Aspartate aminotransferase, Genetically engineered bacteria
Based on 1 publication(s) in Google Scholar
Aspartate aminotransferase (EC 2.6.1.1), Genetically engineered bacteria is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Genetically engineered bacteria comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Genetically engineered bacteria also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Genetically engineered bacteria is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers.
For research use only. We do not sell to patients.
- CAS No.: 9000-97-9
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Aspartate aminotransferase, Genetically engineered bacteria
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Biological Activity
Description
In Vitro
Aspartate aminotransferase, Genetically engineered bacteria has increased synthesis and release in adipocytes treated with rosiglitazone (HY-17386), which catalyzes the aminotransferase reaction between aspartate and α-ketoglutarate[1].
This product can be used as a quality control product for ast kits and as an antigen to prepare anti-cAST antibodies.
Molecular weight: ~58kDa (SDS-PAGE)
pH Stability: 5.0-9.5 (20°C 24 h)
Thermal stability: no deactivation below 60°C for 30 min.
Reconstitution and dilution buffer: It is recommended to use phosphate buffer containing BSA.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
EC Number
2.6.1.1
Enzyme Activity
≥250 U/mL
Chemical Information
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CAS No. 9000-97-9
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Appearance Liquid
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Color Colorless to light yellow
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SMILES
[Aspartate aminotransferase, Genetically engineered bacteria]
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Synonyms
EC 2.6.1.1; GOT; AST
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
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Cell Metab
Hepatocyte-to-intestinal stem cell remote communication regulates blood glucose homeostasis. [Abstract]2026 Jul 7;38(7):1367-1384.e9. PMID: 42309059
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Hepatotoxicity Study
This protocol evaluates hepatotoxicity using complementary in vivo mouse APAP acute liver injury and in vitro hepatocyte-based cytotoxicity readouts. In vivo APAP injury is assessed by serum ALT/AST, liver histology, hepatic glutathione, protein adducts, necrosis, inflammation, and regeneration-related endpoints. In vitro hepatotoxicity is assessed by loss of viability, leakage of ALT/AST/LDH, oxidative-stress markers, mitochondrial function, nuclear morphology, intracellular calcium, and high-content imaging endpoints.
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Liver Histomorphometry
Liver histomorphometry is a quantitative histological approach used to measure structural alterations in hepatic tissue, including parenchymal loss, steatosis, fibrosis, and vascular remodeling, by combining stained tissue section analysis with stereological or computerized image-based measurements. Classical morphometric frameworks quantify volume fractions of liver compartments and fibrotic regions using systematic sampling and image analysis, enabling objective comparison of pathological changes across experimental groups. These approaches are widely applied in liver cirrhosis and fibrosis studies to reduce subjectivity in histological scoring and improve reproducibility of tissue evaluation. Recent methodological advances integrate automated image analysis and radiomics-based extraction of histological features from standard liver stains (e. g. , H&E and fibrotic stains), enabling quantitative correlation between morphometric features and fibrosis stages in non-alcoholic fatty live
Purity & Documentation
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Data Sheet (267 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)