Anti_Mouse, mab TNFSF6 Source Rat
- Known as:
- Anti_Mouse, mab TNFSF6 Source Rat
- Catalog number:
- 103-M495
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab TNFSF6 Source Rat
Related genes to: Anti_Mouse, mab TNFSF6 Source Rat
- 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: Anti_Mouse, mab TNFSF6 Source Rat
Related articles to: Anti_Mouse, mab TNFSF6 Source Rat
- The OSCs population in postnatal chickens is a potential reservoir for follicular renewal, however, the signals that regulate OSC maintenance and expansion are not well understood. Here, we identify anti-Müllerian hormone (AMH) as a key mitogen for chicken OSCs and define its signaling mechanism. Following the successful isolation and characterization of OSCs from adult hens, we found that these cells exhibit a distinctive hormonal receptor profile: they highly express the AMH type II receptor (AMHR2) while showing negligible expression of canonical gonadotropin receptors (FSHR, LHR) and estrogen receptors (ESR1, ESR2). Functionally, AMH robustly stimulated OSCs proliferation in both culture and ex vivo ovarian explants. Transcriptomic analysis revealed that AMH treatment alters the expression of 305 genes, coordinating the activation of major pro-proliferative pathways-including ErbB, mTOR, and Wnt signaling-and concurrently suppressing apoptotic and necroptotic pathways. This effect is mediated through phosphorylation of Smad1/5/8 without affecting their mRNA or total protein levels. Critically, pharmacological inhibition of Smad1/5/8 phosphorylation completely blocked AMH-induced proliferation and reversed the AMH-driven upregulation of proliferative genes (MYC, EGR4, CDK1, BLK) as well as the downregulation of the pro-apoptotic gene FASLG. Our results establish a novel, pro-proliferative role for AMH in avian ovarian biology, operating through a conserved AMH expand the OSCs pool by dual regulation of cell cycle and survival pathways. This work reframes AMH's physiological role beyond its classical function in follicle recruitment and offers new insights into the hormonal control of OSCs, with implications for enhancing reproductive longevity in poultry. - Source: PubMed
Publication date: 2026/05/20
Sun QingYu ChanghaoSun HongcaiHao JinguiLi ZhenyaMa YuxiaoWang JinZhu Guiyu - Cancer remains a major public health challenge worldwide. Tumor reprogramming has emerged as a novel therapeutic strategy for cancer treatment. However, despite increasing interest in this approach, whether tumor cells can be stably and efficiently reprogrammed into cytotoxic effector cells remains unclear. Here, we engineered multiple types of tumor cells to overexpress T cell effectors including IFNG, FASLG, or PRF1/GZMB and evaluated their cytotoxic potential. We found that tumor cells engineered to overexpress these genes can inhibit cell autonomous proliferation in vitro. Co-culture assays showed that overexpression of IFNG or FASLG enabled tumor cells to kill neighboring tumor cells, whereas PRF1/GZMB overexpression had no such effect. However, the cytotoxic effect mediated by IFNG overexpression was much stronger than that mediated by FASLG overexpression. Moreover, IFNG overexpressing tumor cells suppressed the growth of wild-type tumor cells without evident toxicity in vivo. These findings establish a potent strategy for reprogramming tumor cells to acquire tumor-killing activity and suggest a potential new direction for cancer therapies. - Source: PubMed
Publication date: 2026/05/14
Li HaoyangZhu YunfeiHao YanHu QinlinMa QiongqiongLi JiarongSun YangyangHou YintingZhang RuixingHong ZhangyongLiang HuabinFu XueliZhang Hongru - 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 - Hyperglycemia exacerbates cerebral ischemia/reperfusion (I/R) injury, apoptosis pathways playing a key role. Sodium selenite (SE) exhibits neuroprotective effects, however, whether the Fas/FasL/PUMA pathway is involved in this neuroprotective effects remains unclear. For help to make this clear, hyperglycemic-aggravated cerebral I/R models (SD rats) and in vitro high-glucose oxygen deprivation/reoxygenation (OD/R) models (HT22 cells) were applied in this study. This study showed that the cerebral infarct volume and neuronal damages in the hyperglycemic I/R rat indeed were alleviated by the selenite treatment. And the lost neurological functions were improved by selenite treatment also. In the HT22 cells, the SE treatment enhanced viability and reduced reactive oxygen species (ROS) accumulation. Mechanistically, this study showed that the SE treatment downregulated the expressions of Fas, FasL, p-NF-κB, PUMA, Cleaved Caspase-3, and Cytochrome c, while increased the Bcl-2/Bax expression ratio. The SE's anti-apoptotic effects were potentiated by PUMA knockdown or autophagy inhibitor 3-MA co-treatment. These findings confirm that SE alleviates hyperglycemia-exacerbated cerebral I/R injury by inhibiting the Fas/FasL/PUMA apoptotic pathway, providing a therapeutic strategy for hyperglycemia ischemic stroke. CONCLUSION: Sodium selenite alleviates hyperglycemia-exacerbated cerebral I/R injury by modulating the Fas/FasL/PUMA signaling pathway. SIGNIFICANCE STATEMENT: The finding that sodium selenite alleviates hyperglycemia - exacerbated cerebral I/R injury by modulating the Fas/FasL/PUMA signaling pathway advances knowledge in neuroscience by revealing a novel mechanism through which a compound can mitigate the harmful effects of hyperglycemia on cerebral I/R injury, and it deepens our understanding of how apoptotic pathways in the nervous system can be regulated to protect against such injuries. - Source: PubMed
Publication date: 2026/04/26
Yang LanDing FengYin XidaZhao ShuaiChang YueZhang JingwenHuang NingboWang WenjunJing Li - 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