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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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     Western blot analysis using PLAU mouse mAb against PC-3 (1),MCF-7 (2), LNCap (3),DU145 (4),HCT116 (5),A549 (6),SK-OV-3 (7) and HEK293 (8) cell lysate.    

  
  

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     Immunofluorescence analysis of Hela cells using PLAU mouse mAb (green). Blue: DRAQ5 fluorescent DNA dye. Red: Actin filaments have been labeled with Alexa Fluor- 555 phalloidin. Secondary antibody from Fisher (Cat#: 35503)    

  
  

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

  
  

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     Flow cytometric analysis of HepG2 cells using PLAU mouse mAb (green) and negative control (red).    

  
  

TNFRSF1B (tumor necrosis factor receptor superfamily member 1B), also known as TNFR2. is a transmembrane receptor that binds tumor necrosis factor-alpha (TNF-α) and mediates its inflammatory and immunomodulatory signaling. It belongs to the TNF receptor superfamily and shares structural features, including cysteine-rich domains (CRDs) in its extracellular region. Unlike TNFR1 (TNFRSF1A), which is ubiquitously expressed and linked to pro-apoptotic pathways, TNFR2 is primarily expressed on immune cells (e.g., T cells, macrophages) and certain non-immune cells, playing a role in cell survival, proliferation, and tissue regeneration. Its activation triggers signaling cascades, such as NF-κB and MAPK pathways, often counterbalancing TNFR1-driven inflammation.

Antibodies targeting TNFRSF1B are research tools or therapeutic candidates designed to modulate TNFR2 activity. In cancer, anti-TNFR2 antibodies may block receptor-ligand interactions to inhibit immunosuppressive regulatory T cells (Tregs) or tumor cell survival. Conversely, agonist antibodies might enhance anti-tumor immunity by stimulating effector T cells. In autoimmune diseases, inhibiting TNFR2 could reduce chronic inflammation, while in neurodegenerative disorders, activating TNFR2 might promote neuroprotection. Challenges include ensuring receptor specificity to avoid cross-reactivity with TNFR1 and balancing pro- vs. anti-inflammatory effects. Current research focuses on understanding TNFR2's dual roles and optimizing antibody-based therapies for precision targeting.