TNFRSF11A抗体—艾普蒂

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     Black line: Control Antigen (100 ng);Purple line: Antigen (10ng); Blue line: Antigen (50 ng); Red line:Antigen (100 ng)    

  
  

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     Flow cytometric analysis of Hela cells using TNFRSF11A mouse mAb (green) and negative control (red).    

  
  

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     Flow cytometric analysis of HL-60 cells using TNFRSF11A mouse mAb (green) and negative control (red).    

  
  

TNFRSF11A (tumor necrosis factor receptor superfamily member 11A), also known as RANK (receptor activator of nuclear factor kappa-B), is a transmembrane receptor primarily involved in regulating osteoclast differentiation, bone remodeling, and immune cell activation. It binds to its ligand RANKL (RANK ligand), initiating signaling cascades that influence bone metabolism, lymph node development, and thermoregulation. Dysregulation of the RANKL/RANK/OPG (osteoprotegerin) axis is implicated in osteoporosis, rheumatoid arthritis, bone metastases, and rare genetic disorders like familial expansile osteolysis.

TNFRSF11A antibodies are essential tools for studying this receptor’s expression, signaling, and pathological roles. Polyclonal and monoclonal antibodies targeting specific extracellular or intracellular domains are used in techniques like Western blot, immunohistochemistry (IHC), and flow cytometry to detect RANK expression in tissues or cells. Researchers also employ blocking antibodies to inhibit RANKL-RANK interactions, elucidating their functional roles in bone resorption or cancer progression.

Clinically, anti-RANKL therapies (e.g., denosumab) mimic antibody mechanisms to treat bone loss, but direct TNFRSF11A antibodies remain investigational. Their development faces challenges, including balancing therapeutic efficacy with potential immune-related side effects. Ongoing research explores their utility in targeting RANK-expressing cancer cells or modulating immune responses in autoimmune diseases.