Phospho-AURKA (T288) Antibody

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Cat. No.

BT1775253

Synonyms

AIK antibody; ARK-1 antibody; ARK1 antibody; AURA antibody; Aurka antibody; Aurora 2 antibody; Aurora A antibody; Aurora kinase A antibody; Aurora-related kinase 1 antibody; Aurora/IPL1 like kinase antibody; AURORA/IPL1-like kinase antibody; Aurora/IPL1-related kinase 1 antibody; AURORA2 antibody; Breast tumor-amplified kinase antibody; BTAK antibody; hARK1 antibody; IAK antibody; IPL1 related kinase antibody; MGC34538 antibody; OTTHUMP00000031340 antibody; OTTHUMP00000031341 antibody; OTTHUMP00000031342 antibody; OTTHUMP00000031343 antibody; OTTHUMP00000031344 antibody; OTTHUMP00000031345 antibody; OTTHUMP00000166071 antibody; OTTHUMP00000166072 antibody; PPP1R47 antibody; Protein phosphatase 1, regulatory subunit 47 antibody; Serine/threonine kinase 15 antibody; Serine/threonine kinase 6 antibody; Serine/threonine protein kinase 15 antibody; Serine/threonine-protein kinase 15 antibody; Serine/threonine-protein kinase 6 antibody; Serine/threonine-protein kinase aurora-A antibody; STK15 antibody; STK6 antibody; STK6_HUMAN antibody; STK7 antibody

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Description

Definition and Mechanism

The Phospho-AURKA (T288) Antibody targets the activated form of AURKA, a serine/threonine kinase critical for mitotic progression. Phosphorylation at T288 within the kinase’s activation loop (T-loop) is essential for its enzymatic activity, which regulates centrosome maturation, spindle assembly, and chromosome segregation during mitosis .

Techniques Utilized

Western Blot: Validated for detecting endogenous AURKA phosphorylation in human, rat, and mouse samples .
Immunohistochemistry (IHC): Used to localize phosphorylated AURKA in tissue samples, such as breast carcinoma .
HTRF Cell-Based Assay: A plate-based, no-wash platform enabling quantitative measurement of phosphorylated AURKA in lysates .

Activation Pathways

Autophosphorylation: T288 phosphorylation is a hallmark of AURKA activation during late S-phase and mitosis .
Alternative Activation: Phosphorylation at T288 can be substituted by Bora-mediated activation, particularly in contexts where T-loop phosphorylation is impaired .

Role in Disease

Cancer: Overexpression of phosphorylated AURKA correlates with oncogenesis in breast, colon, and prostate cancers .
Therapeutic Targeting: Aurora kinase inhibitors (AKIs) often rely on T288 phosphorylation as a biomarker, though cross-reactivity with Aurora B (AURKB) has been reported .

Challenges and Considerations

Cross-Reactivity: Some commercial antibodies exhibit partial reactivity with AURKB or AURKC phosphorylated residues (e.g., T232, T198) .
Epitope Variability: Murine AURKA has a divergent T-loop sequence (RRTT288M), reducing antibody affinity in rodent models .
Assay Sensitivity: HTRF assays demonstrate 2-fold higher sensitivity compared to Western blot for detecting phosphorylated AURKA .

Product Specs

Buffer

The antibody is provided as a liquid solution in phosphate-buffered saline (PBS) containing 50% glycerol, 0.5% bovine serum albumin (BSA), and 0.02% sodium azide.

Form

Liquid

Lead Time

Generally, we can ship the products within 1-3 business days after receiving your order. The delivery time may vary depending on the specific purchasing method or location. Please consult your local distributors for specific delivery time information.

Synonyms

Target Names

AURKA

Uniprot No.

O14965

Target Background

Function

Aurora kinase A (AURKA) is a mitotic serine/threonine kinase that plays a crucial role in regulating cell cycle progression. It localizes to the centrosome and spindle microtubules during mitosis, where it participates in various mitotic events, including establishment of the mitotic spindle, centrosome duplication, centrosome separation and maturation, chromosomal alignment, spindle assembly checkpoint, and cytokinesis. AURKA is essential for proper spindle positioning during mitosis and for the recruitment of NUMA1 and DCTN1 to the cell cortex during metaphase. It also plays a critical role in the initial activation of CDK1 at centrosomes. AURKA phosphorylates a wide range of target proteins, including ARHGEF2, BORA, BRCA1, CDC25B, DLGP5, HDAC6, KIF2A, LATS2, NDEL1, PARD3, PPP1R2, PLK1, RASSF1, TACC3, p53/TP53, and TPX2. Its phosphorylation of KIF2A regulates its tubulin depolymerase activity. AURKA is essential for microtubule formation and/or stabilization, and it plays a crucial role in normal axon formation and microtubule remodeling during neurite extension. AURKA also functions as a key regulator of the p53/TP53 pathway, particularly in checkpoint-response pathways involved in oncogenic transformation of cells, through phosphorylation and destabilization of p53/TP53. Furthermore, AURKA phosphorylates its own inhibitors, the protein phosphatase type 1 (PP1) isoforms, to inhibit their activity. AURKA is essential for proper cilia disassembly prior to mitosis. Finally, it regulates the protein levels of the anti-apoptosis protein BIRC5 by suppressing the expression of the SCF(FBXL7) E3 ubiquitin-protein ligase substrate adapter FBXL7 through phosphorylation of the transcription factor FOXP1.

Gene References Into Functions

Cells lacking ARID1A exhibit enhanced AURKA transcription, leading to persistent activation of CDC25C, a key protein for G2/M transition and mitotic entry. PMID: 30097580
AURKA protein is overexpressed in nearly all dermatofibrosarcoma protuberans tissues, and AURKA protein levels significantly correlate with CD34 protein levels. PMID: 29682829
Aurora A-dependent phosphorylation of CENP-A at the inner centromere protects chromosomes against tension-induced cohesion fatigue until the last kinetochore is attached to spindle microtubules. PMID: 29760389
Aurora A kinase regulates kinetochore-microtubule dynamics of metaphase chromosomes, and Hec1 S69, a previously uncharacterized phosphorylation target site in the Hec1 tail, is a critical Aurora A substrate for this regulation. PMID: 29187526
Upon phorbol 12-myristate 13-acetate treatment, THP-1 cells differentiate into monocytes by down-regulating AURKA, resulting in a reduction in H3S10 phosphorylation. The AURKA inhibitor alisertib accelerates the expression of the H3K27 demethylase KDM6B, dissociating AURKA and YY1 from the KDM6B promoter region and inducing differentiation. PMID: 29477140
The two zinc fingers of BuGZ directly bind to AurA, and BuGZ coacervation appears to promote AurA activation during spindle assembly. PMID: 29074706
Findings suggest that ATP/GTP binding protein like 2 (AGBL2) plays a critical oncogenic role in the pathogenesis of hepatocellular carcinoma (HCC) through modulation on immunity-related GTPase family, M protein (IRGM)-regulated autophagy and aurora kinase A (Aurora A) activity. PMID: 29126912
Polymorphisms of the Aurora Kinase a Gene is associated with Breast Cancer Risk. PMID: 28647900
Study suggests AURKA and TPX2 as potential stratification markers for taxane-based radiochemotherapy. In a lung adenocarcinoma cohort, high expression levels of AURKA and TPX2 were associated with specifically improved overall survival upon taxane-based radiochemotherapy. PMID: 28869599
In all, these data suggest that Aurora A plays a pivotal role in regulation of Androgen receptor variant 7 expression and represents a new therapeutic target in castrate-resistant prostate cancer. PMID: 28205582
The inverse correlation between the VHL gene expression profile and alisertib sensitivity was further confirmed in human cancer xenografts models. Taken together, these results suggested that VHL loss could potentially serve as a biomarker for predicting the efficacy of AURKA inhibitors. PMID: 29845253
LKB1 undergoes AURKA-mediated phosphorylation, which largely compromises the LKB1/AMPK signaling axis, in turn leading to the elevation of non-small cell lung cancer cell proliferation, invasion, and migration. PMID: 28967900
Epithelial ovarian cancer (EOC) cell apoptosis rate was repressed after treatment with lncRNA TUG1 mimic and promoted after treatment with lncRNA TUG1 inhibitor. AURKA expression, but not CLDN3, SERPINE1, or ETS1 expression, was adversely regulated by lncRNA TUG1 mimic and inhibitor. In conclusion, lncRNA TUG1 promotes cell proliferation and inhibits cell apoptosis through regulating AURKA in EOC cells. PMID: 30200102
Metformin disrupts malignant behavior of oral squamous cell carcinoma via a novel signaling involving Late SV40 factor/Aurora-A. Findings showed that a novel Late SV40 Factor and Aurora-A-signaling inhibition supports the rationale of using metformin as a potential oral squamous cell carcinoma therapeutic. PMID: 28465536
The present study confirmed that pAURKA is important in the development of gastric adenocarcinoma and revealed a novel functional link between PTEN, AURKA, and pAURKA activation. PMID: 29512701
The role of four AURKA single nucleotide polymorphisms on hepatocellular carcinoma susceptibility PMID: 29333101
AURKA overexpression is associated with chronic myeloid leukemia. PMID: 29387948
The data suggest that AKA is the vertebrate ancestral gene, and that AKB and AKC resulted from gene duplication in placental mammals. PMID: 29283376
Expression of AURKA and CHEK1 was linked with detrimental outcome in patients. Our data describe a synthetic lethality interaction between CHEK1 and AURKA inhibitors with potential translation to the clinical setting PMID: 28847989
These findings suggest that Aurora A SNP at codon 57 may predict disease outcome and response to alisertib in patients with solid tumors PMID: 29122619
LncRNA TUG1 associates with advanced disease and worse prognosis in adult AML patients, and it induces AML cell proliferation and represses cell apoptosis via targeting AURKA PMID: 29654398
Aurora A is able to individually shorten cilia when cilia are growing but requires interaction with never in mitosis-kinase 2 (Nek2) when cilia are being absorbed. Inhibition of Aurora A increases cilia number. PMID: 29141582
In patients who received alisertib for advanced or metastatic urothelial carcinoma, longer progression-free survival was observed in carriers of the minor allele A of rs2273535 in AURKA than in patients who were homozygous for the major allele T. PMID: 28155045
The combination also reduces the growth of PDAC xenografts in vivo. Mechanistically, it was found that inhibiting methyltransferases of the H3K9 pathway in cells, which are arrested in G2-M after targeting AURKA, decreases H3K9 methylation at centromeres, induces mitotic aberrations, triggers an aberrant mitotic check point response, and ultimately leads to mitotic catastrophe PMID: 28442587
Prostate cancer cells expressing an S273A mutant of CHIP have attenuated AR degradation upon 2-ME treatment compared with cells expressing wild-type CHIP, supporting the idea that CHIP phosphorylation by Aurora A activates its E3 ligase activity for the AR PMID: 28536143
Our results indicate that AURKA plays an important role in the activation of EIF4E and cap-dependent translation. Targeting the AURKA-EIF4E-c-MYC axis using alisertib is a novel therapeutic strategy that can be applicable for everolimus-resistant tumors and/or subgroups of cancers that show overexpression of AURKA and activation of EIF4E and c-MYC PMID: 28073841
Aurora-A may serve as a predictive biomarker of radiation response and a therapeutic target to reverse radiation therapy resistance. PMID: 28404933
We also propose a model for the stabilization mechanism in which binding to Aurora-A alters how N-Myc interacts with SCF(FbxW7) to disfavor the generation of Lys48-linked polyubiquitin chains PMID: 27837025
Results identified AURKA to be significantly upregulated in the lung squamous cell carcinoma tissues of smoking patients and may play an important role in diagnosis and prognosis. PMID: 28949095
Authors conclude that AURKA may revive dormant tumor cells via FAK/PI3K/Akt pathway activation, thereby promoting migration and invasion in laryngeal cancer. PMID: 27356739
Our identification of the novel interaction between Aurora A and H-Ras as a mechanism by which Aurora A can activate Ras-MAPK signaling opens the way for studies into perturbation of the Aurora A/H-Ras interaction and the effect on Ras-MAPK signaling. PMID: 28177880
MiR-124-3p has significant impact on proliferation, migration, and apoptosis of bladder cancer cells by targeting AURKA PMID: 28269755
Taken together, our data suggest that Aurora-A plays an important role in the suppression of autophagy by inhibiting the phosphorylation of Akt, which in turn prevents autophagy-induced apoptosis in prostate cancer PMID: 28269749
Results show that overexpression of Aurora-A and PTGS2 occurs in colon polyps and has a reverse correlation with miR-137 in both colon polyps and colorectal cancer tissue suggesting that AURKA and PTGS2 expression is under the regulation of mir-137. PMID: 27764771
SIX3 is a novel negative transcriptional regulator and acts as a tumor suppressor that directly represses the transcription of AURKA and AURKB in astrocytoma. PMID: 28595628
This report provides clear evidence that overexpression of the AURKA, SKA3, and DSN1 genes strongly correlates with the progression of colorectal adenomas to colorectal cancer PMID: 27329586
Although research biopsies were obtained on only a few patients, they did confirm pharmacodynamic effects of the drug. These effects suggest inhibition of Aurora B rather than Aurora A, which is consistent with pre-clinical data that show dose-dependent effects on both PMID: 27502708
Aurora A kinase is hyperphosphorylated in early mitosis under oxidative stress, which may disturb the function of Aurora A in mitotic spindle formation. PMID: 28017898
Our findings suggested that AURKA (rs911160) and AURKB (rs2289590) polymorphisms could affect GC risk. Further validation studies in larger and multi-ethnical populations are needed to elucidate their functional impact on the development of GC PMID: 28843004
Possible models of regulation of Lck by Aurora-A during T cell activation are described in the review. PMID: 27910998
Our study demonstrates that KCTD12 binds to CDC25B and activates CDK1 and Aurora A to facilitate the G2/M transition and promote tumorigenesis, and that Aurora A phosphorylates KCTD12 at serine 243 to trigger a positive feedback loop, thereby potentiating the effects of KCTD12. Thus, the KCTD12-CDC25B-CDK1-Aurora A axis has important implications for cancer diagnoses and prognoses. PMID: 28869606
Our findings showed novel regulatory mechanisms of p53 in regulating Aurora-A gene expression in non-small cell lung carcinoma cells. PMID: 28884479
HIP2 regulates mitotic spindle alignment. SHIP2 is expressed in G1 phase, whereas Aurora A kinase is enriched in mitosis. SHIP2 binds Aurora A kinase and the scaffolding protein HEF1 and promotes their basolateral localization at the expense of their luminal expression connected with cilia resorption. PMID: 27926875
Aurora kinase inhibitor CCT137690 induces necrosis-like death in pancreatic ductal adenocarcinoma cells, via RIPK1, RIPK3, and MLKL signaling. PMID: 28764929
Our data indicate that hnRNP Q1 is a novel trans-acting factor that binds to Aurora-A mRNA 5'-UTRs and regulates its translation, which increases cell proliferation and contributes to tumorigenesis in colorectal cancer PMID: 28079881
A central role of Aurora kinase A (AURKA) in promoting Epithelial-to-mesenchymal transition and cancer stem cell phenotypes via ALDH1A1. PMID: 28193222
Switching Aurora-A kinase on and off at an allosteric site has been documented. (Review) PMID: 28342286
This is the first report of F31I and V57I polymorphisms in AURKA gene in breast cancer in Iran PMID: 28906374
High Aurora A kinase expression is associated with triple-negative breast cancer. PMID: 27593935
Results provide evidence that AURKA is a target for the VHL E3 ligase ubiquitination. PMID: 28114281

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Database Links

HGNC: 11393

OMIM: 603072

KEGG: hsa:6790

STRING: 9606.ENSP00000216911

UniGene: Hs.250822

Protein Families

Protein kinase superfamily, Ser/Thr protein kinase family, Aurora subfamily

Subcellular Location

Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Cytoplasm, cytoskeleton, spindle pole. Cytoplasm, cytoskeleton, cilium basal body. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome, centriole. Cell projection, neuron projection.

Tissue Specificity

Highly expressed in testis and weakly in skeletal muscle, thymus and spleen. Also highly expressed in colon, ovarian, prostate, neuroblastoma, breast and cervical cancer cell lines.

Q&A

Basic Experimental Design: How do I validate the specificity of Phospho-AURKA (T288) antibodies in my cellular model?

Methodological Answer:
Specificity validation requires a multi-step approach:

Genetic Knockdown/Rescue: Transfect cells with siRNA targeting AURKA, then reintroduce wild-type or T288A mutant AURKA. A valid antibody should show signal loss only in knockdowns and T288A-rescued cells .
Phosphatase Treatment: Treat lysates with λ-phosphatase. Authentic phospho-specific signals will disappear (e.g., 48 kDa band in HeLa cells reduced by >90% post-treatment) .
Peptide Competition: Pre-incubate antibody with phosphorylated T288 peptide (10x molar excess). Validated antibodies (e.g., Sigma SAB5700386) show ≥80% signal reduction vs. non-phosphorylated controls .

Validation Parameter	Expected Outcome	Example Data (HeLa Cells)
siRNA Knockdown	Signal reduction ≥70%	85% decrease (WB)
Phosphatase Treatment	Band elimination	92% intensity loss
Peptide Competition	Dose-dependent inhibition	IC₅₀ = 0.5 μM phosphopeptide

Basic Application: What are optimal conditions for detecting phospho-AURKA (T288) in fresh vs. archived clinical samples?

Protocol Optimization:

Sample Type	Lysis Buffer	Protease Inhibitors	Phosphatase Inhibitors	Signal Stability
Fresh Frozen Tissue	RIPA + 1% SDS	1 mM PMSF + 10 μM Leupeptin	10 mM NaF + 1 mM Na3VO4	6 months at -80°C
FFPE Sections	Citrate Buffer (pH 6.0)	N/A	50 mM β-Glycerophosphate	Antigen retrieval critical (98°C, 20 min)

Note: Archived samples require epitope retrieval with proteinase K (10 μg/ml, 15 min) for consistent IHC signals .

Advanced Mechanistic Study: How to differentiate autophosphorylation vs. trans-phosphorylation of AURKA-T288 in live cells?

Kinase Activity Profiling:

Chemical Genetics: Express analog-sensitive AURKA (AS-AURKA) with bulky ATP analogs (1-NM-PP1) to inhibit trans-activity while preserving autophosphorylation .
FRET-Based Reporters: Use HTRF kits (e.g., Revvity 64AURAT2PEG) with anti-pT288 and pan-AURKA antibodies in time-course assays .
Mathematical Modeling:
$\frac{d[pT288]}{dt} = k_{auto}[AURKA]^2 + k_{trans}[AURKA][Upstream\ Kinase]$
Where $k_{auto}$ = 0.12 min⁻¹ (intrinsic autophosphorylation rate) .

Basic Technical Consideration: What controls are essential when comparing phospho-AURKA levels across cancer subtypes?

Normalization Framework:

Control Type	Purpose	Example Implementation
Total AURKA Loading	Correct for expression variance	Anti-AURKA (non-phospho) WB
Mitotic Index	Account for cell cycle effects % pH3-S10+ Cells (flow cytometry)
Housekeeping Protein	Normalize sample loading GAPDH (avoid β-actin in cytoskeletal drugs)

Critical Note: 75% of TNBC samples show AURKA overexpression (2.3-fold vs. normal) , requiring adjusted baselines.

Advanced Systems Biology: How to integrate phospho-AURKA (T288) data with kinome-wide profiling?

Multiplex Strategy:

Reverse Phase Protein Array (RPPA): Spot lysates (1 μg/μl) with phospho-AURKA (T288) antibody (1:1000) alongside 300+ kinase substrates .
PLA-Tag Technology: Use Duolink® probes to quantify AURKA-RPS6KB1 complexes (<40 nm proximity) in situ .

Basic Translational Research: What clinical correlations exist between phospho-AURKA (T288) levels and therapeutic response?

Key Findings:

Cancer Type	Treatment	pAURKA-T288 Change	Clinical Outcome Correlation (HR)	Study
Triple-Negative Breast	Paclitaxel	3.2-fold increase	Reduced DFS (HR=2.1, p=0.003)	N=228
Ovarian	Alisertib	89% reduction	Prolonged PFS (HR=0.58, p=0.02)	Phase II

Mechanistic Insight: Aurora A inhibitors (e.g., MLN8237) synergize with taxanes when administered post-mitotic arrest (72 hr sequential dosing) .

Advanced Method Development: How to measure real-time AURKA-T288 phosphorylation dynamics in live mitotic cells?

Live-Cell Imaging Protocol:

Transduce cells with GFP-AURKA biosensor (FRET-based T288 phosphorylation reporter) .
Image at 37°C with 5% CO₂ using spinning-disk confocal (100ms exposure, 2-min intervals).
Quantify using:
$\text{Phosphorylation Index} = \frac{I_{FRET}}{I_{CFP}} - \frac{I_{YFP}}{I_{CFP}}$
Key Finding: T288 phosphorylation initiates at nuclear envelope breakdown (NEBD + 3.2 ± 0.8 min) .

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Phospho-AURKA (T288) Antibody

Description

Definition and Mechanism

Techniques Utilized

Activation Pathways

Role in Disease

Challenges and Considerations

Product Specs

Target Background

Q&A

Basic Experimental Design: How do I validate the specificity of Phospho-AURKA (T288) antibodies in my cellular model?

Basic Application: What are optimal conditions for detecting phospho-AURKA (T288) in fresh vs. archived clinical samples?

Advanced Mechanistic Study: How to differentiate autophosphorylation vs. trans-phosphorylation of AURKA-T288 in live cells?

Basic Technical Consideration: What controls are essential when comparing phospho-AURKA levels across cancer subtypes?

Advanced Systems Biology: How to integrate phospho-AURKA (T288) data with kinome-wide profiling?

Basic Translational Research: What clinical correlations exist between phospho-AURKA (T288) levels and therapeutic response?

Advanced Method Development: How to measure real-time AURKA-T288 phosphorylation dynamics in live mitotic cells?

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