Tumor Necrosis Factor Ligand Superfamily Member 6 (CD178) Antibody (PE)
429€ (100 tests)
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935106861
info@markelab.com
name
Tumor Necrosis Factor Ligand Superfamily Member 6 (CD178) Antibody (PE)
category
Primary Antibodies
provider
Abbexa
reference
abx139055
tested applications
FCM
Description
CD178 Antibody is a Mouse Monoclonal against CD178.
Documents del producto
Instrucciones
Data sheet
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Tumor Necrosis Factor Ligand Superfamily Member 6 (CD178) |
| Host | Mouse |
| Reactivity | Human |
| Recommended Dilution | FCM: 10 µl/100 µl of whole blood or 106 cells. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Monoclonal |
| Conjugation | PE |
| Isotype | IgG1 |
| Clone ID | U373 |
| Size 1 | 100 tests |
| Tested Applications | FCM |
| Buffer | Stabilizing PBS solution containing 15 mM sodium azide. |
| Availability | Shipped within 5-12 working days. |
| Storage | Store in the dark at 2-8°C. Avoid exposure to light. Do not freeze. |
| Dry Ice | No |
| UniProt ID | P48023 |
| Gene ID | 356 |
| Alias | Tumor necrosis factor ligand superfamily member 6,APTL,FASL,CD178,CD95L,ALPS1B,CD95-L,TNFSF6,TNLG1A,APT1LG1,Apoptosis antigen ligand,Fas antigen ligand |
| Background | Antibody anti-FASLG |
| Status | RUO |
Descripción
Fas Ligand (FASLG), also referred to as CD95L, is a type-II transmembrane protein belonging to the tumor necrosis factor (TNF) family. FASLG plays a pivotal role in regulating apoptosis, particularly in immune system homeostasis and cytotoxic T-cell-mediated killing. It binds to its receptor, Fas (CD95), triggering the formation of the death-inducing signaling complex (DISC) and initiating the caspase cascade, ultimately leading to programmed cell death. This pathway is crucial for eliminating autoreactive lymphocytes, maintaining immune tolerance, and resolving immune responses after infections. Dysregulation of FASLG-Fas signaling has been implicated in various pathological conditions, including autoimmune disorders, cancer, and chronic inflammatory diseases. In cancer, tumor cells often evade apoptosis by downregulating Fas or mutating components of the pathway. Conversely, overexpression of FASLG in the tumor microenvironment can contribute to immune evasion by inducing apoptosis in Fas-expressing tumor-infiltrating lymphocytes. Therapeutic strategies targeting FASLG or its signaling pathway are being explored for their potential in cancer immunotherapy, autoimmune disease modulation, and transplantation tolerance. Additionally, genetic polymorphisms in the FASLG gene have been associated with altered susceptibility to diseases, further highlighting its importance in immune regulation and disease pathology.
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