CINP (Cyclin-Dependent Kinase 2-Interacting Nuclear Protein) is a nuclear protein involved in cell cycle regulation, particularly during the G1/S transition. It interacts with CDK2 and plays a role in DNA replication initiation by aiding the loading of replication factors onto chromatin. Dysregulation of CINP has been implicated in genomic instability and cancer progression.
Anti-CINP antibodies are primarily used as research tools to study its expression, localization, and functional interactions in cellular models. They enable detection via techniques like Western blotting, immunofluorescence, and immunoprecipitation. In clinical contexts, autoantibodies targeting CINP have been identified in certain autoimmune conditions, such as systemic lupus erythematosus (SLE) and Sjögren's syndrome, though their pathogenic role remains unclear. These autoantibodies may serve as biomarkers for disease stratification or activity monitoring.
Recent studies also explore CINP's potential role in neurodegenerative diseases, given its interaction with proteins linked to DNA repair and neuronal survival. However, the exact mechanisms and therapeutic implications require further investigation. Commercially available CINP antibodies are typically validated for specificity across human, mouse, and rat samples, supporting cross-species translational research. Ongoing research aims to clarify CINP's dual roles in both physiological processes and disease pathways.