BNIP1抗体—艾普蒂

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     Gel: 12%SDS-PAGE, Lysate: 40 μg, Lane 1-3: Jurkat cells, A172 cells, human liver cancer tissue, Primary antibody: P07042(BNIP1 Antibody) at dilution 1/275, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 10 seconds    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human esophagus cancer tissue using P07042(BNIP1 Antibody) at dilution 1/30. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human thyroid cancer tissue using P07042(BNIP1 Antibody) at dilution 1/30. (Original magnification: ×200)    

  
  

BNIP1 (Bcl-2/adenovirus E1B 19 kDa-interacting protein 1) is a member of the pro-apoptotic BNIP protein family, which shares homology with the Bcl-2 family in the BH3 domain. It is primarily localized to the endoplasmic reticulum (ER) and mitochondria-associated membranes (MAMs), where it interacts with Bcl-2 and E1B-19K proteins to regulate apoptosis and ER stress responses. BNIP1 is implicated in ER membrane fusion processes through its interaction with syntaxin-18. a SNARE protein critical for vesicle trafficking. Dysregulation of BNIP1 expression has been linked to neurodegenerative diseases, cancer, and hypoxia-related pathologies, as it modulates cell survival under stress conditions.

Antibodies targeting BNIP1 are essential tools for studying its expression, localization, and functional roles. They are widely used in techniques like Western blotting, immunohistochemistry, and immunofluorescence to investigate BNIP1's involvement in apoptosis, autophagy, and cellular adaptation to hypoxia. Commercial BNIP1 antibodies are typically developed in rabbits or mice, validated for specificity against human, mouse, or rat samples. Research utilizing these antibodies has highlighted BNIP1's dual role—promoting apoptosis under certain stresses while supporting cell survival in others—making it a potential therapeutic target. Recent studies also explore its crosstalk with mitochondrial pathways and implications in tumor progression, emphasizing its context-dependent regulatory mechanisms.