 103-63-9 Formula: C8H9Br(2_Bromoethyl)benzene beta_Bromoethylbenze(Ala286)-Calmodulin-Dependent Protein Kinase II (281-302) 98% C111H191N39O29S2 CAS:(Phenylthio)acetic acid Phenylmercaptoacetic(Tyr0)-Prepro-Atrial Natriuretic Factor (104-123) (human)
(Tyr0)-Kaliuretic Peptide (human), (Tyr0)-Prepro-Atrial Natriuretic Factor (103-122) (bovine), (Tyr0)-pro-hANF (79-98) 98% C103H180N32O30 C([125I]-Tyr)-Prepro-Neuromedin S (70-103) (human)([125I]-Tyr)-Prepro-Neuromedin S (70-103) (human), CE-marked, Lyophilized([125I]-Tyr)-Prepro-Neuromedin S (70-103) (human), CE-marked, Lyophilized([125I]-Tyr)-Prepro-NeuromedinS (70-103) (human)([125I]-Tyr)-Prepro-NeuromedinS (70-103) (human), CE-marked, Liquid Related articles to: CD178 _ Fas Ligand (103_281)
- One of the key hallmarks of aging is the age-related decline in immune system function, accompanied by a chronic low-grade inflammation, or "inflammaging". Simultaneously, a reduced capacity of immune cells to recognize and eliminate pathogens, along with immune exhaustion, is also defined as a sign of aging. Cynomolgus macaques () belong to a group of non-human primates evolutionarily close to humans and are often used for preclinical research. - Source: PubMed
Publication date: 2026/08/13
Petrova Viktoria MBulgin Dmitry VRadomskaya Elena YuShevelov Vsevolod AZhukova Darya SChzhu Olga PManakhov Andrey DPopov Alexander VRybtsov Stanislav A - Photodynamic priming (PDP), a fallout of photodynamic therapy, transiently modulates the tumor microenvironment (TME), enhances therapeutic susceptibility, and promotes immunogenic cell death through the release of damage-associated molecular patterns (DAMPs). Pancreatic ductal adenocarcinoma (PDAC) remains non-responsive to current therapies with a desmoplastic and immunosuppressive TME that limits drug delivery and blunts responses to immune checkpoint blockade. We investigated whether PDP could enhance anti-PD1 therapy responses in PDAC using patient-derived organoids (PDOs). PDOs were treated with Visudyne and red light (25, 75, and 100 J/cm²), followed by assessment of cytotoxicity, DAMP expression (HSP60, calreticulin, HMGB1), and transcriptomic changes. Monocyte-derived dendritic cells (mDCs) from healthy donors were cocultured with PDP-treated (25 J/cm) PDOs, then with matched naïve T cells. mDC and T cell activation markers were analyzed. Pembrolizumab (anti-PD1) was added to PDO-mDC-T cell cocultures to evaluate combined effects on PDO viability and T cell activation. PDP induced dose-dependent cytotoxicity and upregulated DAMPs. Gene profiling in PDOs showed increased , , and , with reduced , , and expression. mDCs exposed to PDP-treated PDOs upregulated CD40, CD86, and MHC-II, driving activation of CD4 and CD8 T cells, evidenced by elevated PD1 expression. Addition of pembrolizumab further decreased PDO viability and amplified effector cytokines (, , , B, , ). PDP was associated with modulation of the PDAC TME toward a more immunogenic phenotype by enhancing tumor immunogenicity, activating dendritic cells and T cells, and potentiating PD1 blockade. These findings provide mechanistic support for further preclinical and clinical evaluation of PDP combined with checkpoint inhibition in PDAC. - Source: PubMed
Publication date: 2026/08/11
De Silva PushpamaliWekking DemiChoe Joanna JoeunKidd Madeline DPearce Josie LRocha Castellanos Dario MissaelZelga PiotrJenkins RussellWang Kenneth KChandrasekhara VinayMaytin Edward VLiss Andrew ScottHasan Tayyaba - Colorectal cancer (CRC) remains a major global health burden, while current therapeutic strategies are often constrained by limited efficacy and adverse side effects. This study evaluated the anticancer activity and DNA-binding properties of a novel platinum-Mesalazine complex (Pt-MES) compared with Mesalazine (MES) in human CRC cells. Cytotoxicity was assessed using the MTT assay, gene expression was analyzed by qPCR, and drug-DNA interactions were investigated through viscosimetry, UV-visible spectroscopy, and molecular docking. Both compounds exhibited dose-dependent cytotoxicity; however, Pt-MES demonstrated superior antiproliferative activity, with a lower IC₅₀ value (2.694 µg/mL) than MES (3.503 µg/mL), indicating enhanced efficacy following platinum complexation. Gene expression analysis revealed that Pt-MES promoted apoptosis by upregulating FASLG, BAX, and miRNA-122, while suppressing Bcl-2, telomerase, and miRNA-21. In contrast, MES exerted weaker regulatory effects on these molecular targets. Biophysical studies showed a slight reduction in DNA viscosity accompanied by hyperchromic shifts in UV-visible spectra, suggesting a predominantly non-intercalative mode of DNA interaction. Molecular docking further supported preferential binding within the DNA minor groove. These findings indicate that Pt-MES may interact with DNA grooves and facilitate platinum coordination with nucleophilic sites, particularly guanine residues, leading to DNA structural perturbation and activation of apoptotic pathways. In addition, Pt-MES may influence key pathways implicated in CRC progression, including NF-κB, Wnt/β-catenin, and COX-2 signaling. Collectively, the results demonstrate that Pt-MES exhibits enhanced in vitro anticancer activity relative to MES and represents a promising multi-targeted candidate for further preclinical investigation in colorectal cancer. - Source: PubMed
Publication date: 2026/08/09
Ghasemi KimiyaSabokrouh AbdolrezaNoohi BahareModarresi Farrokh - - Source: PubMed
Tang MingxiangPan HongweiZheng ZhaofenGuo YinPeng JianqiangYang JunLuo YangpingHe JinYan SulanWang PengZhang YiZhou Yulu - Transcriptome analysis relies on intact RNA, and RNA integrity relies on intact cells. Death and cardiac arrest cause hypoxia and result in cell death and RNA fragmentation. Our study aims to systematically define the organ-specific post-mortem intervals (PMIs) at which RNA fragmentation has reached a level that hampers transcriptome analysis and at which apoptosis marker gene expression starts and reaches its maximum. A total of 453 biopsies were harvested from nine organs of seven body donors at 8, 10, 12, 18, and 24 hrs (h), and in four of them also at 6 h after confirmed death. From the livers, two biopsies were harvested. The material was used for calculating the percentage of RNA fragments > 200 nucleotides (DV200) and for determining the expression levels of marker genes of the intrinsic (BAX; CASP9) and extrinsic (FADD; FASLG; CASP8) apoptosis pathways. Additional material was collected from all organs and used for preparing histological sections. These were checked for pathologies. Detailed DV200 values and details of the expression levels of the selected genes of both apoptotic pathways are provided for each time point and organ. The DV200 and apoptosis marker expression levels of the different liver segments were almost identical. Our findings characterize post-mortem RNA fragmentation and the dynamics of apoptotic marker gene expression in nine organs. They define the time frame during which material harvested from these organs can be successfully used for transcriptomics projects, such as the Human Cell Atlas and similar programs. - Source: PubMed
Publication date: 2026/07/06
Baghrsad Sara SamanianMoghaddam Atieh SeyedianPruidze PaataHainfellner AndreasGeyer Stefan HWeninger Jeremias TBauer Stefan AMallik AromitaWeninger Wolfgang J