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Our data suggest a model whereby SPATA5, C1ORF109, SPATA5L1, and CINP cooperate to promote the recycling of RSL24D1 off of cytoplasmic pre-60S subunits back to the nucleolus, thereby promoting 60S maturation. In the absence of these factors, this recycling is disrupted, resulting in the aberrant cytoplasmic retention of RSL24D1 and a decrease in fully functional 60S ribosomal subunits.
