Phospho-Rad17 (Ser656)抗体;Phospho-Rad17 (Ser656) Antibody—艾普蒂

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     Western blot analysis of Rad17 (Phospho-Ser656) in Hela, Ramos lysates using Rad17 (Phospho-Ser656) antibody.    

  
  

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     Immunocytochemistry analysis of Phospho-Rad17 (Ser656) (green) in Hela using Phospho-Rad17 (Ser656) antibody,and DAPI(blue).    

  
  

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     Immunohistochemistry analysis of paraffin-embedded Human lung cancer tissue using Rad17 (Phospho-Ser656) antibody. High-pressure and temperature Sodium Citrate pH 6.0 was used for antigen retrieval.    

  
  

The Phospho-Rad17 (Ser656) antibody is a specialized tool used to detect Rad17 protein phosphorylated at serine residue 656. a post-translational modification critical for its role in DNA damage response and cell cycle regulation. Rad17. a key component of the Rad9-Rad1-Hus1 (9-1-1) complex-related family, functions as a checkpoint clamp loader. It facilitates the recruitment of DNA repair and signaling proteins to sites of genomic lesions, particularly during replication stress or ionizing radiation-induced damage. Phosphorylation of Rad17 at Ser656 is mediated by ATM/ATR kinases in response to DNA damage, marking its activation and promoting checkpoint signaling to halt cell cycle progression until repairs are completed.

This antibody is widely utilized in research to study the molecular mechanisms of DNA damage checkpoints, replication stress, and genomic stability. It helps assess Rad17 activation status in experimental models, including cancer cells, where dysregulated DNA repair pathways contribute to tumorigenesis or therapeutic resistance. Detection of phosphorylated Rad17 (Ser656) via Western blot, immunofluorescence, or immunohistochemistry provides insights into cellular responses to genotoxic agents, such as chemotherapy or radiation. Its specificity for the phosphorylated form makes it valuable for distinguishing active Rad17 from its inactive state, aiding in the exploration of checkpoint adaptation, apoptosis, and cancer biology. Proper validation using phosphorylation-deficient mutants or kinase inhibitors is recommended to confirm signal specificity.