Identifying the translational targets of the shuttling protein, SRSF1, reveals that it is needed for normal cell division, and suggests that it couples pre-mRNA splicing and translation.

Aneuploidy can cause chromosome mis-segregation and specific cellular phenotypes driven by expression of genes on the extra chromosome.

To control centriole duplication, centriolar satellite proteins assemble a microcephaly-associated protein complex at the centrosome and activate cyclin-dependent kinase 2.

Ciliogenesis is regulated by a certain group of centriolar satellite proteins, among which an E3 ligase is tethered by PCM1 to maintain the normal level of pro-ciliogenic protein on centrioles.

Extensive periodic regulation of alternative splicing during the cell cycle in genes is linked to cell cycle functions, and involves an auto-inhibitory mechanism that uses the protein kinase CLK1.

TRIM37 prevents the formation of centriolar protein assemblies through an atypical de novo assembly pathway that would otherwise threaten genome integrity.

Analysis of mutant cells combined with biochemical experiments reveals that CEP78 is recruited to the centrosome by CEP350 and regulates ciliogenesis and ciliary length control through CP110-dependent and CP110-independent mechanisms, respectively.

5-Hydroxymethylcytosine-mediated active DNA demethylation occurs in postmitotic neurons, and is required for their terminal differentiation and function.

Genetically modified mouse model and comprehensive analysis reveal the molecular mechanisms regulating early T-cell development through intracellular TCRβ expression-mediated β-selection and independent cell survival signaling.

Genome-wide CRISPR screens in human cells identifies a role for TRIM37 in growth arrest after chemical inhibition of PLK4.