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     The image is immunohistochemistry of paraffin-embedded Human esophagus cancer tissue using P10417(CCNI Antibody) at dilution 1/65. (Original magnification: ×200)    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human colorectal cancer tissue using P10417(CCNI Antibody) at dilution 1/65. (Original magnification: ×200)    

  
  

CCNI (Cyclin I) is a member of the cyclin protein family, known for regulating cell cycle progression by interacting with cyclin-dependent kinases (CDKs). Unlike classical cyclins such as Cyclin D or B, Cyclin I exhibits distinct expression patterns and functional roles. It is primarily expressed in post-mitotic cells, including neurons and kidney podocytes, suggesting involvement in non-proliferative processes. Studies reveal that Cyclin I forms complexes with CDK5. a kinase linked to neuronal signaling and survival, rather than canonical cell cycle CDKs. This interaction is critical for modulating apoptosis; Cyclin I overexpression inhibits caspase activation, enhancing cell survival under stress conditions like oxidative damage or DNA injury.

Research highlights its role in neurodegenerative diseases and kidney disorders. For instance, reduced Cyclin I levels correlate with increased neuronal death in Alzheimer's disease models, while mutations are implicated in glomerular dysfunction. CCNI antibodies, essential tools in these studies, enable detection of Cyclin I expression in tissues and cell lines, facilitating investigations into its molecular mechanisms. They are widely used in Western blotting, immunohistochemistry, and co-immunoprecipitation assays to explore Cyclin I-CDK5 interactions and downstream pathways. Recent interest also focuses on its potential as a therapeutic target or biomarker in diseases marked by dysregulated apoptosis. Despite progress, questions remain about its tissue-specific regulation and broader signaling networks.