Target intelligence / Profile preview

Centrosomal P4.1-associated protein (CPAP)

Target
CPAP
Molecular classification
Other (centrosomal structural protein, centromere protein family)
01

Overview

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].

Other names
Centromere protein JCENPJSASS4SAS-4MCPH6BM032LIP1LAPSCKL4Seckel syndrome 4Spindle assembly abnormal 4LYST-interacting protein 1
02

Mechanism of action

no drugs targeting CPAP directly; mechanistic roles described in biological functions

03

Biological functions

Centriole biogenesis and duplicationRegulation of centriole lengthMaintenance of centrosome integrityMicrotubule organization and stabilizationSpindle formation and function during mitosisMicrotubule disassembly at centrosomeTranscriptional coactivator in STAT5 and NF-κB signaling pathwaysEndocytic vesicular transport and lysosome targeting of surface receptors (e.g., EGFR)
04

Disease associations

Primary autosomal recessive microcephalySeckel syndromeNeurodevelopmental disorders(Evidence for potential links to cancer through centrosome and mitotic defects, but not established as a canonical cancer biomarker or target)
05

Safety considerations

Mutations can cause severe neurodevelopmental phenotypes (e.g., microcephaly, Seckel syndrome)Disruption leads to defective cell division, abnormal spindle assembly, and genomic instabilityNo direct targeting, so no drug-specific toxicity data

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