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Centromere protein T, abbreviated as CENPT, is an essential component of the inner kinetochore that plays a foundational role in chromosome segregation during cell division by mediating the assembly of the kinetochore complex and establishing kinetochore–microtubule interactions[1][2][7][9][10]. Centromere protein T (CENP-T) is a protein encoded by the *CENPT* gene and is a key component of the centromere–kinetochore complex in human cells[2][7][9]. CENP-T forms part of the heterotetramer_CENP-T-W-S-X complex, which binds centromeric DNA and organizes kinetochore nucleosomes[7][9]. It acts as a structural hub that physically links centromeric chromatin (where the histone H3 variant CENP-A is present) to downstream outer kinetochore components[2][10]. The N-terminal region of CENP-T recruits major outer kinetochore modules, including the MIS12 and NDC80 complexes, upon phosphorylation by cyclin-dependent kinases in mitosis; this enables microtubule–kinetochore attachment and is essential for accurate chromosome segregation[1][2][8][10]. CENP-T activity is tightly regulated during the cell cycle, with localization to centromeres established in late interphase independent of DNA replication, and functionally linked in parallel with CENP-C[4]. Loss or dysfunction of CENP-T disrupts kinetochore formation and chromosome segregation, leading to aneuploidy and cell death[1][7]. No drugs, biomarkers, or direct safety concerns are linked to CENP-T in current therapeutic practice; its roles are central to cell division machinery and it is not currently a recognized therapeutic target.
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