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TIMELESS-interacting protein (TIPIN) is a nuclear protein essential for the integrity of DNA replication and cell cycle checkpoints, especially under conditions of replication stress[1][2][3]. TIPIN forms a stoichiometric complex with TIMELESS, together operating as a key sensor and effector in the maintenance and stability of replication forks, associating with components of the replicative helicase (MCM complex) and with Replication Protein A (RPA) during stress[1][3]. Loss of TIPIN leads to defects in checkpoint signaling, genomic instability, increased sensitivity to DNA damage, cell cycle arrest deficiencies, and higher rates of apoptosis—making TIPIN a critical factor in genome maintenance and a potential therapeutic target in oncology contexts[1][3][4]. Aliases and orthologs include "CSM3 homolog" (in yeast), reflecting conservation of function across eukaryotes[1]. Currently, no approved drugs target TIPIN directly, nor is it used as a clinical biomarker, but decreased TIPIN expression promotes apoptosis in cancer cell models and may implicate it in disease susceptibility and therapy response[4].
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