Hamster Anti-Mouse CD178
- Known as:
- Hamster Antibody toMouse CD178
- Catalog number:
- 129-10107
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Hamster Anti-Mouse CD178
Related genes to: Hamster Anti-Mouse CD178
- 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: Hamster Anti-Mouse CD178
Related articles to: Hamster Anti-Mouse CD178
- Vesicular cutaneous lupus erythematosus (VCLE) is a rare autoimmune disease in dogs and is considered the canine counterpart of human subacute cutaneous lupus erythematosus (SCLE). However, the molecular mechanisms underlying VCLE remain incompletely defined. - Source: PubMed
Publication date: 2026/05/11
Keating TreasaStranahan LaurenWiener DominiqueKeating M KellyLeon RenatoBanovic Frane - Glioblastoma (GBM), a rare, highly aggressive and chemoresistant brain cancer, exhibits profound metabolic plasticity that relies, in part, on aberrant transforming growth factor-β (TGF-β) signaling. Such plasticity was recently associated with TGF-β-regulated apoptosis and autophagy. Here, we questioned whether TGF-β-regulated apoptotic/autophagic phenotypes are recapitulated in a preclinical in vitro 3D spheroid culture model of human U87 GBM-derived cells, and how metabolic alterations affect such phenotypes. - Source: PubMed
Publication date: 2026/03/30
Payet-Desruisseaux MaellisZgheib AlainDanalache Bogdan AlexandruDesjarlais MichelAnnabi Borhane - Metastatic breast cancer (mBC) remains a major therapeutic challenge. Increasing evidence suggests that metastatic dissemination and resistance to treatment are sustained by systemic immune dysfunction and vascular remodeling. Yet, the underpinning mechanisms remain incompletely understood. Therefore, we applied a multilayered liquid biopsy strategy to characterize the systemic immunovascular landscape of mBC and identify clinically actionable circulating biomarkers of disease progression and risk stratification. - Source: PubMed
Publication date: 2026/04/18
Kurma KeerthiBardol ThomasMollevi CarolineEslami-S ZahraGarima FrançoiseAlexandre MarieBobrie AngéliqueLossaint GeraldMassemin BlandineD'Hondt VéroniqueGuiu SéverineCayrefourcq LaureJacot WilliamAlix-Panabières Catherine - The discovery of heterozygous germline mutations in FAS 30 years ago led to an understanding of the pathophysiology associated with familial forms of autoimmune lymphoproliferative syndrome (ALPS). Ten years later, the identification of somatic mutations in FAS was the first description of an acquired mutation in a non-cancerous disease. It was subsequently observed that haploinsufficient germline mutations are accompanied by a somatic mutation in the second FAS allele or by somatic loss of heterozygosity. More recently, germline and combined mutations in FADD have also been described in ALPS. In contrast, mutations in other proteins of the signaling pathway, such as caspases 8 and 10, do not appear to be associated with ALPS. Finally, biallelic mutations in the FAS ligand (FASLG) can also lead to an ALPS phenotype. In all these genetic forms of ALPS, hyperactivation of the mTOR pathway, observed in animal models and subsequently in humans, has demonstrated the efficacy of mTOR inhibitors as a standard treatment for ALPS. Since the discovery of FAS in ALPS, mutations in numerous other genes (CTLA4, LRBA, STAT3) have been described in patients presenting with ALPS symptoms combined with signs of immunodeficiency. It has been proposed to distinguish these monogenic ALPID disorders to avoid confusing them with ALPS, which is specifically associated with a defect in the FASLG/FAS pathway. - Source: PubMed
Publication date: 2026/04/15
Rieux-Laucat Frédéric - 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