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Article ; Online: Midzone activation of aurora B in anaphase produces an intracellular phosphorylation gradient.

Fuller, Brian G / Lampson, Michael A / Foley, Emily A / Rosasco-Nitcher, Sara / Le, Kim V / Tobelmann, Page / Brautigan, David L / Stukenberg, P Todd / Kapoor, Tarun M

Nature

2008 Volume 453, Issue 7198, Page(s) 1132–1136

Abstract: ... we examine the anaphase dynamics of protein phosphorylation by aurora B kinase, a key mitotic regulator ... immunofluorescence of native aurora B substrates. Quantitative analysis of phosphorylation dynamics, using chromosome ... early in anaphase that is centred at the spindle midzone. This gradient depends on aurora B targeting ...

Abstract	Proper partitioning of the contents of a cell between two daughters requires integration of spatial and temporal cues. The anaphase array of microtubules that self-organize at the spindle midzone contributes to positioning the cell-division plane midway between the segregating chromosomes. How this signalling occurs over length scales of micrometres, from the midzone to the cell cortex, is not known. Here we examine the anaphase dynamics of protein phosphorylation by aurora B kinase, a key mitotic regulator, using fluorescence resonance energy transfer (FRET)-based sensors in living HeLa cells and immunofluorescence of native aurora B substrates. Quantitative analysis of phosphorylation dynamics, using chromosome- and centromere-targeted sensors, reveals that changes are due primarily to position along the division axis rather than time. These dynamics result in the formation of a spatial phosphorylation gradient early in anaphase that is centred at the spindle midzone. This gradient depends on aurora B targeting to a subpopulation of microtubules that activate it. Aurora kinase activity organizes the targeted microtubules to generate a structure-based feedback loop. We propose that feedback between aurora B kinase activation and midzone microtubules generates a gradient of post-translational marks that provides spatial information for events in anaphase and cytokinesis.
MeSH term(s)	Anaphase/physiology ; Animals ; Aurora Kinase B ; Aurora Kinases ; Cell Compartmentation ; Centromere/metabolism ; Chromatin/metabolism ; Enzyme Activation ; Fluorescence Resonance Energy Transfer ; HeLa Cells ; Humans ; Intracellular Space/metabolism ; Microtubules/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Spindle Apparatus/metabolism ; Xenopus
Chemical Substances	Chromatin ; AURKB protein, human (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1) ; Aurora Kinases (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2008-05-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature06923
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Article ; Online: Bcl-XL represents a druggable molecular vulnerability during aurora B inhibitor-mediated polyploidization.

Shah, O Jameel / Lin, Xiaoyu / Li, Leiming / Huang, Xiaoli / Li, Junling / Anderson, Mark G / Tang, Hua / Rodriguez, Luis E / Warder, Scott E / McLoughlin, Shaun / Chen, Jun / Palma, Joann / Glaser, Keith B / Donawho, Cherrie K / Fesik, Stephen W / Shen, Yu

Proceedings of the National Academy of Sciences of the United States of America

2010 Volume 107, Issue 28, Page(s) 12634–12639

Abstract: Aurora kinase B inhibitors induce apoptosis secondary to polyploidization and have entered ... 263, which inhibits Bcl-XL, Bcl-2, and Bcl-w. The combination of ABT-263 with aurora B inhibitors ... more sustained tumor growth inhibition in vivo compared with aurora B inhibitor monotherapy. These data ...

Abstract	Aurora kinase B inhibitors induce apoptosis secondary to polyploidization and have entered clinical trials as an emerging class of neocytotoxic chemotherapeutics. We demonstrate here that polyploidization neutralizes Mcl-1 function, rendering cancer cells exquisitely dependent on Bcl-XL/-2. This "addiction" can be exploited therapeutically by combining aurora kinase inhibitors and the orally bioavailable BH3 mimetic, ABT-263, which inhibits Bcl-XL, Bcl-2, and Bcl-w. The combination of ABT-263 with aurora B inhibitors produces a synergistic loss of viability in a range of cell lines of divergent tumor origin and exhibits more sustained tumor growth inhibition in vivo compared with aurora B inhibitor monotherapy. These data demonstrate that Bcl-XL/-2 is necessary to support viability during polyploidization in a variety of tumor models and represents a druggable molecular vulnerability with potential therapeutic utility.
MeSH term(s)	Aniline Compounds ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Apoptosis/genetics ; Aurora Kinase B ; Aurora Kinases ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Male ; Mice ; Neoplasms/drug therapy ; Neoplasms/genetics ; Protein-Serine-Threonine Kinases ; Sulfonamides
Chemical Substances	Aniline Compounds ; Antineoplastic Agents ; Enzyme Inhibitors ; Sulfonamides ; Aurkb protein, mouse (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1) ; Aurora Kinases (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; navitoclax (XKJ5VVK2WD)
Language	English
Publishing date	2010-06-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0913615107
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Article ; Online: Expression, purification, stability optimization and characterization of human Aurora B kinase domain from E. coli.

Sheth, Payal R / Ramanathan, Lata / Ranchod, Ashwin / Basso, Andrea D / Barrett, Dianah / Zhao, Jia / Gray, Kimberly / Liu, Yan-Hui / Zhang, Rumin / Le, Hung V

Archives of biochemistry and biophysics

2010 Volume 503, Issue 2, Page(s) 191–201

Abstract: Aurora B kinase plays a critical role in regulating mitotic progression, and its dysregulation has ... been linked to tumorigenesis. The structure of the kinase domain of human Aurora B and ... we sought to identify a human Aurora B construct that would be amenable for large-scale protein production ...

Abstract	Aurora B kinase plays a critical role in regulating mitotic progression, and its dysregulation has been linked to tumorigenesis. The structure of the kinase domain of human Aurora B and the complementary information of binding thermodynamics of known Aurora inhibitors is lacking. Towards that effort, we sought to identify a human Aurora B construct that would be amenable for large-scale protein production for biophysical and structural studies. Although the designed AurB(69-333) construct expressed at high levels in Escherichia coli, the purified protein was largely unstable and prone to aggregation. We employed thermal-shift assay for high-throughput screening of 192 conditions to identify optimal pH and salt conditions that increased the stability and minimized aggregation of AurB(69-333). Direct ligand binding analyses using temperature-dependent circular dichroism (TdCD) and TR-FRET-based Lanthascreen™ binding assay showed that the purified protein was folded and functional. The affinity rank-order obtained using TdCD and Lanthascreen™ binding assay correlated with enzymatic IC50 values measured using full-length Aurora B protein for all the inhibitors tested except for AZD1152. The direct binding results support the hypothesis that the purified human AurB(69-333) fragment is a good surrogate for its full-length counterpart for biophysical and structural analyses.
MeSH term(s)	Amino Acid Sequence ; Aurora Kinase B ; Aurora Kinases ; Circular Dichroism ; Cloning, Molecular ; Enzyme Stability ; Escherichia coli/metabolism ; Fluorescence Resonance Energy Transfer ; Humans ; Inhibitory Concentration 50 ; Mass Spectrometry ; Molecular Sequence Data ; Molecular Weight ; Protein Folding ; Protein Structure, Tertiary/genetics ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/isolation & purification ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Homology, Amino Acid ; Thermodynamics
Chemical Substances	Recombinant Fusion Proteins ; AURKB protein, human (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1) ; Aurora Kinases (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2010-11-15
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2010.08.004
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Article ; Online: Discovery of (7-aryl-1,5-naphthyridin-2-yl)ureas as dual inhibitors of ERK2 and Aurora B kinases with antiproliferative activity against cancer cells.

Defaux, Julien / Antoine, Maud / Logé, Cédric / Le Borgne, Marc / Schuster, Tilmann / Seipelt, Irene / Aicher, Babette / Teifel, Michael / Günther, Eckhard / Gerlach, Matthias / Marchand, Pascal

Bioorganic & medicinal chemistry letters

2014 Volume 24, Issue 16, Page(s) 3748–3752

Abstract: A novel series of (7-aryl-1,5-naphthyridin-2-yl)ureas was discovered as dual ERK2 and Aurora B ... Aurora B, associated with very promising antiproliferative activity toward various cancer cell lines ...

Abstract	A novel series of (7-aryl-1,5-naphthyridin-2-yl)ureas was discovered as dual ERK2 and Aurora B kinases inhibitors. Several analogues were active at micromolar and submicromolar range against ERK2 and Aurora B, associated with very promising antiproliferative activity toward various cancer cell lines. Synthesis, structure activity relationship and docking study are reported. In vitro ADME properties and safety data are also discussed.
MeSH term(s)	Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Aurora Kinase B/antagonists & inhibitors ; Aurora Kinase B/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Dose-Response Relationship, Drug ; Drug Discovery ; Drug Screening Assays, Antitumor ; HCT116 Cells ; Humans ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 1/metabolism ; Models, Molecular ; Molecular Structure ; Protein Kinase Inhibitors/chemical synthesis ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Structure-Activity Relationship ; Urea/analogs & derivatives ; Urea/chemistry ; Urea/pharmacology
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; Urea (8W8T17847W) ; Aurora Kinase B (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24)
Language	English
Publishing date	2014-08-15
Publishing country	England
Document type	Journal Article
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2014.06.078
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Zs.A 3203: Show issues

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Article ; Online: Identification of genes that confer tumor cell resistance to the aurora B kinase inhibitor, AZD1152.

Guo, J / Anderson, M G / Tapang, P / Palma, J P / Rodriguez, L E / Niquette, A / Li, J / Bouska, J J / Wang, G / Semizarov, D / Albert, D H / Donawho, C K / Glaser, K B / Shah, O J

The pharmacogenomics journal

2009 Volume 9, Issue 2, Page(s) 90–102

Abstract: AZD1152 is a highly selective Aurora B kinase inhibitor currently undergoing Phase I and II ... resistant to the pan-Aurora kinase inhibitor, VX-680/MK0457. Using whole-genome microarray analysis and ... for resistance to Aurora kinase inhibitors, which could be utilized to predict clinical response to therapy. ...

Abstract	AZD1152 is a highly selective Aurora B kinase inhibitor currently undergoing Phase I and II clinical evaluation in patients with acute myelogenous leukemia and advanced solid malignancies. We have established two AZD1152-resistant cell lines from SW620 colon and MiaPaCa pancreatic carcinoma lines, which are >100-fold resistant to the active metabolite of AZD1152, AZD1152 HQPA and interestingly, cross-resistant to the pan-Aurora kinase inhibitor, VX-680/MK0457. Using whole-genome microarray analysis and comparative genomic hybridization, we were able to identify MDR1 and BCRP as the causative genes that underlie AZD1152 HQPA-resistance in these models. Furthermore, the upregulation of either of these genes is sufficient to render in vivo tumor growth insensitive to AZD1152. Finally, the upregulation of MDR1 or BCRP is predictive of tumor cell sensitivity to this agent, both in vitro and in vivo. The data provide a genetic basis for resistance to Aurora kinase inhibitors, which could be utilized to predict clinical response to therapy.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B ; ATP Binding Cassette Transporter, Subfamily B, Member 1/genetics ; ATP Binding Cassette Transporter, Subfamily B, Member 1/metabolism ; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Animals ; Antineoplastic Agents/pharmacology ; Aurora Kinase B ; Aurora Kinases ; Cell Line, Tumor ; Cell Survival/drug effects ; Comparative Genomic Hybridization ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm/genetics ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic ; Humans ; Inhibitory Concentration 50 ; Mice ; Mice, SCID ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Organophosphates/pharmacology ; Piperazines/pharmacology ; Protein Kinase Inhibitors/pharmacology ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Quinazolines/pharmacology ; RNA Interference ; RNA, Small Interfering/metabolism ; Time Factors ; Up-Regulation ; Xenograft Model Antitumor Assays
Chemical Substances	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate ; ABCB1 protein, human ; ABCG2 protein, human ; ATP Binding Cassette Transporter, Subfamily B ; ATP Binding Cassette Transporter, Subfamily B, Member 1 ; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; ATP-Binding Cassette Transporters ; Antineoplastic Agents ; Neoplasm Proteins ; Organophosphates ; Piperazines ; Protein Kinase Inhibitors ; Quinazolines ; RNA, Small Interfering ; tozasertib (234335M86K) ; AURKB protein, human (EC 2.7.11.1) ; Aurkb protein, mouse (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1) ; Aurora Kinases (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2009-02-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2106831-8
ISSN	1473-1150 ; 1470-269X
ISSN (online)	1473-1150
ISSN	1470-269X
DOI	10.1038/tpj.2008.20
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Article: Basal aurora kinase B activity is sufficient for histone H3 phosphorylation in prophase.

Le, Ly-Thuy-Tram / Vu, Hong-Lien / Nguyen, Chi-Hung / Molla, Annie

Biology open

2013 Volume 2, Issue 4, Page(s) 379–386

Abstract: Histone H3 phosphorylation is the hallmark of mitosis deposited by aurora kinase B. Benzo[e ... chromosome compaction involve the basal activity of aurora kinase B. Our data suggest that aurora kinase B is ... progressively activated at mitosis entry and at anaphase onset. The full activation of aurora kinase B ...

Abstract	Histone H3 phosphorylation is the hallmark of mitosis deposited by aurora kinase B. Benzo[e]pyridoindoles are a family of potent, broad, ATP-competitive aurora kinase inhibitors. However, benzo[e]pyridoindole C4 only inhibits histone H3 phosphorylation in prophase but not in metaphase. Under the C4 treatment, the cells enter into mitosis with dephosphorylated histone H3, assemble chromosomes normally and progress to metaphase, and then to anaphase. C4 also induces lagging chromosome in anaphase but we demonstrated that these chromosome compaction defects are not related to the absence of H3 phosphorylation in prophase. As a result of C4 action, mitosis lasts longer and the cell cycle is slowed down. We reproduced the mitotic defects with reduced concentrations of potent pan aurora kinase as well as with a specific aurora B ATP-competitive inhibitor; we therefore propose that histone H3 phosphorylation and anaphase chromosome compaction involve the basal activity of aurora kinase B. Our data suggest that aurora kinase B is progressively activated at mitosis entry and at anaphase onset. The full activation of aurora kinase B by its partners, in prometaphase, induces a shift in the catalytic domain of aurora B that modifies its affinity for ATP. These waves of activation/deactivation of aurora B correspond to different conformations of the chromosomal complex revealed by FRAP. The presence of lagging chromosomes may have deleterious consequences on the daughter cells and, unfortunately, the situation may be encountered in patients receiving treatment with aurora kinase inhibitors.
Language	English
Publishing date	2013-02-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2632264-X
ISSN	2046-6390
ISSN	2046-6390
DOI	10.1242/bio.20133079
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Article ; Online: Basal aurora kinase B activity is sufficient for histone H3 phosphorylation in prophase

Ly-Thuy-Tram Le / Hong-Lien Vu / Chi-Hung Nguyen / Annie Molla

Biology Open, Vol 2, Iss 4, Pp 379-

2013 Volume 386

Abstract: Summary Histone H3 phosphorylation is the hallmark of mitosis deposited by aurora kinase B. Benzo[e ... chromosome compaction involve the basal activity of aurora kinase B. Our data suggest that aurora kinase B is ... progressively activated at mitosis entry and at anaphase onset. The full activation of aurora kinase B ...

Abstract	Summary Histone H3 phosphorylation is the hallmark of mitosis deposited by aurora kinase B. Benzo[e]pyridoindoles are a family of potent, broad, ATP-competitive aurora kinase inhibitors. However, benzo[e]pyridoindole C4 only inhibits histone H3 phosphorylation in prophase but not in metaphase. Under the C4 treatment, the cells enter into mitosis with dephosphorylated histone H3, assemble chromosomes normally and progress to metaphase, and then to anaphase. C4 also induces lagging chromosome in anaphase but we demonstrated that these chromosome compaction defects are not related to the absence of H3 phosphorylation in prophase. As a result of C4 action, mitosis lasts longer and the cell cycle is slowed down. We reproduced the mitotic defects with reduced concentrations of potent pan aurora kinase as well as with a specific aurora B ATP-competitive inhibitor; we therefore propose that histone H3 phosphorylation and anaphase chromosome compaction involve the basal activity of aurora kinase B. Our data suggest that aurora kinase B is progressively activated at mitosis entry and at anaphase onset. The full activation of aurora kinase B by its partners, in prometaphase, induces a shift in the catalytic domain of aurora B that modifies its affinity for ATP. These waves of activation/deactivation of aurora B correspond to different conformations of the chromosomal complex revealed by FRAP. The presence of lagging chromosomes may have deleterious consequences on the daughter cells and, unfortunately, the situation may be encountered in patients receiving treatment with aurora kinase inhibitors.
Keywords	Cancer ; Chromosome compaction ; Aurora kinase ; Kinase inhibitors ; Survivin ; Chromosomal passenger complex ; Histone H3 phosphorylation ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2013-02-01T00:00:00Z
Publisher	The Company of Biologists
Document type	Article ; Online
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Article ; Online: The need for a multi-level approach to occupational safety and health among Asian and Asian American beauty service workers.

Lê, Aurora B / Huỳnh, Trân B

Journal of occupational and environmental hygiene

2023 Volume 20, Issue 11, Page(s) 495–505

Abstract: Asian and Asian Americans (A/AA) are a group overlooked in general health outcomes but especially occupational safety and health outcomes. In the United States, the beauty service microbusiness industry (e.g., nail salons) predominantly employs immigrant ...

Abstract	Asian and Asian Americans (A/AA) are a group overlooked in general health outcomes but especially occupational safety and health outcomes. In the United States, the beauty service microbusiness industry (e.g., nail salons) predominantly employs immigrant Asian women who regularly encounter a plethora of occupational hazards (e.g., harmful chemical exposures -toluene, formaldehyde, bloodborne pathogens, fungi. However, due to the precariousness of beauty service jobs, cultural and linguistic barriers, and social determinants of health, A/AA beauty service workers face complex occupational safety and health challenges that require interdisciplinary collaboration and cultural competency to address. This commentary will discuss a multi-level approach including specific outreach partners that will offer the required diverse skillsets necessary for improving the occupational safety and health for this worker population in this microbusiness industry. Implications and suggestions for interventions and policy changes are also recommended utilizing the National Institute on Minority Health and Health Disparities' Research Framework.
MeSH term(s)	Humans ; Female ; United States ; Asian ; Occupational Exposure/prevention & control ; Occupational Exposure/analysis ; Occupational Health ; Beauty Culture ; Toluene/analysis
Chemical Substances	Toluene (3FPU23BG52)
Language	English
Publishing date	2023-08-04
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2131820-7
ISSN	1545-9632 ; 1545-9624
ISSN (online)	1545-9632
ISSN	1545-9624
DOI	10.1080/15459624.2023.2245447
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Article ; Online: The Health Impacts of COVID-19-Related Racial Discrimination of Asian Americans Extend Into the Workplace.

Le, Aurora B

American journal of public health

2021 Volume 111, Issue 4, Page(s) e17–e18

MeSH term(s)	Asian/statistics & numerical data ; COVID-19/ethnology ; COVID-19/mortality ; Health Personnel/organization & administration ; Health Personnel/statistics & numerical data ; Humans ; Occupational Health/standards ; Racism ; Social Discrimination/ethnology ; Workplace
Language	English
Publishing date	2021-03-08
Publishing country	United States
Document type	Letter
ZDB-ID	121100-6
ISSN	1541-0048 ; 0090-0036 ; 0002-9572
ISSN (online)	1541-0048
ISSN	0090-0036 ; 0002-9572
DOI	10.2105/AJPH.2020.306139
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Article ; Online: The Relationship Between Workplace Drug Policies, Opioid Misuse, and Psychological Distress: Evidence From the 2020 National Survey on Drug Use and Health.

Le, Aurora B / Urban-Wojcik, Emily / Seewald, Meghan / Mezuk, Briana R

New solutions : a journal of environmental and occupational health policy : NS

2024 Volume 34, Issue 1, Page(s) 22–37

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Adult ; Humans ; Adolescent ; Analgesics, Opioid/therapeutic use ; Opioid-Related Disorders/epidemiology ; Opioid-Related Disorders/drug therapy ; Workplace ; Public Policy
Chemical Substances	Analgesics, Opioid
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1236515-4
ISSN	1541-3772 ; 1048-2911
ISSN (online)	1541-3772
ISSN	1048-2911
DOI	10.1177/10482911241231523
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