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Centrosomal P4.1-associated protein (CPAP), encoded by the CENPJ gene, is a highly conserved component of the **centrosome** and a member of the **centromere protein family**[1][2][5]. It plays an essential structural role in **centriole biogenesis** and the strict regulation of **centriole length**, ensuring accurate duplication of centrosomes and maintenance of spindle morphology during mitosis[1][2][5]. CPAP acts by controlling microtubule nucleation and stabilization specifically at centrioles, modulating microtubule plus-end growth and preventing abnormal extension from centriolar ends[5]. It is also required for recruiting other key proteins to centrioles and enabling proper chromosome segregation[2][5]. Disruption of CPAP, due to genetic mutations, is associated with diseases such as **primary autosomal recessive microcephaly** and **Seckel syndrome**, characterized by reduced brain size and developmental disability[1][2][4]. Beyond its canonical roles, CPAP also participates non-canonically in **transcriptional co-activation** and **intracellular vesicular transport**—notably influencing the endocytic trafficking and lysosomal targeting of cell surface receptors such as EGFR, implicating it in broader cellular communication and homeostasis[3]. No approved drugs currently target CPAP directly, nor is it routinely used as a biomarker; defects in its function are primarily of interest in the context of rare neurodevelopmental disorders and basic cell biology[1][2][3][5].
no drugs targeting CPAP directly; mechanistic roles described in biological functions
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