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Cyclin-dependent kinase 2-interacting protein (CINP) is a chromatin-associated protein that acts as a component of the DNA replication complex, physically and functionally linking CDK2 and CDC7 during the origin firing step of DNA replication[2]. It regulates ATR-mediated checkpoint signaling in response to DNA damage, and functions in maintaining replication fork progression, sister chromatid cohesion, and chromosome stability[2]. CINP also participates in the 55LCC heterohexameric ATPase complex to promote replisome proteostasis and ribosomal large subunit biogenesis[2][4][5]. Loss-of-function mutations have been linked with syndromes such as microcephaly and Seckel syndrome[2]. CINP is not considered a direct therapeutic target or receptor such as a kinase, receptor, or enzyme; rather, it serves as a protein-protein interaction partner and scaffolding factor in DNA replication and genome maintenance[2][4]. There are currently no known drugs that directly target CINP, nor is it established as a clinical biomarker or primary disease driver[2].
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