STIL centriolar assembly protein (STIL)

STIL centriolar assembly protein (STIL) is a cytoplasmic protein crucial for centriole replication and for de novo centriole biogenesis, which is essential during mammalian embryogenesis[1]. It regulates the mitotic spindle checkpoint to monitor chromosome segregation, ensuring proper distribution of chromosomes during cell division, and is required for activating the spindle checkpoint through its interaction with mitotic regulators. STIL has fundamental roles in cell cycle progression, cell proliferation, and embryonic development. Loss-of-function mutations in STIL are linked to autosomal recessive primary microcephaly (MCPH7), and chromosomal deletions involving STIL are seen in some forms of T-cell leukemia[2][3]. At a molecular level, STIL interacts with other centriolar proteins such as CPAP and PLK4, participating in the assembly and duplication of centrioles via its coiled-coil domain[1][3]. No approved drugs directly target STIL, but its genetic alterations function as disease biomarkers in some contexts[2][3].

Other names

SCL-interrupting locus proteinSILMCPH7TAL-1-interrupting locus proteinSCL/TAL1 interrupting locusSTIL_HUMANSCL-interrupting locusSTIL

Not applicable for drugs, as no direct pharmacological modulators are known.