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TopBP1-interacting checkpoint and replication regulator (TICRR), also known as Treslin, is a chromatin-associated protein essential for the initiation of DNA replication and regulation of cell cycle checkpoints, especially the S/M and G2/M transitions[1][2][4][5][6]. TICRR forms a stable complex with TopBP1, facilitating the transition from the pre-replication complex (pre-RC) to the pre-initiation complex (pre-IC) by regulating origin firing at the beginning of S phase[2][4][5][6]. Loss or depletion of TICRR disrupts DNA replication, impairs the assembly of pre-IC, and abrogates checkpoint activation, leading to premature mitotic entry with incompletely replicated genomes and mitotic catastrophe[2][5][1]. TICRR is overexpressed in various human cancers, correlating with poor prognosis, and its depletion suppresses tumor cell proliferation and survival, highlighting its potential as a prognostic biomarker and therapeutic target in oncology[3][7].
Not applicable (no drugs currently reported that selectively target TICRR); theoretical: inhibition of TICRR could suppress cancer cell proliferation by inducing DNA replication defects and checkpoint activation leading to apoptosis
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