FasL (tet_on)
- Known as:
- FasL (tet_on)
- Catalog number:
- 000134A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FasL (tet_on)
Related genes to: FasL (tet_on)
- 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: FasL (tet_on)
Related articles to: FasL (tet_on)
- Calcium Oxalate (CaOx) kidney stones with high recurrence are a major clinical and economic health burden. Randall's Plaques (RP) serve as a nidus for CaOx stones, but it remains poorly understood how renal interstitial hydroxyapatite (HAP) deposition erodes through the papillary urothelium to create sites for urinary CaOx crystal adherence. Here, it is observed loss of urothelium above interstitial HAP deposition, and revealed that Fas Ligand (FASLG) derived from renal interstitial fibroblasts (RIFs) in HAP-rich microenvironment induced anoikis of urothelium to trigger RP exposure to urine. Mechanistically, HAP interacted with membrane protein THY1 of RIFs, which increased the affinity of THY1 to SFRP1 but suppressed its affinity to NDP, leading to activation of GSK3α/β-β-catenin pathway and thus upregulating FASLG. Moreover, the upregulated FASLG is identified as the predictor for recurrence in patients with CaOx stones following lithotripsy. Furthermore, Benarthin, a small compound binding to THY1, is found to inhibit HAP-induced FASLG and thus attenuate the anoikis of urothelium in RP mice. It is anticipated that investigations of urothelial anoikis caused by FASLG from HAP-induced fibroblasts will offer novel insights into RP exposure, enabling preventive strategies for CaOx stone formation. - Source: PubMed
Publication date: 2026/04/02
Liu MinghuiWu MaolanGao MengLi YongchaoYuan MiaoLiao ZhangchengLiu ZhiWang YizhouCui YuChen JinboHe ChengChen ZhiyongZeng FengChen HequnZhu Zewu - Apoptosis and tumor suppression prevent cell proliferation in response to genomic damage. Polymorphisms in genes involved in these pathways can alter their function, facilitating the onset of cancer. Detecting these polymorphisms would assess the individual risk of developing different types of cancer. Therefore, the main goal of this study is to analyze the association between a set of genetic polymorphisms involved in apoptosis and tumor suppression and the risk of developing prostate cancer (PCa) in a population from Galicia. Accordingly, we performed a case-control study with 291 patients diagnosed with PCa and 249 healthy controls. A total of 19 genetic polymorphisms located in loci BCL2, CASP9, CASP8, CASP7, FAS, FASLG, BIRC5, TP53, MDM2, and MDM4 were genotyped. Their association with PCa was approached from a global perspective and stratified by the body mass index (BMI). Globally, a statistically significant association with PCa was found for polymorphisms rs1052576 (CASP9) and rs990431 (BIRC5), with carriers of the G allele (OR = 2.14; p = 0.002) or the CC genotype (OR = 1.92; p = 0.037), respectively, manifesting greater susceptibility to the disease. The analyses stratified by BMI yielded statistically significant results for polymorphisms rs1052576 (CASP9), rs3740286 (FAS), rs9904341 (BIRC5), rs2279744 (MDM2), rs937283 (MDM2), and rs1380576 (MDM4), with odds ratios between 2.47 and 8.00 in overweight or obese participants. These results indicate the differential effect of allelic variants of six SNPs on prostate cancer risk in patients with overweight or obesity. Further studies in larger cohorts should be conducted to confirm these findings. - Source: PubMed
Publication date: 2026/03/31
López-Trigo NCaeiro BPérez-Pérez JRodríguez-Alonso AAguín NRodríguez J ALuis J R - Bioinformatics analysis. - Source: PubMed
Publication date: 2026/02/27
Wang ZhengSun HaojunLiu BinWang YuWang DanniHan Wenfeng - FAS/FAS-ligand (FAS-L) complex is implicated in critical cell functions including programmed cell death (apoptosis) and immune response regulation. FAS and FAS-ligand are members of the tumor necrosis factor (TNF) superfamily. Their activation triggers the caspase-mediated apoptotic cataract. The aim of this study was to investigate the role of their altered co-expression in a series of laryngeal squamous cell carcinomas (LSCCs). - Source: PubMed
Athanasopoulos MichailPapanikolaou VasileiosRoukas DimitriosChrysovergis AristeidisPapanastasiou GeorgiosAdamopoulou MariaMetaxas Ioanna ETsiambas EvangelosTsouvelas GeorgiosMastronikolis NicholasKyrodimos EythimiosKavantzas NikolaosAgrogiannis Georgios - The ecological and health risks of 6PPDQ (N-(1,3-Dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone) have raised significant concerns. We recently demonstrated that the Aryl Hydrocarbon Receptor (AhR) mediates 6PPDQ-caused extrinsic apoptosis and heart defects; however, the underlying molecular pathways remain elucidated. In this study, we observed that inhibition of Protein Kinase A (PKA) effectively mitigated 6PPDQ-caused apoptosis and cardiac dysfunction in zebrafish larvae. Subsequent experiments revealed significant increases in both PKA levels and cyclic adenosine monophosphate (cAMP) concentrations within the hearts of zebrafish embryos exposed to 6PPDQ. Notably, pharmacological inhibition or genetic knockdown of AhR abolished 6PPDQ-induced PKA overexpression. Dual-luciferase reporter assays indicated that AhR activation by 6PPDQ directly enhance the transcription of adcy6a, which encodes an adenylate cyclase (AC) isoform predominately expressed in the heart of zebrafish. Inhibition of β-adrenergic receptors did not significantly influence the AC/cAMP/PKA cascade. Furthermore, exposure to 6PPDQ induced phosphorylation of cAMP response element-binding protein (CREB), an effect that was mitigated by PKA inhibition. Activated CREB subsequently promoted the expression of Fos, a component of the activator protein-1 (AP-1) transcription factor family. Inhibition of Fos (AP-1) counteracted the 6PPDQ-induced overexpression of fas and faslg, as well as the subsequent extrinsic apoptosis. In conclusion, our findings indicate that AhR activation by 6PPDQ triggers AC/cAMP/PKA cascade through direct transcriptional upregulation of adcy6a. PKA-mediated phosphorylation of CREB then facilitates the overexpression of fas and faslg via AP-1, resulting in extrinsic apoptosis and cardiac defects. - Source: PubMed
Publication date: 2026/02/04
Zhai MengyaLi JinhaoZhang MingxuanYang XinyueGan QianqianJiang YanChen Tao