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Validated All-in-One™ qPCR Primer for AURKB(NM_001313951.1) Search again
Product ID:
HQP116033
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AIK2, AIM-1, AIM1, ARK-2, ARK2, AurB, IPL1, PPP1R48, STK-1, STK12, STK5, aurkb-sv1, aurkb-sv2
Gene Description:
aurora kinase B
Target Gene Accession:
NM_001313951.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Chromosomal segregation during mitosis as well as meiosis is regulated by kinases and phosphatases. The Aurora kinases associate with microtubules during chromosome movement and segregation. Aurora kinase B localizes to microtubules near kinetochores, specifically to the specialized microtubules called K-fibers, and Aurora kinase A (MIM 603072) localizes to centrosomes (Lampson et al., 2004 [PubMed 14767480]).[supplied by OMIM].
Gene References into function
- Aurora B kinase. Human Aurora-B is activated by okadaic acid and forms complexes with the protein serine/threonine phosphatase type 1 (PP1) or PP2A, but not with PP5. Human Aurora-B is likely a mitotic histone H3 kinase.
- These results indicate that survivin stimulates Aurora-B kinase activity and helps correctly target Aurora-B to its substrates during the cell cycle, thus providing a mechanism as to how survivin exerts its function in human cells.
- topoisomerase II alpha is an Aurora B substrate on metaphase chromosomes
- Aurora B kinase activity is stimulated by INCENP and C-terminal region of INCENP is sufficient for activation
- aurora-B may regulate targeting of survivin by phosphorylating it at threonine 117
- Aurora-B might undergo degradation by binding to HC8 in a proteasome-dependent manner during mitosis
- phosphorylation of Thr-232 is an essential regulatory mechanism for Aurora-B activation
- aurora B mRNA level is regulated by its cell cycle-dependent element (CDE) and cell cycle-gene homology region and a subset of E2F/DP family proteins binds to the CDE
- Aurora B knocked down prevents the formation of the midbody - and consequently affects TACC1 localization at this site - and leads to abnormal cell division and multinucleated cells
- Aurora-B/AIM-1 was highly expressed in high-grade gliomas and its expression was well correlated with histological malignancy and clinical outcomes.
- results suggest that endomitotic MKs appropriately express functional Aurora-B kinase and related proteins in early anaphase, making a simple deficiency of this protein an unlikely explanation for polyploidy in this cell type.
- propose that MKlp2 is involved in the localization of Plk1, Aurora B, and Cdc14A to the central spindle during anaphase, and that the integration of signaling by these proteins is necessary for proper cytokinesis.
- Changes in rates of survivin turnover at centromeres were regulated by stage of the cell cycle, microtubule attachment, and Aurora B kinase activity.
- Aurora-B interacts with the inner centromere protein (INCENP) at the carboxyl terminal end spanning the conserved IN box domain.
- a small C-terminal sequence of Aurora B is essential for the distinct localization and function of Aurora B
- Block of Aurora B expression induced by RNA interference or by using an inhibitor of Aurora kinase activity significantly reduced the growth of thyroid anaplastic carcinoma cells.
- multinucleated giant tumor cells remain in the early mitotic phase because of aurora-B dysfunction, effecting aberrations in cytoplasmic cleavage without affecting nuclear division.
- An important protein in the progresesion of anaplastic carcinoma of the thyroid.
- Aurora-C is a chromosomal passenger protein that disrupts the association of INCENP with Aurora-B and may serve as a key regulator in cell division
- Aurora B is responsible for mitotic arrest in the absence of aurora A.
- Results identify the degradation pathway for Aurora-B, and show that overexpression of a stable form of Aurora-B alone induces aneuploidy and anchorage-independent growth.
- Rebamipide significantly downregulates in AGS cell survivin expression, its association with Aurora-B and cell proliferation. Rebamipide-induced downregulation of survivin is at the transcription level and does not involve ubiquitin-proteasome pathway.
- The two spindle checkpoint arms respond to different spindle cues: whereas the Bub1 arm monitors kinetochore-microtubule attachment, the aurora B arm monitors biorientation.
- Anti-proliferative effect of p53 tumor suppressor is activated by aurora B in normal and glioblastoma cells containing intact p53.
- Aurora-B binds and phosphorylates Septin1.
- The specific inhibition of Aurora-B kinase activity by PARP-1 contributes to the physiological response to DNA damage.
- H3 phosphorylation by Aurora B is therefore part of a 'methyl/phos switch' mechanism that displaces HP1 and perhaps other proteins from mitotic heterochromatin
- Overexpression of aurora B kinase leading to genetic instability is associated with primary non-small cell lung carcinoma
- Overexpression of aurora kinase B is associated with Esophageal Neoplasms
- the direct interaction of Survivin and Aurora B was critical for the correct location of Survivin and the function of the Survivin complex in cell division
- Data show that small molecule-mediated inhibition of Aurora A and Aurora B yields distinct phenotypes, suggesting that the Auroras may present two avenues for anti-cancer drug discovery.
- These results indicate that RKIP regulates Aurora B kinase and the spindle checkpoint via the Raf-1/MEK/ERK cascade and demonstrate that small changes in the MAP kinase (MAPK) pathway can profoundly impact the fidelity of the cell cycle.
- Deacetylation of H3 in mitosis requires AKAP95/HA95 and HDAC3 and provides a hypoacetylated H3 tail that is the preferred substrate for Aurora B kinase.
- chromosome passenger complex, consisting of multiple proteins including Aurora B kinase and INCENP is thought to be responsible for H3 phosphorylation, chromosome condensation and the subsequent segregation of chromosomes
- Aurora B regulates cohesin removal through its effect on the localization of Shugoshin.
- Aberrant alterative splicing of Aurora-B kinase is associated with hepatocarcinogenesis
- role of DNA methylation in Aurora-B targeting to pericentromeres
- These results indicate that Aurora-B participates to regulate the assembly of nucleolar RNA-processing machinery and the RNA methyltransferase activity of NSUN2 via phosphorylation at Ser139 during mitosis.
- Aurora-B may be involved in tumor progression and can be a new diagnostic and therapeutic target for oral squamous cell carcinoma.
- data indicate that Aurora B contributes to chromosome rigidity and segregation by promoting the binding of condensin I to chromatin
- Phosphorylation by aurora-B negatively regulates survivin function during mitosis.
- These results identify a GEF-H1-dependent mechanism to modulate localized RhoA activation during cytokinesis under the control of mitotic kinases.
- Chromatid axial shortening was not affected in condensin-depleted cells, but depended instead on dynamic microtubules and Aurora kinase.
- Sgo1 is phosphorylated by both AurB and Plk1 in vitro.
- ectopically BRCA2-expressing cells have different intracellular levels of Aurora A, Aurora B, p21, E2F-1, and pRb, suggesting a BRCA2-mediated suppression of polyploidy via stabilization of the checkpoint proteins levels
- aurora B kinase activity is required for proper regulation of microtubule dynamics to ensure that cytokinesis occurs precisely at the cell equator
- phosphorylates MgcRacGAP in conjunction with Cdk1 and is dephosphorylated by PP2A
- the anaphase dynamics of protein phosphorylation by aurora B kinase
- Aurora-B is an EB1-interacting protein; EB1 stimulates Aurora-B activity through antagonizing its dephosphorylation/inactivation by PP2A
- Aurora B has a significant role in the biologic behavior of endometrial carcinoma
- These observations suggest that most endopolyploid tumour cells are not reproductively inert and that Aurora-B may contribute to the establishment of resistant tumours post-irradiation.
- Aurora B expression was not associated with survival in breast cancer
- HsMis13 phosphorylation by Aurora B is required for organizing a stable bi-oriented microtubule kinetochore attachment that is essential for faithful chromosome segregation in mitosis.
- AURB is a novel target of transcriptional regulation by histone deacetylase inhibitors in non-small cell lung cancer.
- Ajuba is a microtubule-associated protein that collaborates with Aurora B and BUBR1 at the metaphase-anaphase transition and this may be important to ensure proper chromosome segregation.
- Conserved together throughout eukaryotic evolution, I-2, PP1 and Aurora B function interdependently during mitosis.
- These observations suggest Usp39 to be involved in splicing of Aurora B and other mRNAs that are essential for proper spindle checkpoint function.
- Data have concluded that INCENP plays a catalytic role in AurB autophosphorylation, and AurB/INCENP-catalysed phosphorylation of a peptide substrate proceeds through a rapid equilibrium random Bi Bi kinetic mechanism.
- The Aurora B kinase is required for mitotic chromosome segregation, spindle checkpoint function, cytokinesis and histone H3 phosphorylation
- Aurora kinases A and B overexpression is a relatively early phenomenon in the genesis of malignant epithelial neoplasm tumorigenesis.
- the mitotic kinases Aurora A and Aurora B are regulated by EWS-Fli1 fusion protein in Ewing sarcoma cells
- This is the first study to report clinicopathological significance of aberrant expression of AURKB-Sv2 variant form in hepatocellular carcinoma.
- study found that centromere tension can be sensed by increased spatial separation of Aurora B from kinetochore substrates, which reduces phosphorylation and stabilizes kinetochore microtubules
- Chromosome bridges sustained Aurora B activity to posttelophase stages and thereby delayed abscission at stabilized intercellular canals; this suppresses tetraploidization by furrow regression in a pathway further involving the phosphorylation of Mklp1.