| 别名 | FAS;APT1;FAS1;TNFRSF6;Tumor necrosis factor receptor superfamily member 6;Apo-1 antigen;Apoptosis-mediating surface antigen FAS;FASLG receptor;CD antigen CD95 |
| 基因名称 | FAS |
| 蛋白名称 | Tumor necrosis factor receptor superfamily member 6 |
| 推荐应用 | |
| 反应物种 | Human, |
| 存储缓冲液 | PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA |
| Human Gene Link | 355 |
| Human Swissprot No. | P25445 |
| Mouse Swissprot No. | P25446 |
| 特异性 | endogenous |
| 稀释度 | IHC 1:200-1:1000;WB 1:1000-1:2500;IF 1:200-1:1000;ELISA 1:5000-1:20000;IP 1:50-1:200, |
| 参考分子量 | MW(Observed):40kD |
| 预测分子量 | MW(Calculated):38kD |
| 运输及保存条件 | -15°C to -25°C/1 year(Do not lower than -25°C) |
| 宿主 | Rabbit |
| 同种型 | IgG,Kappa |
| 背景介绍 | The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, s |
| 细胞定位 | Membranous |
| 功能 | Disease:Defects in FAS are the cause of autoimmune lymphoproliferative syndrome type 1A (ALPS1A) [MIM:601859]; also known as Canale-Smith syndrome (CSS). ALPS is a childhood syndrome involving hemolytic anemia and thrombocytopenia with massive lymphadenopathy and splenomegaly.,Domain:Contains a death domain involved in the binding of FADD, and maybe to other cytosolic adapter proteins.,Function:Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. The secreted isoforms 2 to 6 block apoptosis (in vitro).,online information:Mutations in TNFRSF6 causing ALPS type Ia,similarity:Contains 1 death domain.,similarity:Contains 3 TNFR-Cys repeats.,subunit:Binds DAXX. Interacts with HIPK3. Part of a complex containing HIPK3 and FADD (By similarity). Binds RIPK1 and FAIM2. Interacts with BRE and FEM1B.,tissue specificity:Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6., |
| 纯化 | Protein A |
| Clonality | Monoclonal |
| 修饰类型 | Unmodified |
| 细胞定位 | Membranous |
| 组织表达 | Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6. |
| 研究领域 | >>Platinum drug resistance;>>MAPK signaling pathway;>>Cytokine-cytokine receptor interaction;>>p53 signaling pathway;>>Apoptosis;>>Necroptosis;>>Natural killer cell mediated cytotoxicity;>>TNF signaling pathway;>>Non-alcoholic fatty liver disease;>>Alcoholic liver disease;>>Type I diabetes mellitus;>>Alzheimer disease;>>Pathways of neurodegeneration - multiple diseases;>>Pathogenic Escherichia coli infection;>>Chagas disease;>>African trypanosomiasis;>>Hepatitis C;>>Hepatitis B;>>Measles;>>Human cytomegalovirus infection;>>Influenza A;>>Human papillomavirus infection;>>Kaposi sarcoma-associated herpesvirus infection;>>Herpes simplex virus 1 infection;>>Epstein-Barr virus infection;>>Human immunodeficiency virus 1 infection;>>Pathways in cancer;>>Proteoglycans in cancer;>>Autoimmune thyroid disease;>>Allograft rejection;>>Graft-versus-host disease;>>Lipid and atherosclerosis |
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