NUBP2抗体—艾普蒂

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     Gel: 12%SDS-PAGE, Lysate: 40 μg, Lane: Human Bladder transitional cell carcinoma grade 2-3 tissue lysate, Primary antibody: P02637(NUBP2 Antibody) at dilution 1/300, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 1 minute    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human breast cancer tissue using P02637(NUBP2 Antibody) at dilution 1/25. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human esophagus cancer tissue using P02637(NUBP2 Antibody) at dilution 1/25. (Original magnification: ×200)    

  
  

The NUBP2 (Nucleotide-Binding Protein 2) antibody is a tool used to study the NUBP2 protein, a member of the cytosolic iron-sulfur cluster assembly (CIA) machinery. NUBP2. along with its homolog NUBP1. forms a heterotetrameric complex critical for the maturation and transfer of iron-sulfur (Fe-S) clusters to target apoproteins, which are essential for diverse cellular processes, including DNA repair, enzyme catalysis, and mitochondrial function. Dysregulation of NUBP2 has been implicated in diseases such as cancer and neurodegenerative disorders, where Fe-S cluster biogenesis is compromised.

The NUBP2 antibody is typically developed in hosts like rabbits or mice using immunogenic peptides or recombinant protein fragments. It is widely employed in techniques such as Western blotting, immunohistochemistry (IHC), and immunofluorescence (IF) to detect NUBP2 expression levels, localization, and interactions in cell lines or tissues. Researchers use this antibody to explore NUBP2's role in cellular proliferation, redox homeostasis, and mitochondrial dynamics. Specificity is validated via knockout/knockdown controls or siRNA experiments. Commercial NUBP2 antibodies are often accompanied by validation data (e.g., species reactivity, application suitability) to ensure reproducibility. Studies utilizing this antibody have contributed to understanding molecular mechanisms underlying cancer progression, particularly in contexts where Fe-S cluster deficiency drives genomic instability or metabolic reprogramming.