抗Human Aurora Kinase B 抗体:
抗Mouse (Murine) Aurora Kinase B 抗体:
抗Rat (Rattus) Aurora Kinase B 抗体:
Human Polyclonal Aurora Kinase B Primary Antibody for ELISA, WB - ABIN129612
Mackay, Makise, Ullman: Defects in nuclear pore assembly lead to activation of an Aurora B-mediated abscission checkpoint. in The Journal of cell biology 2011
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Human Polyclonal Aurora Kinase B Primary Antibody for ICC, IF - ABIN151760
Adams, Eckley, Vagnarelli, Wheatley, Gerloff, Mackay, Svingen, Kaufmann, Earnshaw: Human INCENP colocalizes with the Aurora-B/AIRK2 kinase on chromosomes and is overexpressed in tumour cells. in Chromosoma 2001
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Cow (Bovine) Polyclonal Aurora Kinase B Primary Antibody for IF, ELISA - ABIN538167
Yasui, Urano, Kawajiri, Nagata, Tatsuka, Saya, Furukawa, Takahashi, Izawa, Inagaki: Autophosphorylation of a newly identified site of Aurora-B is indispensable for cytokinesis. in The Journal of biological chemistry 2004
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Human Polyclonal Aurora Kinase B Primary Antibody for ICC, IF - ABIN152999
Qi, Tang, Yu: Phosphorylation- and polo-box-dependent binding of Plk1 to Bub1 is required for the kinetochore localization of Plk1. in Molecular biology of the cell 2006
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Human Monoclonal Aurora Kinase B Primary Antibody for ELISA, WB - ABIN1724660
Song, So, Cheng, Tang, Croft: Sustained survivin expression from OX40 costimulatory signals drives T cell clonal expansion. in Immunity 2005
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Human Monoclonal Aurora Kinase B Primary Antibody for ELISA, WB - ABIN965626
Kapoor, Lavoie, Frappier: EBP2 plays a key role in Epstein-Barr virus mitotic segregation and is regulated by aurora family kinases. in Molecular and cellular biology 2005
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Human Polyclonal Aurora Kinase B Primary Antibody for EIA, WB - ABIN117978
Honda, Asato, Tanaka, Endo, Nishimura, Ito: Vidian nerve schwannoma with middle cranial fossa extension resected via a maxillary swing approach. in Head & neck 2008
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Human Polyclonal Aurora Kinase B Primary Antibody for ELISA, WB - ABIN129590
Slawson, Lakshmanan, Knapp, Hart: A mitotic GlcNAcylation/phosphorylation signaling complex alters the posttranslational state of the cytoskeletal protein vimentin. in Molecular biology of the cell 2008
Human Polyclonal Aurora Kinase B Primary Antibody for WB - ABIN2441645
Bailey, Fields, Cheng, Lee, Wagenaar, Lagrois, Schmidt, Xia, Ma: WD repeat-containing protein 5 (WDR5) localizes to the midbody and regulates abscission. in The Journal of biological chemistry 2015
Chimpanzee Polyclonal Aurora Kinase B Primary Antibody for ELISA, WB - ABIN2477557
Klever, Grond-Ginsbach, Hager, Schroeder-Kurth: Chorionic villus metaphase chromosomes and interphase nuclei analysed by chromosomal in situ suppression (CISS) hybridization. in Prenatal diagnosis 1992
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The study provides a mechanism by which gastric tumor cells maintain their high proliferation rate via coordination of AURKB and CREPT on the expression of CCNB1.
Data revealed that Aurora B kinase expression was higher in osteosarcoma compared with normal tissue.
identified phosphorylation of RV[S/T]F motifs in known and previously unidentified PP1 regulatory proteins as a cell cycle-dependent event. We show that Aurora B was the primary kinase responsible for this phosphorylation event during mitosis.
Mitotic kinase Aurora B interacts with and phosphorylates Cdt1. Aurora B-phosphomimetic Cdt1 exhibited attenuated MT binding, and its cellular expression induced defective kinetochore-microtubule attachments with a concomitant delay in mitotic progression.
Results showed that Aurora B kinase phosphorylation by KNL1 results in distinct patterns of KNL1 complex disruption.
Aurora-B may promote the malignant phenotype of osteosarcoma cells.
These results indicate structural and functional destabilization of p53 upon phosphomimetic substitution, which provides a molecular basis toward understanding the process that drives the fate of p53 upon phosphorylation by Aurora B kinase.
temporal and spatial Aurora kinase-mediated regulation of SPICE1 is important for correct chromosome segregation.
this study identifies Aurora B kinase activity-dependent and -independent roles for the chromosomal passenger complex in regulating centromeric cohesion during mitosis in human cells.
Study have demonstrated that acquisition of resistance to EGFR tyrosine kinase inhibitors in EGFR-mut cell line models and non-small cell lung cancer patients is often associated with AURKB activation and increased levels of histone H3 phosphorylation.
nhibition of AURKB enhanced GC-induced expression of cell death genes, resulting in potentiation of GC cytotoxicity in cell lines and relapsed B-ALL patient samples. This function for AURKB is distinct from its canonical role in the cell cycle. These results show the utility of functional genomics in understanding mechanisms of resistance and rapidly identifying combination chemotherapeutics.
Aurora kinase B (AKB) siRNA-loaded nanoparticles (AKB-LfNPs) were prepared with milk protein, lactoferrin, by water in oil emulsion method.Treatment of AKB-LfNPs to GBM mice improves life expectancy and has potential to combine with conventional chemotherapy.
VRK1 and AURKB for a complex that inhibits their kinase activity and H3 histone phosphorylation. In locations where the two kinases interact, there is a different pattern of histone modifications, indicating that there is a local difference in chromatin during mitosis because of the local complexes formed by these kinases and their asymmetric intracellular distribution.
We also suggested Aurora-B as a promising therapeutic target in non-small cell lung cancer treatment.
The epigenetic targets AURKB, AURKC and DNMT3B, and the global DNA methylation profile are regulated during HIV-1 replication in CD4+ T cells, and this regulation can be influenced by the activation state of the cell at the time of infection.
findings suggest that USP35 regulates the stability and function of Aurora B by blocking APC(CDH1)-induced proteasomal degradation, thereby controlling mitotic progression
PKCvarepsilon directly modulates the Aurora B-dependent abscission checkpoint by phosphorylating Aurora B at S227. This phosphorylation invokes a switch in Aurora B specificity, with increased phosphorylation of a subset of target substrates, including the CPC subunit Borealin.
The results propose a model in which Aurora B-mediated H2AX-phosphorylated serine 121 probably provide a platform for Aurora B autoactivation circuitry at centromeres and thus play a pivotal role in proper chromosome segregation.
The data suggest that AKA is the vertebrate ancestral gene, and that AKB and AKC resulted from gene duplication in placental mammals.
Study reveals the mechanism controlling abscission through integration of Aurora B kinase and B56-bound PP2A phosphatase activities on the kinesin motor protein MKlp2. MKlp2 is an essential protein for promoting abscission, which may regulate tethering and stabilizing of the PM to the microtubule cytoskeleton at the intercellular bridge through its previously uncharacterized lipid association motif.
in the absence of AURKC, AURKA localizes to chromosomes in a CPC-dependent manner. These data suggest that AURKC prevents AURKA from localizing to chromosomes by competing for CPC binding. This competition is important for adequate spindle length to support meiosis I. There is also a unique requirement for AURKB to negatively regulate AURKC to prevent aneuploidy.
Aurora B causes mitotic arrest and participates in spindle assembly checkpoint via Mad2 and H3S10P, which is required for self-correction of aneuploidies
Data show that phosphorylated Ku70 S155 interacts with the Aurora B kinase and leads to inhibition of its activity.
Loss of AURKB function affects TERF1 telomere binding and results in aberrant telomere structure.
The high sequence similarity among the AURK family members has made discerning the individual kinase functions in meiosis challenging. Technical limitations in specifically targeting AURKB or AURKC using small-molecule inhibitors and compensatory abilities in single-knockout animals add to this challenge...proper regulation of AURKA expression is crucial for spindle formation in meiosis
Aurkb phosphorylates Oct4(S229) during G2/M phase, leading to the dissociation of Oct4 from chromatin, whereas PP1 binds Oct4 and dephosphorylates Oct4(S229) during M/G1 transition, which resets Oct4-driven transcription for pluripotency and the cell cycle.
Overexpression of Aurora B also results in a reduced DNA damage response and decreased levels of the p53 target p21(Cip1) in vitro and in vivo.
Chromsome stability is on of the tumor-suppressive functions of ARF as well as regulation of Aurora B expression in tumors.
Using this mutant we show for the first time that AURKC has functions that do not overlap with AURKB. These functions include regulating localized CPC activity and regulating chromosome alignment and K-MT attachments at metaphase of meiosis I (Met I).
reduced accumulation of Aurora B at the inner centromere region in cells lacking Pds5B impairs its error correction function, promoting chromosome mis-segregation and aneuploidy
Aurora B and Ring1B co-occupy active promoters in resting lymphocytes.
These results provide a scientific rationale for investigating ABK inhibitors as a treatment for intestinal cancer
FBXL2 mediates Aurora B ubiquitination and degradation within the midbody, which is sufficient to induce mitotic arrest and apoptosis.
Inhibitions of Aurora B and Cyclin-dependent kinase 1 activity in vertebrate cells also have opposite effects on the timing of abscission.
Aurora B represses p21(Cip1), preventing delayed DNA replication, Cdk inhibition and premature mitotic exit.
Calmodulin protects Aurora B on the midbody to regulate the fidelity of cytokinesis.
the BRAF/ERK axis controls Aurora B expression at the transcriptional level, likely through the transcription factor FOXM1.
These findings suggest a model for the presence of AURKC in oocytes: that AURKC compensates for loss of AURKB through differences in both message recruitment and protein stability.
Results indicated that the activity of AURKB was required for regulating multiple stages of mitotic progression in the early development of mouse zygotes and was correlated with the activation of the MAPK pathway.
Aurora A and B kinases directly phosphorylate Lgl to promote its mitotic relocalization.
Regulation of Polo by Aurora B and Map205 is required for cytokinesis.
We propose that mutual inhibitions between Aurora B and Cyclin B regulate the duration of abscission and thereby the number of sister cells in each cyst.
Aurora B kinase activity is not required during contractile ring ingression, providing insight into the mechanism of cytokinesis.
Aurora B interacts with and requires the Cdc37/Hsp90 complex for its stability.
This protein accumulates at the mid-zones of chromosome-free spindles.
INCENP binds to the cohesion protector protein MEI-S332, which is also an excellent in vitro substrate for Aurora B kinase.
Alterations in PGRMC1 and/or AURKB localization account in part for the increased aneuploidy and low development competence of oocytes from ovaries with reduced antral follicle counts.
AURKB associated with metaphase chromosomes.
Results suggest a role of AurkB in regulating neuronal development and axonal outgrowth.
Aurora B kinase is essential for furrow induction and maturation in the zebrafish embryo.
Data suggest a model in which microtubules act as scaffolds for the enzymatic activity of Aurora-B.
Data report the crystal structure of Aurora B in complex with the IN-box segment of the inner centromere protein (INCENP) activator and with the small molecule inhibitor Hesperadin.
ICIS and Aurora B coregulate the microtubule depolymerase Kif2a.
the Aurora B chromosome passenger protein complex, including INCENP and survivin, is regulated during oocyte maturation in Xenopus laevis
This study reveals a new role for Aurora B, which is to prevent excess MCAK binding to chromatin to facilitate chromatin-nucleated spindle assembly.
MCAK regulation of cytoplasmic and spindle-associated microtubules can be differentiated by Aurora B-dependent phosphorylation
results suggest an essential combined function of AurA and AurB in chromosome segregation and anaphase MT dynamics
Aurora B pathway is suppressed in the cytoplasm of Xenopus egg extract by phosphatases, but that it becomes activated by chromatin via a Ran-independent mechanism.
This gene encodes a member of the aurora kinase subfamily of serine/threonine kinases. The genes encoding the other two members of this subfamily are located on chromosomes 19 and 20. These kinases participate in the regulation of segregation of chromosomes during mitosis and meiosis through association with microtubules. A pseudogene of this gene is located on chromosome 8. Multiple transcript variants encoding different isoforms have been found for this gene.
, aurora 1
, aurora kinase B-Sv1
, aurora kinase B-Sv2
, aurora- and Ipl1-like midbody-associated protein 1
, aurora-related kinase 2
, aurora/IPL1-related kinase 2
, protein phosphatase 1, regulatory subunit 48
, serine/threonine kinase 12
, serine/threonine-protein kinase 12
, serine/threonine-protein kinase 5
, serine/threonine-protein kinase aurora-B
, aurora B
, aurora- and IPL1-like midbody-associated protein 1
, serine/threonine kinase 5
, aurora B kinase
, dAurora B
, Serine/threonine-protein kinase 12
, cellular island
, serine/threonine kinase a
, aurora kinase B
, serine/threonine-protein kinase 12-like
, Aurora/IPL1-related kinase 2-B
, Serine/threonine-protein kinase 12-B
, Serine/threonine-protein kinase aurora-B-B
, aurora kinase B-B
, aurora/IPL1-related kinase 2-B
, serine/threonine-protein kinase 12-B
, serine/threonine-protein kinase aurora-B-B