Affinage

AURKB

Aurora kinase B · UniProt Q96GD4

Round 2 corrected
Length
344 aa
Mass
39.3 kDa
Annotated
2026-04-28
130 papers in source corpus 46 papers cited in narrative 46 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

Aurora kinase B (AURKB) is the catalytic serine/threonine kinase subunit of the chromosomal passenger complex (CPC, comprising AURKB, INCENP, Survivin, and Borealin), which orchestrates chromosome segregation, kinetochore–microtubule error correction, and cytokinesis during cell division. AURKB phosphorylates histone H3 at Ser10 to drive HP1 dissociation from chromatin at the G2–M transition and to modulate mitotic chromatin architecture, and it phosphorylates KMN network components (Ndc80, KNL1, Dam1) in a tension-sensitive manner—governed by spatial separation from outer-kinetochore substrates—to selectively destabilize erroneous kinetochore–microtubule attachments and promote chromosome bi-orientation (PMID:19150808, PMID:20471944, PMID:16222244). CPC centromeric recruitment depends on Survivin recognition of Haspin-generated H3T3ph intersecting with Bub1-mediated H2A-S121ph, while INCENP-mediated autophosphorylation is required for full kinase activation (PMID:20705812, PMID:20929775, PMID:12925766). Beyond mitosis, AURKB delays cytokinetic abscission at chromosome bridges to prevent tetraploidization, phosphorylates Oct4 to reset pluripotency gene expression in embryonic stem cells, and restrains glucocorticoid-driven transcription in lymphoid cells by phosphorylating EHMT1/2 (PMID:19203582, PMID:26880562, PMID:30733284).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1998 High

    Establishing AURKB as a cytokinesis-essential kinase resolved the question of whether this Aurora family member acts in late mitotic events; dominant-negative kinase-dead mutants disrupted cleavage furrow formation without affecting nuclear division.

    Evidence Dominant-negative overexpression and immunofluorescence in mammalian cells

    PMID:9450992 PMID:9809983

    Open questions at the time
    • Identity of cytokinetic substrates was unknown
    • Relationship to chromosome segregation functions was not addressed
  2. 2000 High

    Discovery that the Ipl1/Aurora–Glc7/PP1 kinase–phosphatase axis controls histone H3-Ser10 phosphorylation and chromosome segregation established the first chromatin substrate and revealed an antagonistic phosphatase circuit governing Aurora activity.

    Evidence Genetic epistasis in S. cerevisiae and C. elegans with histone phosphorylation assays

    PMID:10975519 PMID:11098131

    Open questions at the time
    • Whether H3S10ph was the sole mitotic chromatin function of Aurora was unclear
    • Direct regulation of PP1 at centromeres was not dissected
  3. 2001 High

    Three concurrent studies demonstrated that Ipl1/Aurora B promotes chromosome bi-orientation by destabilizing improper kinetochore–spindle connections, activates the spindle checkpoint specifically in response to tension defects, and is directly stimulated by INCENP/Sli15—establishing the core CPC regulatory logic.

    Evidence Live-cell imaging of kinetochore dynamics, checkpoint epistasis, co-immunoprecipitation, and in vitro kinase assays in yeast

    PMID:11724818 PMID:11731476 PMID:11853667

    Open questions at the time
    • How tension is transduced to kinase–substrate accessibility was unknown
    • Full CPC composition had not been determined
  4. 2003 High

    Identification that INCENP phosphorylation by Aurora B at Thr893/Ser894/Ser895 constitutes a positive-feedback activation loop resolved how the CPC achieves switch-like kinase activation and proper centromere/spindle localization.

    Evidence Reconstituted in vitro kinase assay with site-directed mutagenesis plus RNAi depletion

    PMID:12925766

    Open questions at the time
    • Structural basis of the activation loop was not determined
    • Whether additional kinases prime INCENP was unclear
  5. 2004 High

    Borealin was identified as the fourth CPC subunit, completing the complex architecture, and the CPC was shown to promote spindle assembly by negatively regulating the microtubule depolymerase MCAK.

    Evidence Co-IP/in vitro reconstitution of four-subunit CPC; MCAK co-depletion epistasis in Xenopus egg extracts

    PMID:14767480 PMID:15249581 PMID:15260989

    Open questions at the time
    • MCAK phosphorylation sites by Aurora B were not fully mapped
    • How CPC transitions from centromere to spindle midzone was unknown
  6. 2005 High

    The 'methyl/phos switch' mechanism was elucidated: Aurora B phosphorylation of H3S10 adjacent to K9me3 ejects HP1 from heterochromatin at G2/M, explaining how mitotic chromatin condensation is coupled to histone code readout.

    Evidence In vitro kinase/binding reconstitution, immunofluorescence, and phosphorylation inhibitor experiments

    PMID:16222244 PMID:16687578

    Open questions at the time
    • Whether the switch operates at all chromatin loci or only pericentric heterochromatin was unresolved
    • Kinetics of HP1 rebinding after Aurora B inactivation were not measured
  7. 2009 High

    Two landmark mechanisms were established: (1) FRET biosensors showed that Aurora B senses bi-orientation through spatial separation from outer-kinetochore substrates, explaining tension-dependent error correction; (2) Aurora B was found to delay cytokinetic abscission at chromosome bridges via MKLP1 phosphorylation, preventing tetraploidization.

    Evidence FRET-based biosensors with Aurora B relocalization in living cells; live-cell imaging with RNAi and chemical inhibition

    PMID:19150808 PMID:19203582

    Open questions at the time
    • Phosphatase contribution to the spatial gradient was not quantified
    • How the abscission checkpoint integrates with ESCRT machinery was unknown
  8. 2009 High

    Aurora B phosphorylation of Ndc80 and Dam1 was shown to reduce microtubule binding in vitro and to be tension-regulated in vivo, identifying key outer-kinetochore substrates for the error-correction mechanism.

    Evidence In vitro microtubule binding assays, phospho-specific antibodies, genetic analysis in yeast

    PMID:19822728 PMID:19923271

    Open questions at the time
    • Relative contribution of each KMN substrate to error correction was not determined
    • Whether mammalian Dam1-equivalent Ska complex is similarly regulated was untested
  9. 2010 High

    The molecular basis of CPC centromere targeting was resolved: Survivin binds Haspin-generated H3T3ph and Bub1-generated H2A-S121ph marks intersect to define the inner centromere, explaining the precision of Aurora B localization.

    Evidence Direct binding assay (Survivin–H3T3ph), mutagenesis, antibody microinjection, and two-organism genetic epistasis

    PMID:20471944 PMID:20705812 PMID:20929775

    Open questions at the time
    • How Haspin and Bub1 activities are themselves spatially restricted was not fully resolved
    • Whether centromere targeting differs in meiosis was not addressed
  10. 2011 High

    Aurora B autophosphorylation of INCENP/Sli15 was shown to prevent premature CPC binding to the spindle, while Cdk1 phosphorylation of Aurora B itself suppresses plus-end tracking until anaphase, revealing layered temporal control of CPC redistribution.

    Evidence Phosphosite mutagenesis with in vitro microtubule binding and live-cell imaging in yeast

    PMID:21727193 PMID:22521784

    Open questions at the time
    • Whether Cdk1 regulation of Aurora B is conserved in mammalian cells was not tested
    • Structural basis for phosphorylation-dependent spindle binding was lacking
  11. 2016 High

    Discovery that Aurora B phosphorylates Oct4 at Ser229 during G2/M to dissociate it from chromatin—with PP1-mediated dephosphorylation resetting pluripotency transcription—extended AURKB function beyond mitosis into stem cell gene regulation.

    Evidence In vitro kinase assay, ChIP, phospho-specific antibodies, ESC pluripotency and reprogramming assays

    PMID:26880562

    Open questions at the time
    • Whether other pluripotency factors are Aurora B substrates was not examined
    • Relevance to in vivo embryonic development was not tested
  12. 2019 Medium

    AURKB was found to restrain glucocorticoid signaling in lymphoid cells by phosphorylating EHMT1/2, reducing GC-induced cell death gene expression—identifying a non-mitotic role in transcriptional repression relevant to drug resistance in B-ALL.

    Evidence Genome-wide shRNA screen, AURKB inhibitor treatment, gene expression analysis, patient sample validation

    PMID:30733284

    Open questions at the time
    • Direct phosphorylation sites on EHMT1/2 by AURKB were not mapped
    • Whether this mechanism operates in other hematopoietic lineages is unknown
  13. 2022 High

    Haspin kinase was confirmed to be required for Aurora B centromeric recruitment in mammalian meiosis (spermatocytes), extending the Haspin–H3T3ph–Survivin recruitment paradigm from mitosis to meiotic divisions.

    Evidence Chemical inhibition and Haspin knockout mice with immunofluorescence for meiotic AURKB/MCAK localization

    PMID:35694956

    Open questions at the time
    • Whether female meiosis uses the identical recruitment mechanism was not shown
    • Interaction between Haspin pathway and Bub1 pathway in meiosis was not dissected
  14. 2024 High

    USP29 was identified as a deubiquitinase that stabilizes AURKB by removing K48-linked polyubiquitin chains, revealing a post-translational mechanism controlling AURKB protein abundance.

    Evidence Co-IP, in vitro ubiquitination assay, CRISPR KO, Usp29 knockout mice

    PMID:38233848

    Open questions at the time
    • The E3 ubiquitin ligase targeting AURKB for degradation was not identified
    • Whether USP29 regulation of AURKB operates in normal (non-cancer) physiology is unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for the Aurora B spatial phosphorylation gradient at the centromere–kinetochore axis, the full extent of non-mitotic AURKB substrates, and how the abscission checkpoint mechanistically integrates with ESCRT-mediated membrane scission.
  • No high-resolution structure of the full CPC bound to centromeric nucleosomes
  • Comprehensive phosphoproteomics of AURKB substrates across cell cycle stages is lacking
  • Mechanism coupling Aurora B activity to ESCRT-III recruitment at the midbody is undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 15 GO:0016740 transferase activity 6 GO:0042393 histone binding 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005694 chromosome 5 GO:0005856 cytoskeleton 3 GO:0005815 microtubule organizing center 2
Pathway
R-HSA-1640170 Cell Cycle 11 R-HSA-4839726 Chromatin organization 5 R-HSA-1643685 Disease 4 R-HSA-74160 Gene expression (Transcription) 3
Partners
BIRC5CDCA8DAM1INCENPMKLP1NDC80POU5F1VRK1
Complex memberships
Chromosomal passenger complex (CPC)

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 AIM-1 (AURKB) is a mammalian serine/threonine kinase that localizes to the equator of central spindles during late anaphase and to the midbody during telophase and cytokinesis; overexpression of kinase-inactive AIM-1 disrupts cleavage furrow formation without affecting nuclear division, demonstrating that AURKB kinase activity is required for cytokinesis. Dominant-negative overexpression, immunofluorescence localization, cell ploidy analysis The EMBO journal High 9450992
1998 AURKB overexpression in human cancer cells produces multinuclearity and increased ploidy due to cytokinesis errors, establishing that excess AURKB disrupts chromosomal integrity. Exogenous overexpression in tumor cell lines, flow cytometry for ploidy Cancer research Medium 9809983
2000 Ipl1/Aurora kinase (AURKB ortholog) and the Glc7/PP1 phosphatase together govern the balance of histone H3 serine-10 phosphorylation during mitosis, and both activities are required for proper chromosome segregation in S. cerevisiae and C. elegans. Genetic epistasis in yeast and C. elegans, histone phosphorylation assays Cell High 10975519
2000 AIM-1 (rat AURKB) phosphorylates myosin II regulatory light chain (MRLC) at Ser19 in vitro and colocalizes with monophosphorylated MRLC at the cleavage furrow, implicating AURKB in MRLC phosphorylation during cytokinesis. In vitro kinase assay, two-dimensional phosphopeptide mapping, MRLC mutant analysis, immunofluorescence colocalization Journal of biochemistry High 11098131
2001 The yeast AURKB ortholog Ipl1 promotes chromosome bi-orientation by facilitating turnover of kinetochore-spindle pole connections; in ipl1 mutants, kinetochores remain inappropriately attached to old spindle pole bodies, indicating Ipl1 resolves syntelic attachments. Live-cell imaging, genetic analysis of spindle pole body attachment in DNA-replication-deficient cells Cell High 11853667
2001 Ipl1 (AURKB ortholog) is required for spindle checkpoint activation in response to lack of kinetochore tension but not for checkpoint arrest induced by spindle depolymerization, positioning Ipl1 as a tension-specific checkpoint activator. Genetic analysis, Mps1 overexpression checkpoint assays in ipl1 mutant yeast Genes & development High 11731476
2001 Sli15 (INCENP ortholog) directly associates with Ipl1 (AURKB) in vivo, stimulates Ipl1 kinase activity in vitro, and facilitates Ipl1 association with the mitotic spindle; both Sli15 and Dam1 are phosphorylated by Ipl1 in vitro and show reduced phosphorylation in ipl1 mutants in vivo. Co-immunoprecipitation, in vitro kinase assay, spindle localization imaging, in vivo phosphorylation assays The Journal of cell biology High 11724818
2002 AURKB overexpression causes increased mitotic histone H3 Ser10 phosphorylation with concomitant induction of lagging chromosomes; expression of phosphomimetic H3(S10E) recapitulates this phenotype, demonstrating that excess H3-S10 phosphorylation is a precipitating factor of chromosome instability. Exogenous overexpression, histone mutant transfection, cytogenetic analysis of lagging chromosomes Cancer research Medium 12234980
2002 AURKB (AIM-1) expression is regulated by E2F transcription factors; doxorubicin-induced sustained G2/M arrest involves E2F-dependent downregulation of AIM-1 (AURKB), and abrogation of E2F function prevents this downregulation and leads to premature exit from G2. Dominant-negative E2F expression, E7 papillomavirus protein expression, gene expression analysis, cell cycle assays The Journal of biological chemistry Medium 12446714
2002 Aurora-B (AURKB) and Aurora-A physically interact with histone H3 tail and phosphorylate H3-Ser10 both in vitro and in vivo; Aurora-B colocalizes with H3 phosphorylation at the centromeric region during prophase/metaphase and translocates to the midbody during cytokinesis. In vitro kinase assay, co-immunoprecipitation, immunofluorescence colocalization, cell cycle staging Molecular and cellular biology High 11784863
2003 Aurora B kinase activity is required for proper localization of the entire Aurora B/INCENP/survivin complex to centromeres and central spindle; INCENP directly activates Aurora B kinase activity and is itself phosphorylated by Aurora B at Thr893/Ser894/Ser895 — a non-phosphorylatable mutant (TSS→AAA) is a poor activator, demonstrating that INCENP phosphorylation is required for full kinase activation. Dominant-negative overexpression, RNAi depletion, in vitro kinase assay with recombinant proteins, mass spectrometry phosphosite identification, site-directed mutagenesis Molecular biology of the cell High 12925766
2004 Borealin is a novel subunit of the chromosomal passenger complex (CPC) containing Aurora B/INCENP/Survivin; approximately half of Aurora B in mitotic cells is in the four-subunit complex; Borealin binds Survivin and INCENP in vitro; Borealin depletion causes kinetochore-spindle misattachments and ectopic spindle poles. Co-immunoprecipitation, in vitro binding, RNAi depletion, immunofluorescence The Journal of cell biology High 15249581
2004 The chromosomal passenger complex (containing Aurora B) is required for chromatin-induced microtubule stabilization and spindle assembly; Aurora B negatively regulates MCAK (a microtubule-depolymerizing kinesin), and co-depletion of MCAK rescues microtubule stabilization failure caused by CPC depletion. Xenopus egg extract biochemistry, CPC depletion, MCAK co-depletion epistasis Cell High 15260989
2004 Controlled Aurora kinase reactivation in living vertebrate cells corrects improper chromosome-spindle attachments by selective disassembly of kinetochore-microtubule fibers at mal-oriented kinetochores, revealing a mechanism for error correction during chromosome bi-orientation. Small-molecule inhibitor washout in living cells, real-time high-resolution microscopy of chromosome and microtubule dynamics Nature cell biology High 14767480
2005 Ipl1/Aurora (AURKB) activates the spindle checkpoint in response to tension defects by creating unattached kinetochores; when Ipl1 function is impaired in kinetochore mutants, kinetochore-microtubule attachments are restored and the checkpoint is silenced, demonstrating that Ipl1 converts syntelic tension defects into the unattached-kinetochore signal. Chemical-genetic kinase inhibition, kinetochore attachment analysis, spindle checkpoint assays in budding yeast Nature cell biology High 16327780
2005 Aurora B kinase (AURKB) phosphorylates histone H3 at Ser10, causing dissociation of HP1alpha from chromodomain binding at the G2-M transition; depletion of AURKB inhibits HP1alpha dissociation from chromosome arms, and SUV39H1 methyltransferase is mislocalized in AURKB-depleted cells. RNAi depletion, immunofluorescence of HP1alpha dynamics, in vitro H3 phosphorylation and HP1 dissociation assay Molecular biology of the cell High 16687578
2005 Aurora B-mediated phosphorylation of histone H3 Ser10 causes HP1 dissociation from heterochromatin during mitosis via a 'methyl/phos switch'; H3K9me3S10ph is generated at pericentric heterochromatin in a Suv39h- and Aurora B-dependent manner, and inhibiting H3 Ser10 phosphorylation prevents HP1 chromosome release throughout mitosis. In vitro kinase assay, immunofluorescence, phosphorylation inhibitor experiments, ChIP-like analysis of autoimmune antibody recognition Nature High 16222244
2005 Aurora-B kinase activity augments Ras-mediated cell transformation; RNAi knockdown of Aurora-B inhibits transformation by Ras and Src (but not downstream Raf), and INCENP (a passenger protein associated with Aurora-B) has a similar potentiating effect. RNAi knockdown, focus formation assay in BALB/c 3T3 cells, epistasis with Ras/Src/Raf oncogenes Oncogene Medium 16027732
2009 Aurora B kinase (AURKB) mediates an abscission checkpoint that prevents tetraploidization: chromosome bridges sustain Aurora B activity at posttelophase stages, delaying abscission at stabilized intercellular canals; this involves Aurora B phosphorylation of MKLP1 (Mklp1); Aurora B inactivation promotes premature abscission and furrow regression. Live-cell imaging, RNAi, chemical inhibition, phosphorylation assays in human cells Cell High 19203582
2009 Aurora B kinase senses chromosome bi-orientation by spatial separation from its kinetochore substrates: FRET-based biosensors showed that phosphorylation of Aurora B substrates at the kinetochore depends on their distance from Aurora B at the inner centromere; repositioning Aurora B closer to the kinetochore prevents stabilization of bi-oriented attachments and activates the spindle checkpoint. FRET-based phosphorylation biosensors in living cells, Aurora B relocalization experiments Science High 19150808
2009 Aurora B (AURKB) plays an unexpected role in regulating XIST RNA binding to the inactive X chromosome: RNAi knockdown of AURKB causes mitotic retention of XIST RNA, and H3 phosphorylation (H3S10ph but not H3S28ph) precedes XIST RNA release, linking AURKB-mediated chromatin modification to RNA chromosome binding. RNAi knockdown, kinase inhibitor treatment, RNA FISH, immunofluorescence The Journal of cell biology Medium 19704020
2009 Aurora B phosphorylates the Ndc80 kinetochore protein to reduce its microtubule binding activity; kinetochore-bound Ndc80 is phosphorylated at Ipl1 sites in vivo, but this phosphorylation alone is not essential — additional Ipl1 targets contribute to segregation and checkpoint. In vitro microtubule binding assay, in vivo phosphorylation analysis, genetic analysis of phospho-mutants in yeast Genetics Medium 19822728
2009 Ipl1-dependent phosphorylation of Dam1 is maximal during S phase and minimal during metaphase; when tension is reduced (by failure to establish sister chromatid cohesion), Dam1 phosphorylation persists in metaphase-arrested cells, demonstrating that Aurora B/Ipl1-facilitated bi-orientation is stabilized in response to kinetochore tension by dephosphorylation of Dam1. In vivo phosphorylation assays with phospho-specific antibodies, genetic manipulation of sister chromatid cohesion in yeast Journal of cell science High 19923271
2010 Histone H3 threonine-3 phosphorylation (H3T3ph) by Haspin is necessary for CPC (Aurora B complex) accumulation at centromeres; the CPC subunit Survivin binds directly to H3T3ph; non-binding Survivin-D70A/D71A mutation diminishes centromere localization of Aurora B and compromises centromeric Aurora B functions. Biochemical binding assay (Survivin-H3T3ph), site-directed mutagenesis, microinjection of phospho-specific antibody, immunofluorescence Science High 20705812
2010 The inner centromere is defined by the intersection of two histone kinase pathways: Haspin-mediated H3-pT3 and Bub1-mediated H2A-S121 phosphorylation cooperate to recruit the CPC (Aurora B/Survivin) to the inner centromere in fission yeast and human cells. Genetic and biochemical epistasis in S. pombe and human cells, histone mutant analysis, CPC localization imaging Science High 20929775
2010 Aurora B phosphorylates three spatially distinct targets within the KMN network (KNL1, Mis12, Ndc80 complexes) at the outer kinetochore; combinatorial phosphorylation generates graded levels of microtubule-binding activity with full phosphorylation severely compromising binding; spatial distribution of targets along the kinetochore axis leads to their differential phosphorylation in response to tension vs. attachment state. In vitro phosphorylation assay, microtubule binding assay, phospho-specific antibodies, chromosome segregation phenotype analysis Molecular cell High 20471944
2011 Ipl1/Aurora-dependent phosphorylation of Sli15/INCENP modulates microtubule dynamics by preventing CPC binding to the preanaphase spindle; decreased Ipl1-dependent Sli15 phosphorylation drives direct CPC binding to microtubules, revealing how the CPC influences microtubule dynamics through spatiotemporal control of CPC-spindle interaction. Phosphorylation site mutagenesis, in vitro microtubule binding of Sli15 mutants, live-cell imaging, genetic analysis in yeast The Journal of cell biology High 21727193
2012 Cdk1 directly phosphorylates Ipl1/Aurora at two N-terminal serine residues, suppressing its association with the microtubule plus-end tracking protein Bim1 until anaphase onset; failure to phosphorylate Ipl1 leads to premature metaphase spindle targeting and constitutive Bim1 phosphorylation. In vitro kinase assay (Cdk1 phosphorylation of Ipl1), site-directed mutagenesis, in vivo localization, genetic growth analysis Current biology High 22521784
2014 Ipl1/Aurora B phosphorylation of Sli15 (INCENP) on sites within its central microtubule-binding domain inhibits Sli15 association with microtubules both in vitro and in vivo; mimicking constitutive phosphorylation delocalizes the CPC in metaphase, while blocking phosphorylation drives excessive spindle association; the phosphorylation state also affects the tension checkpoint mechanism. Phospho-site mutagenesis (sli15-20A/20D), in vitro microtubule binding assay, chromosome instability assay, tension checkpoint assay PloS one High 24558497
2016 Aurkb phosphorylates Oct4 at Ser229 during G2/M phase, causing dissociation of Oct4 from chromatin; PP1 then binds Oct4 and dephosphorylates Oct4(S229) during M/G1 transition to reset Oct4-driven transcription for pluripotency; phosphomimetic and PP1-binding-deficient Oct4 mutations alter the cell cycle and impair pluripotency in embryonic stem cells. In vitro kinase assay, phospho-specific antibody detection, ChIP, ESC pluripotency assays, somatic cell reprogramming efficiency eLife High 26880562
2017 Ipl1/Aurora B phosphorylation of Dam1 is critical for faithful chromosome segregation in vivo: phospho-deficient dam1-3A mutants show stabilized kinetochore-microtubule attachment, delay establishment of bipolar attachment after nocodazole washout, and exhibit dramatic chromosome mis-segregation with premature SAC silencing. Phospho-deficient mutant analysis in vivo, chromosome bi-orientation assay, SAC checkpoint analysis in S. cerevisiae Scientific reports High 28928489
2018 VRK1 and AURKB form a stable protein complex (detected after nocodazole release); each kinase inhibits the kinase activity of the other and inhibits the other's specific phosphorylation of histone H3 (VRK1→H3-Thr3; AURKB→H3-Ser10); VRK1 is required for survivin expression (which recognizes H3-T3ph) and thereby for AURKB recruitment to centromeres. Co-immunoprecipitation, in vitro cross-inhibition kinase assay, RNAi depletion, immunofluorescence of centromere markers Cellular and molecular life sciences Medium 29340707
2018 In mouse oocyte meiosis, AURKC is the predominant CPC kinase; AURKB can compensate in the absence of AURKC; AURKB negatively regulates AURKC to prevent aneuploidy; in the absence of AURKC, AURKA localizes to chromosomes in a CPC-dependent manner, revealing inter-kinase competition for CPC binding. Oocyte-specific Aurkb/Aurkc single- and double-knockout mice, immunofluorescence localization, chromosome segregation and fertility assays Current biology High 30415701
2019 Aurora B (AURKB) activation is associated with acquired resistance to EGFR TKIs in NSCLC; AURKB inhibitors reduce phospho-histone H3 (a major AURKB product), triggering G1/S arrest and polyploidy in resistant cells, and pH3 levels are increased in NSCLC patients after progression on EGFR TKIs. AURKB inhibitor treatment, pH3 quantification by Western blot/IHC, cell cycle analysis, patient tissue analysis Nature communications Medium 31000705
2019 AURKB is overexpressed in relapsed B-ALL and restrains glucocorticoid (GC) signaling by phosphorylating EHMT1-2 (histone methyltransferases), thereby reducing GC-induced expression of cell death genes; AURKB inhibition enhances GC-induced expression of cell death genes. Genome-wide shRNA screen, gene expression analysis, AURKB inhibitor treatment, patient sample validation PNAS Medium 30733284
2019 The COMA complex (Ame1/Okp1 heterodimer with Ctf19/Mcm21) positions Sli15/Ipl1(INCENP/Aurora B) at the budding yeast inner kinetochore through a direct interaction between the Sli15/Ipl1 core-CPC and the Ctf19 C-terminus; tethering Sli15 to Ame1/Okp1 rescues synthetic lethality, establishing the molecular architecture for centromeric CPC recruitment. In vitro reconstitution of kinetochore complexes, crosslink-guided co-purification, yeast genetics (synthetic lethality, rescue) eLife High 31112132
2019 Oncoviral antigen LANA (KSHV) cleaves AURKB at Asp76 in a serine protease-dependent manner; the N-terminal cleavage product (N'-AURKB) relocalizes to the spindle pole and promotes metaphase-to-telophase transition; introduction of N'-AURKB promotes colony formation and malignant tumor growth in vivo. Identification of cleavage isoforms in virus-infected cells, serine protease inhibitor experiments, subcellular localization imaging, xenograft tumor model Cell reports Medium 30917319
2020 AURKB promotes gastric cancer cell proliferation by mediating H3 Ser10 phosphorylation (H3S10ph) at the CCND1 (cyclin D1) promoter, thereby epigenetically activating CCND1 expression; AURKB silencing reduces CCND1 and arrests cells in G2/M. AURKB knockdown/inhibition, ChIP for H3S10ph at CCND1 promoter, CCND1 expression analysis, in vitro and in vivo proliferation assays Aging Medium 31982864
2020 CCAT2 lncRNA stabilizes BOP1 protein, which in turn increases the active form of Aurora kinase B (AURKB), promoting chromosomal missegregation; BOP1 knockdown reduces CIN phenotypes, placing BOP1 upstream of AURKB activation in a CCAT2-BOP1-AURKB axis. MS2 pulldown, RNA immunoprecipitation, mass spectrometry, BOP1 overexpression/knockdown, CIN cytogenetic assays, AURKB activity measurement Gastroenterology Medium 32805281
2021 BRAFV600E induces mitotic arrest in human melanocytes via microRNA-mediated suppression of AURKB; MIR211-5p and MIR328-3p converge on AURKB targeting, causing mitotic failure, genome duplication, and proliferation arrest; ectopic AURKB expression rescues arrested human nevus cells. miRNA overexpression, luciferase reporter assay for target validation, AURKB rescue expression, immunofluorescence, proliferation assays eLife High 34812139
2022 Haspin kinase activity is required for AURKB recruitment to meiotic centromeres in mouse spermatocytes; haspin inhibition or Haspin gene deletion reduces Aurora B and MCAK (KIF2C) centromeric localization and impairs chromosome congression during meiotic divisions. Chemical inhibition (LDN-192960), Haspin knockout mice, immunofluorescence for AURKB and meiotic markers Journal of cell science High 35694956
2022 AURKB interacts with MAD2L2 and modulates its expression in bladder cancer cells; AURKB knockdown induces senescence and cell cycle arrest in a p53-dependent manner, and overexpression of MAD2L2 rescues AURKB knockdown effects in vitro and in vivo, establishing an AURKB-MAD2L2-p53 DDR axis. Co-immunoprecipitation, siRNA knockdown, rescue overexpression, xenograft assays, Western blot, senescence assays Journal of translational medicine Medium 38515112
2023 AURKB and TTK inhibitors abrogate the spindle assembly checkpoint; tumor cell sensitivity to these inhibitors is determined by BID (BH3-interacting domain death agonist) levels — high BID cells undergo SAC abrogation-induced CASP-2 activation leading to CASP-3 cleavage and cell death, while BID-low cells are resistant; BID silencing renders sensitive cells resistant and ectopic BID expression sensitizes resistant cells. CRISPR KO, doxycycline-inducible ectopic expression, 53-cell-line panel, PDX in vivo models, CASP-2/3 activation assays Molecular cancer High 37443114
2023 PLK1 and AURKB both phosphorylate survivin to regulate cell proliferation; AURKB inhibition with barasertib significantly inhibited growth of African American (AA) TNBC xenografts, with AA TNBC cells showing higher phospho-survivin levels reflecting higher AURKB activity. Western blot for phospho-survivin, siRNA silencing, barasertib treatment, xenograft tumor models Cell death & disease Medium 36627281
2024 AURKB interacts with DHX9 (DExH-Box helicase 9) and targets its expression; AURKB promotes hepatocellular carcinoma progression through the PI3K/AKT/mTOR pathway in a DHX9-dependent manner, as demonstrated by rescue experiments. Co-immunoprecipitation, knockdown/rescue experiments, Western blot for PI3K/AKT/mTOR markers, in vitro and in vivo tumor models Molecular carcinogenesis Medium 38874176
2024 USP29, activated by transcription factor FUBP1, deubiquitinates AURKB protein by suppressing K48-linked polyubiquitination, thereby stabilizing AURKB protein levels and promoting its oncogenic functions in gastric cancer; Usp29 knockout mice show reduced Aurkb levels. Co-immunoprecipitation, ubiquitination assay, ChIP, qRT-PCR, CRISPR KO, Usp29 knockout mice Cancer cell international High 38233848

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Regulation of chromatin structure by site-specific histone H3 methyltransferases. Nature 2204 10949293
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
1998 Control of apoptosis and mitotic spindle checkpoint by survivin. Nature 1620 9859993
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2001 Mitotic kinases as regulators of cell division and its checkpoints. Nature reviews. Molecular cell biology 1272 11413462
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2000 Mitotic phosphorylation of histone H3 is governed by Ipl1/aurora kinase and Glc7/PP1 phosphatase in budding yeast and nematodes. Cell 723 10975519
2012 Quantitative analysis of HSP90-client interactions reveals principles of substrate recognition. Cell 708 22939624
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2002 Evidence that the Ipl1-Sli15 (Aurora kinase-INCENP) complex promotes chromosome bi-orientation by altering kinetochore-spindle pole connections. Cell 602 11853667
2002 Mitotic phosphorylation of histone H3: spatio-temporal regulation by mammalian Aurora kinases. Molecular and cellular biology 563 11784863
2005 High-throughput mapping of a dynamic signaling network in mammalian cells. Science (New York, N.Y.) 553 15761153
2005 Histone H3 serine 10 phosphorylation by Aurora B causes HP1 dissociation from heterochromatin. Nature 540 16222244
2009 Aurora B-mediated abscission checkpoint protects against tetraploidization. Cell 512 19203582
2003 Exploring the functional interactions between Aurora B, INCENP, and survivin in mitosis. Molecular biology of the cell 453 12925766
2009 Sensing chromosome bi-orientation by spatial separation of aurora B kinase from kinetochore substrates. Science (New York, N.Y.) 448 19150808
2008 Implications for kinetochore-microtubule attachment from the structure of an engineered Ndc80 complex. Cell 445 18455984
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
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