CFHR1抗体

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     Gel: 10%SDS-PAGE, Lysate: 40 μg, Lane: Human liver cancer tissue, Primary antibody: P07337(CFHR1 Antibody) at dilution 1/300, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 30 seconds    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human brain tissue using P07337(CFHR1 Antibody) at dilution 1/40. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human tonsil tissue using P07337(CFHR1 Antibody) at dilution 1/40. (Original magnification: ×200)    

  
  

**Background of CFHR1 Antibody**

The CFHR1 (Complement Factor H-Related 1) protein, encoded by the *CFHR1* gene on chromosome 1. is part of the complement factor H (CFH) protein family involved in regulating the alternative complement pathway. Structurally similar to CFH, CFHR1 contains conserved domains (SCRs) that mediate interactions with complement components and host cell surfaces. While its precise biological role remains debated, CFHR1 is implicated in fine-tuning complement activation, potentially competing with CFH to modulate C3 convertase activity or binding to damaged cells.

CFHR1 antibodies, either therapeutic or autoantibodies, have gained attention in autoimmune and kidney diseases. Autoantibodies targeting CFHR1 are associated with atypical hemolytic uremic syndrome (aHUS) and lupus nephritis, where they may disrupt complement regulation, leading to uncontrolled activation and tissue injury. Conversely, monoclonal anti-CFHR1 antibodies are explored as therapeutic tools to block pathogenic complement activation in diseases like age-related macular degeneration.

Research also links *CFHR1* gene deletions or mutations to autoimmune conditions, suggesting CFHR1's role in immune homeostasis. Assays detecting CFHR1 antibodies (e.g., ELISA) aid in diagnosing autoimmune complement disorders. Ongoing studies aim to clarify CFHR1's functional mechanisms and therapeutic potential, highlighting its dual role as both a target and modulator in complement-driven pathologies.