Tag: Survivin

Aurora C kinase is a germ‑cell‑enriched member of the Chromosomal Passenger Complex that safeguards meiotic chromosome segregation. By regulating kinetochore–microtubule interactions and cytokinesis, Aurora C ensures gamete quality and genomic stability. Its dysregulation contributes to infertility and tumour progression.

Aurora B kinase is the catalytic core of the Chromosomal Passenger Complex, ensuring accurate chromosome segregation, correcting kinetochore–microtubule attachment errors and coordinating cytokinesis. Its central role in mitotic fidelity and frequent dysregulation in cancer make Aurora B a major therapeutic target.

Borealin (CDCA8) is the structural stabiliser of the Chromosomal Passenger Complex. By anchoring Aurora B, INCENP and Survivin to centromeres and guiding CPC relocation to the spindle midzone, Borealin ensures accurate chromosome segregation and successful cytokinesis.

INCENP is the structural and regulatory scaffold of the Chromosomal Passenger Complex. By activating Aurora B kinase, binding microtubules and directing CPC movement from centromeres to the spindle midzone, INCENP ensures accurate chromosome segregation and successful cytokinesis.

The IAP family consists of intracellular proteins that regulate apoptosis, ubiquitination and immune signalling. Through their BIR domains and RING ligase activity, IAPs control caspase inhibition, NF‑κB activation, inflammasome signalling and tumour cell survival, making them central players in cell biology and cancer research.

The Chromosomal Passenger Complex (CPC) is a dynamic mitotic regulator composed of Aurora B, INCENP, Borealin and Survivin. It ensures accurate chromosome segregation, corrects spindle attachment errors and coordinates cytokinesis, making it essential for genomic stability and highly relevant in cancer biology.

Survivin (BIRC5) is a tumour‑specific IAP that integrates apoptosis suppression with essential mitotic functions. As part of the chromosomal passenger complex, Survivin ensures proper chromosome segregation while stabilising anti‑apoptotic pathways, making it a central driver of tumour progression and therapy resistance.