| Catalog No. | Host/Clonality | Reactivity | Applications | Immunogen Region |
|---|---|---|---|---|
| ABIN6265492 | Rabbit/Polyclonal | Human, Mouse, Rat | WB, IHC, ELISA, IF, ICC | N-terminal amino acids |
| 67371-1-Ig | Mouse/Monoclonal | Human, Mouse, Pig | WB, IHC, FC (Intra), ELISA | Fusion protein Ag29177 |
| Application | Dilution Range |
|---|---|
| Western Blot (WB) | 1:5,000 – 1:50,000 |
| IHC | 1:1,000 – 1:4,000 |
| Flow Cytometry | 0.80 µg/10^6 cells |
Breast Cancer: TBXAS1 is overexpressed in breast tumors and precancerous lesions (4.6-fold higher than normal tissues) . Knockdown of TBXAS1 in breast cancer cell lines (MCF-7, T47D, SK-BR-3) reduced anchorage-independent growth by 60–80% and impaired metastasis in murine 4T1 models .
Mechanistic Role: TBXAS1 enhances tumor invasion via thromboxane A2 (TXA2) signaling, which is attenuated by inhibitors like aspirin .
Ghosal Hematodiaphyseal Dysplasia: Mutations in TBXAS1 reduce enzyme activity, leading to elevated prostaglandin E2 levels, bone marrow fibrosis, and anemia . TBXAS1 antibodies aid in studying these molecular pathways.
Western Blot: Detects endogenous TBXAS1 at ~52–60 kDa in human platelets, placenta, and A549 cells .
Immunohistochemistry: Strong cytoplasmic staining observed in lung cancer tissues and mammary ducts .
Flow Cytometry: Validated for intracellular detection in A549 cells .
TBXAS1 antibodies are pivotal in exploring TXA2’s role in cancer metastasis , cardiovascular diseases, and bone disorders . Ongoing studies focus on therapeutic targeting of TBXAS1 in HER2-driven cancers and inflammatory conditions .
TBXAS1 (thromboxane A synthase 1) is an enzyme that catalyzes the conversion of prostaglandin endoperoxide (PGH2) into thromboxane A2 (TXA2). This enzyme plays crucial roles in vascular biology and hemostasis. TXA2 functions as a potent vasoconstrictor and inducer of platelet aggregation, making it essential for regulating vascular tension, maintaining blood fluidity, and proper hemostatic mechanisms . Additionally, TBXAS1 has been identified as a novel airway fibroblast-specific marker alongside integrin-8 (ITGA8) . Recent research reveals its involvement in multiple pathological processes, including cardiovascular diseases, cancer metastasis, and even psychiatric conditions like depression .
TBXAS1 antibodies demonstrate versatility across multiple experimental techniques. Based on validation data, these antibodies are particularly effective in Western Blot (WB), Immunohistochemistry (IHC), Flow Cytometry (FC), and ELISA applications . For researchers designing experiments, it's worth noting that TBXAS1 antibodies show validated reactivity with human, mouse, and pig samples, making them suitable for comparative cross-species studies . The choice of application should align with specific research questions - WB for protein expression quantification, IHC for localization in tissues, FC for cellular expression patterns, and ELISA for quantitative protein detection in complex samples.
TBXAS1 has a calculated molecular weight of 60 kDa, though it is typically observed at approximately 52 kDa in experimental settings, likely due to post-translational modifications or specific isoforms . The gene is located on chromosome 7q34 and comprises 13 exons and 12 introns . When designing experiments or interpreting results, researchers should account for this discrepancy between calculated and observed molecular weights to avoid misidentification. The TBXAS1 gene (GenBank accession number BC014117, Gene ID 6916, UNIPROT ID P24557) encodes the full protein, which is predominantly expressed in platelets but also present in other cell types .
Optimal antibody dilutions vary significantly depending on the experimental technique. Based on extensive validation, the following dilutions are recommended:
| Application | Recommended Dilution | Notes |
|---|---|---|
| Western Blot (WB) | 1:5000-1:50000 | High dilution range indicates good sensitivity |
| Immunohistochemistry (IHC) | 1:1000-1:4000 | Antigen retrieval with TE buffer pH 9.0 recommended; citrate buffer pH 6.0 as alternative |
| Flow Cytometry (FC) (INTRA) | 0.80 μg per 10^6 cells in 100 μl suspension | Optimized for intracellular detection |
It is strongly recommended to titrate the antibody for each specific experimental system to achieve optimal results, as sensitivity may vary depending on sample type and preparation methods . For IHC applications specifically, antigen retrieval conditions significantly impact staining quality and should be optimized for different tissue types.
Recent findings demonstrate that TBXAS1 and its product TXA2 play significant roles in cancer metastasis through immunosuppressive mechanisms . When designing experiments to investigate this relationship, researchers should consider:
T-cell function assays: Measure T-cell receptor-driven kinase signaling, proliferation, and effector functions in the presence and absence of TXA2 or TBXAS1 inhibitors.
Conditional knockout models: Utilize T cell-specific conditional deletion of genes like Arhgef1 (which mediates TXA2 immunosuppressive signaling) to assess impact on metastasis.
Pharmacological interventions: Include COX-1 inhibitors (such as aspirin) or selective TBXAS1 inhibitors in experimental designs to modulate the TXA2 pathway.
Metastasis quantification: Employ lung and liver metastasis models which have demonstrated particular sensitivity to TBXAS1-mediated effects .
This experimental approach allows for mechanistic understanding of how platelet-derived TXA2 suppresses anti-tumor immunity at metastatic sites, potentially revealing new therapeutic targets.
When selecting experimental models, researchers should prioritize systems with confirmed TBXAS1 expression. The following models have been validated for TBXAS1 antibody applications:
| Model Type | Validated Samples | Application |
|---|---|---|
| Cell lines | A549 cells | WB, FC (Intracellular) |
| Primary cells | Human peripheral blood platelets | WB |
| Tissues | Human placenta tissue, Human lung cancer tissue | WB, IHC |
| Animal samples | Pig blood | WB |
For IHC applications in human lung cancer tissue, proper antigen retrieval is critical for specific detection . These validated models provide reliable systems for investigating TBXAS1 expression and function across different physiological and pathological contexts.
TBXAS1 gene polymorphisms have been associated with various pathological conditions, including ischemic stroke, myocardial infarction, and depression . When designing studies to investigate these relationships, researchers should consider:
SNP selection: Focus on validated polymorphisms with functional consequences, such as NC_000007.14:g.139985896C>T, which has been associated with ischemic stroke risk, or rs6945590, which is linked to depression risk .
Genotyping methodologies: Utilize precise techniques such as Sequenom MassArray systems or PCR-based approaches for accurate genotyping .
Expression correlation analysis: Assess how specific polymorphisms affect TBXAS1 expression levels. For example, as the number of risk alleles (A) of rs6945590 increases, TBXAS1 expression decreases, correlating with increased depression symptoms .
Mendelian randomization (MR) studies: Employ MR methodologies to establish causality between TBXAS1 expression and disease phenotypes. This approach has successfully demonstrated that decreased TBXAS1 expression causally increases depression risk (β = –0.785; P = 3.82 × 10^-3) .
Symptom correlation analysis: Analyze associations between specific polymorphisms and individual disease symptoms or subtypes for more nuanced understanding of TBXAS1's role in pathophysiology .
When encountering contradictory results with TBXAS1 antibodies, consider these methodological approaches:
Antibody validation: Confirm antibody specificity using positive and negative controls. For TBXAS1, human peripheral blood platelets serve as excellent positive controls, while cell lines with TBXAS1 knockdown can function as negative controls .
Molecular weight verification: TBXAS1 has a calculated molecular weight of 60 kDa but is typically observed at 52 kDa. Ensure bands are analyzed at the correct molecular weight .
Cross-validation: Employ multiple detection methods (e.g., combine WB with IHC or FC) to verify findings through orthogonal techniques .
Isoform consideration: TBXAS1 has multiple splice variants that may be expressed differently across tissues. Verify which isoform your antibody targets and whether this matches your experimental system .
Sample preparation optimization: For intracellular proteins like TBXAS1, permeabilization conditions in FC significantly impact detection sensitivity. Optimize fixation and permeabilization protocols for your specific cell type .
Technical replication: Perform at least three independent experiments with appropriate technical replicates to establish reproducibility and statistical significance.
Recent research has revealed TBXAS1's crucial role in immune regulation, particularly through TXA2's effects on T cell function in cancer metastasis contexts . To functionally assess TBXAS1's immunological impact:
T cell signaling assays: Measure TCR-driven kinase signaling in the presence of TXA2 or TBXAS1 inhibitors to assess how the TBXAS1/TXA2 axis modulates T cell activation.
ARHGEF1 pathway analysis: Investigate the guanine exchange factor ARHGEF1-dependent pathway, which mediates TXA2's immunosuppressive effects on T cells .
In vivo models with conditional knockouts: Utilize T cell-specific deletion of genes like Arhgef1 to assess immune-mediated rejection of metastases in cancer models .
Pharmacological intervention studies: Employ COX-1 inhibitors (aspirin), selective TBXAS1 inhibitors, or TXA2 receptor antagonists to modulate the pathway and assess functional outcomes .
Immune cell proliferation and effector function assays: Quantify T cell proliferation, cytokine production, and cytotoxic activity in the presence of TXA2 or pathway inhibitors .
This multifaceted approach allows researchers to comprehensively assess how TBXAS1-derived TXA2 influences immune cell function in both physiological and pathological contexts.
TBXAS1 and its product TXA2 have emerged as critical factors in cancer metastasis through previously unrecognized immunosuppressive mechanisms. Recent groundbreaking research published in Nature (2025) has revealed that platelet-derived TXA2 suppresses anti-tumor immunity at metastatic sites . This research demonstrates:
Immunosuppressive pathway: TXA2 acts on T cells to trigger an immunosuppressive pathway dependent on the guanine exchange factor ARHGEF1, suppressing T cell receptor-driven kinase signalling, proliferation, and effector functions .
Genetic validation: T cell-specific conditional deletion of Arhgef1 in mice increases T cell activation at metastatic sites, promoting immune-mediated rejection of lung and liver metastases .
Pharmacological intervention: Aspirin, selective COX-1 inhibitors, or platelet-specific deletion of COX-1 reduces metastasis rates in a manner dependent on T cell-intrinsic expression of ARHGEF1 and TXA2 signaling .
These findings provide mechanistic insights into aspirin's anti-metastatic activity and open avenues for developing more effective anti-metastatic immunotherapies targeting the TBXAS1/TXA2 axis.
Recent genome-wide association studies have implicated TBXAS1 in psychiatric conditions, particularly depression. A 2024 study in a Korean population revealed:
Genetic association: The SNP rs6945590 was significantly associated with depressive symptoms (P = 2.83 × 10^-8; odds ratio = 1.23; 95% CI: 1.15–1.33) .
Expression correlation: Predicted expression levels of TBXAS1 were significantly decreased in whole blood tissues of participants with depressive symptoms .
Causal relationship: Mendelian randomization analysis demonstrated a causal association between decreased TBXAS1 expression and increased risk of depressive symptoms (β = –0.785; P = 3.82 × 10^-3) .
Symptom specificity: TBXAS1 expression was most significantly associated with specific depressive symptoms, particularly lack of satisfaction (item 4) and sleep disturbance (item 16) .
For researchers investigating this emerging field, approaches should include:
Gene expression studies in relevant neural tissues
Investigation of how TBXAS1/TXA2 signaling affects neuronal function
Analysis of potential inflammatory mechanisms linking TBXAS1 to mood regulation
Exploration of the arachidonic acid cascade in neural contexts, as TBXAS1 participates in this pathway
As TBXAS1 research expands into diverse fields, advanced methodological approaches for sensitive and specific detection have emerged:
Mass spectrometry-based proteomics: For absolute quantification of TBXAS1 protein levels in complex samples, particularly useful for comparing expression across different physiological states.
Single-cell analysis: Techniques such as single-cell RNA sequencing or mass cytometry allow identification of cell-specific TBXAS1 expression patterns within heterogeneous tissues.
Proximity ligation assays: For detecting TBXAS1 interactions with other proteins in situ, providing insights into protein complexes and signaling networks.
Live-cell imaging with tagged antibody fragments: For tracking TBXAS1 dynamics in real-time experimental systems.
Multiplexed immunohistochemistry: For co-localization studies of TBXAS1 with other proteins of interest in tissue samples.
When implementing these advanced methods, researchers should follow the validated sample preparation protocols for TBXAS1 detection, including appropriate buffer conditions (PBS with 0.1% sodium azide and 50% glycerol pH 7.3) and storage parameters (−20°C, stable for one year after shipment) .
Several promising research directions for TBXAS1 are emerging based on recent findings:
Immunometabolism: Investigating how TBXAS1/TXA2 signaling intersects with metabolic pathways in immune cells, particularly in the tumor microenvironment.
Precision medicine applications: Exploring TBXAS1 gene polymorphisms as biomarkers for disease risk stratification and treatment response, especially in cardiovascular disease and depression .
Novel inhibitor development: Designing selective TBXAS1 inhibitors that could provide therapeutic benefits with fewer side effects than general COX inhibitors like aspirin.
Neuroinflammatory mechanisms: Elucidating how TBXAS1 contributes to neuroinflammation in psychiatric and neurodegenerative conditions, building on recent findings linking it to depression .
T cell programming: Exploiting the newly discovered TBXAS1-ARHGEF1 immunosuppressive axis to enhance T cell responses in cancer immunotherapy approaches .