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Centrosomal AT-AC splicing factor (CENATAC/CCDC84) is a protein that serves as a component of the minor (U12-dependent) spliceosome, specifically promoting the splicing of a rare subtype of minor introns known as A-type (AT-AN splice sites)[1][4]. Loss or mutation of CENATAC leads to retention of these minor introns in many genes, including those regulating nucleocytoplasmic transport and the cell cycle, resulting in chromosome segregation defects and aneuploidy, and is implicated in congenital chromosomal instability syndromes and microcephaly[1][4]. It is also a negative regulator of centrosome duplication, functioning by modulating the acetylation status and degradation of the centrosome-duplication factor HsSAS-6: deacetylated CENATAC promotes centrosome targeting, while acetylated CENATAC facilitates SASS6 proteasome degradation, thus controlling centriole number[6][2]. There are multiple transcript variants of this gene, indicating alternate splicing[4]. CENATAC is not recognized as a conventional therapeutic target (receptor, transporter, etc.), and there are currently no known drugs that directly interact with or modulate this protein. Its core roles are in RNA processing and cell division fidelity[1][4][6].
Not applicable (no drugs targeting CENATAC are described)
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