AURKB
AURKB Gene
Aurora Kinase B (AURKB) is a serine/threonine protein kinase encoded by the AURKB gene located on chromosome 17p13.1. As a member of the Aurora kinase family, AURKB plays essential roles in cell division and has recently been implicated in neurodegenerative disease pathways. The protein's involvement in chromosome segregation, cytokinesis, and cellular stress responses makes it a subject of growing research interest for understanding neuronal dysfunction and death. The AURKB gene is also known by several aliases including AURORA-B and STK12, with an NCBI Gene ID of 921, and it produces a 344-amino acid catalytic protein known as Aurora B kinase that exhibits ubiquitous expression with highest levels during mitosis.
| Property | Details |
|----------|---------|
| Gene Symbol | AURKB |
| Gene Name | Aurora Kinase B |
| Aliases | AURORA-B, STK12 |
| Chromosomal Location | 17p13.1 |
| NCBI Gene ID | 921 |
| Protein Product | Aurora B kinase (AurB) |
| Expression Pattern | Ubiquitous; highest during mitosis |
Overview
...AURKB
AURKB Gene
Aurora Kinase B (AURKB) is a serine/threonine protein kinase encoded by the AURKB gene located on chromosome 17p13.1. As a member of the Aurora kinase family, AURKB plays essential roles in cell division and has recently been implicated in neurodegenerative disease pathways. The protein's involvement in chromosome segregation, cytokinesis, and cellular stress responses makes it a subject of growing research interest for understanding neuronal dysfunction and death. The AURKB gene is also known by several aliases including AURORA-B and STK12, with an NCBI Gene ID of 921, and it produces a 344-amino acid catalytic protein known as Aurora B kinase that exhibits ubiquitous expression with highest levels during mitosis.
| Property | Details |
|----------|---------|
| Gene Symbol | AURKB |
| Gene Name | Aurora Kinase B |
| Aliases | AURORA-B, STK12 |
| Chromosomal Location | 17p13.1 |
| NCBI Gene ID | 921 |
| Protein Product | Aurora B kinase (AurB) |
| Expression Pattern | Ubiquitous; highest during mitosis |
Overview
The AURKB gene encodes a serine/threonine protein kinase that belongs to the Aurora kinase family. Aurora kinases comprise three members in mammals—Aurora A (AURKA), Aurora B (AURKB), and Aurora C (AURKA)—which regulate critical aspects of cell division. AURKB produces a catalytic protein essential for proper chromosome segregation, cytokinesis, and cell cycle progression. Unlike Aurora A, which localizes primarily to centrosomes and spindle poles, Aurora B functions as the catalytic core of the chromosomal passenger complex (CPC), a multiprotein assembly that coordinates mitotic progression and genome stability. [@carmena2009] The protein's dysfunction has emerged as a significant factor in cellular pathology relevant to neurodegenerative diseases.
Function/Biology
Aurora B kinase regulates multiple processes during mitosis and cytokinesis through its catalytic activity and subcellular localization. The CPC, composed of Aurora B, survivin (BIRC5), INCENP, and Borealin, targets Aurora B to the inner centromere during metaphase, where it phosphorylates numerous substrates including histone H3, CENP-A, and Dasra B (also known as Bora). This localization is crucial for establishing proper tension across sister kinetochores and for the spindle assembly checkpoint, which prevents premature anaphase entry. Aurora B activity directly regulates kinetochore-microtubule attachments by phosphorylating the KMN network proteins, particularly NDC80. Following anaphase, Aurora B relocalizes to the central spindle and contractile ring, where it phosphorylates regulators of cytokinesis, including MgcRacGAP and MKLP1, promoting cleavage furrow formation and cell division completion. Beyond mitosis, Aurora B also participates in DNA damage responses and contributes to maintaining genomic stability through checkpoint control mechanisms. [@hindriksen2017]
Role in Neurodegeneration
Aberrant Aurora B activity has been implicated in multiple neurodegenerative disease pathways, particularly through its effects on cellular proliferation, chromosome segregation fidelity, and stress responses in neurons and glia. In Alzheimer's disease, increased Aurora B kinase activity has been observed in brain tissue, correlating with enhanced phosphorylation of tau protein and exacerbation of neurofibrillary pathology. The kinase's involvement in cell cycle re-entry—a phenomenon where post-mitotic neurons abnormally enter cell cycle phases—suggests that dysregulated AURKB expression may contribute to neuronal loss through aberrant proliferation signaling and subsequent apoptosis. In Parkinson's disease models, Aurora B dysfunction impairs proper mitochondrial segregation during cytokinesis, potentially leading to accumulation of dysfunctional mitochondria and cellular bioenergetic stress. Additionally, defective Aurora B-mediated cytokinesis in oligodendrocytes and astrocytes may compromise glial support functions critical for neuronal survival.
Molecular Mechanisms
Aurora B exerts neurodegenerative effects through multiple molecular pathways. Overactive Aurora B promotes aberrant phosphorylation of tau at serine-threonine residues, promoting tau aggregation and paired helical filament formation—hallmark pathologies of tauopathies. The kinase also phosphorylates p53 and other cell cycle checkpoint regulators, potentially triggering p53-dependent apoptotic programs in neurons exposed to proteotoxic stress. Aurora B dysregulation impairs the mitotic checkpoint, leading to chromosomal instability and aneuploidy in cycling cells, which generates additional cellular stress. Furthermore, Aurora B activity influences mitochondrial dynamics and autophagy regulation through phosphorylation of proteins controlling mitochondrial fission-fusion processes, directly affecting cellular energy homeostasis critical to neurons.
Clinical/Research Significance
Aurora B kinase inhibitors represent emerging therapeutic targets for neurodegenerative diseases, particularly those involving tau pathology. Pan-Aurora kinase inhibitors and Aurora B-selective compounds have shown promise in preclinical models of Alzheimer's disease by reducing tau phosphorylation and improving neuronal viability. The potential of AURKB modulation is also being explored in polyglutamine expansion disorders and other neurodegenerative conditions characterized by cell cycle dysregulation.
The AURKB gene is related to several other entities within the Aurora kinase family and the chromosomal passenger complex. AURKA (Aurora Kinase A) is another family member involved in centrosome maturation and spindle pole organization, while AURKC (Aurora Kinase C) is primarily expressed in meiotic cells. Within the cell, AURKB functions as the catalytic core of the Chromosomal Passenger Complex (CPC), a multiprotein assembly that also includes survivin (BIRC5), INCENP, and Borealin. INCENP (Inner Centromere Protein) serves as a key regulatory component that directs Aurora B localization and activity during mitosis.
Pathway Diagram
The following diagram shows the key molecular relationships involving AURKB Gene discovered through SciDEX knowledge graph analysis:
Mermaid diagram (expand to render)