Tag: Chromosomal passenger complex
Aurora C
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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.
Spindle Assembly Checkpoint
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The spindle assembly checkpoint (SAC) is a mitotic surveillance system that prevents premature anaphase onset by monitoring kinetochore–microtubule attachment and tension. Through coordinated action with Aurora B kinase and the Chromosomal Passenger Complex, the SAC ensures accurate chromosome segregation and protects cells from aneuploidy.
Mitotic Error Correction
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Mitotic error correction is a tension‑sensing mechanism that detects and destabilises incorrect kinetochore–microtubule attachments. Driven by Aurora B kinase and the Chromosomal Passenger Complex, this process ensures accurate chromosome segregation and prevents aneuploidy, making it essential for genomic stability.
Aurora B
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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.
Chromosomal Passenger Complex
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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
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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.
Aurora C
![]()
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.
Spindle Assembly Checkpoint
![]()
The spindle assembly checkpoint (SAC) is a mitotic surveillance system that prevents premature anaphase onset by monitoring kinetochore–microtubule attachment and tension. Through coordinated action with Aurora B kinase and the Chromosomal Passenger Complex, the SAC ensures accurate chromosome segregation and protects cells from aneuploidy.
Mitotic Error Correction
![]()
Mitotic error correction is a tension‑sensing mechanism that detects and destabilises incorrect kinetochore–microtubule attachments. Driven by Aurora B kinase and the Chromosomal Passenger Complex, this process ensures accurate chromosome segregation and prevents aneuploidy, making it essential for genomic stability.
Aurora B
![]()
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.
Chromosomal Passenger Complex
![]()
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
![]()
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.
