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Trehalase (prokaryote)

Product code: E-TREH
€122.00

8,400 Units

Prices exclude VAT

This product is currently unavailable, please contact cs@megazyme.com.

Content: 8,400 Units
Shipping Temperature: Ambient
Storage Temperature: 2-8oC
Formulation: In 3.2 M ammonium sulphate
Physical Form: Suspension
Stability: > 4 years at 4oC
Enzyme Activity: Other Activities
EC Number: 3.2.1.28
CAZy Family: GH37
CAS Number: 9025-52-9
Synonyms: alpha,alpha-trehalase; alpha,alpha-trehalose glucohydrolase
Source: Prokaryote
Molecular Weight: 63,636
Concentration: Supplied at ~ 4,200 U/mL
Expression: Recombinant from a Prokaryotic source
Specificity: Catalyses the reaction:
Trehalose + H2O = β-D-glucose + α-D-glucose
Specific Activity: ~ 180 U/mg (40oC, pH 5.5 on trehalose)
Unit Definition: One Unit of trehalase activity is defined as the amount of enzyme required to release two µmoles of D-glucose per minute from trehalose (5 mg/mL) in sodium maleate buffer (100 mM), pH 5.5 at 40oC.
Temperature Optima: 40oC
pH Optima: 5.5
Application examples: Applications established for the measurement of trehalose in the food, fermentation, wine, beverage and dairy industries.

This product has been discontinued (read more).

High purity Trehalase (prokaryote) for use in research, biochemical enzyme assays and in vitro diagnostic analysis.

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Documents
Certificate of Analysis
Safety Data Sheet
Data Sheet
Publications
Publication

Metabolomics provide new insights into mechanisms of Wolbachia-induced paternal defects in Drosophila melanogaster.

Zhang, H. B., Cao, Z., Qiao, J. X., Zhong, Z. Q., Pan, C. C., Liu, C., Zhang, L. & Wang, Y. F. (2021). PLoS pathogens, 17(8), e1009859.

Wolbachia is a group of intracellular symbiotic bacteria that widely infect arthropods and nematodes. Wolbachia infection can regulate host reproduction with the most common phenotype in insects being cytoplasmic incompatibility (CI), which results in embryonic lethality when uninfected eggs fertilized with sperms from infected males. This suggests that CI-induced defects are mainly in paternal side. However, whether Wolbachia-induced metabolic changes play a role in the mechanism of paternal-linked defects in embryonic development is not known. In the current study, we first use untargeted metabolomics method with LC-MS to explore how Wolbachia infection influences the metabolite profiling of the insect hosts. The untargeted metabolomics revealed 414 potential differential metabolites between Wolbachia-infected and uninfected 1-day-old (1d) male flies. Most of the differential metabolites were significantly up-regulated due to Wolbachia infection. Thirty-four metabolic pathways such as carbohydrate, lipid and amino acid, and vitamin and cofactor metabolism were affected by Wolbachia infection. Then, we applied targeted metabolomics analysis with GC-MS and showed that Wolbachia infection resulted in an increased energy expenditure of the host by regulating glycometabolism and fatty acid catabolism, which was compensated by increased food uptake. Furthermore, overexpressing two acyl-CoA catabolism related genes, Dbi (coding for diazepam-binding inhibitor) or Mcad (coding for medium-chain acyl-CoA dehydrogenase), ubiquitously or specially in testes caused significantly decreased paternal-effect egg hatch rate. Oxidative stress and abnormal mitochondria induced by Wolbachia infection disrupted the formation of sperm nebenkern. These findings provide new insights into mechanisms of Wolbachia-induced paternal defects from metabolic phenotypes.

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Publication

Separate immobilization of glucose oxidase and trehalase, and optimization of enzyme-carbon nanotube layers for the anode of enzymatic fuel cells utilizing trehalose.

Wang, X., Zhang, Y. Q., Kim, H. H. & Kim, C. J. (2021). Electrochimica Acta, 392, 138974.

Insect cyborgs can be used as search robots in disaster areas and as environmental monitoring robots. In this study, we aimed to develop an anode for compact enzymatic fuel cells (EFCs) utilizing trehalose to power electronic devices implanted in such insects. Conventional trehalose-EFCs are fabricated by co-immobilization of glucose oxidase (GOx) and trehalase (TREH) on the surface of the anode. Here, we showed that current generation can be enhanced by separate immobilization of GOx and TREH using agarose. The effects of GOx-redox mediator layers, TREH loading, and the incorporation of single-walled carbon nanotubes (SWCNTs) on the performance of GOx-TREH anodes were investigated. The optimal arrangement of GOx-redox mediator layers with or without SWCNTs was determined. The highest oxidation current density (494 μA/cm2) was obtained at an electrode composed of three GOx-redox mediator layers and three GOx-redox mediator-SWCNTs layers, and agarose containing TREH. The bilirubin oxidase (BOD)-redox mediator layers and SWCNTs also influenced the performance of cathode. The highest reduction current intensity was obtained for the cathode with six BOD-redox mediator-SWCNTs layers. EFCs with the optimized anode and cathode showed a power density of ca. 15 μW/cm2 at a cell voltage of 0.3 V under a discharge current density of 50 μA/cm2.

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Publication

Roles of PINK1 in regulation of systemic growth inhibition induced by mutations of PTEN in Drosophila.

Han, Y., Zhuang, N., & Wang, T. (2021). Cell Reports, 34(12), 108875.

The maintenance of mitochondrial homeostasis requires PTEN-induced kinase 1 (PINK1)-dependent mitophagy, and mutations in PINK1 are associated with Parkinson’s disease (PD). PINK1 is also downregulated in tumor cells with PTEN mutations. However, there is limited information concerning the role of PINK1 in tissue growth and tumorigenesis. Here, we show that the loss of pink1 caused multiple growth defects independent of its pathological target, Parkin. Moreover, knocking down pink1 in muscle cells induced hyperglycemia and limited systemic organismal growth by the induction of Imaginal morphogenesis protein-Late 2 (ImpL2). Similarly, disrupting PTEN activity in multiple tissues impaired systemic growth by reducing pink1 expression, resembling wasting-like syndrome in cancer patients. Furthermore, the re-expression of PINK1 fully rescued defects in carbohydrate metabolism and systemic growth induced by the tissue-specific pten mutations. Our data suggest a function for PINK1 in regulating systemic growth in Drosophila and shed light on its role in wasting in the context of PTEN mutations.

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Publication

Metabolic profiling identifies trehalose as an abundant and diurnally fluctuating metabolite in the microalga Ostreococcus tauri.

Liverani, S., Mahlow, S., Bouget, F. Y., Pohnert, G., & Sasso, S. (2017). Metabolomics, 13, 68.

The picoeukaryotic alga Ostreococcus tauri (Chlorophyta) belongs to the widespread group of marine prasinophytes. Despite its ecological importance, little is known about the metabolism of this alga. Objectives: In this work, changes in the metabolome were quantified when O. tauri was grown under alternating cycles of 12 h light and 12 h darkness. Methods: Algal metabolism was analyzed by gas chromatography-mass spectrometry. Using fluorescence-activated cell sorting, the bacteria associated with O. tauri were depleted to below 0.1% of total cells at the time of metabolic profiling. Results: Of 111 metabolites quantified over light–dark cycles, 20 (18%) showed clear diurnal variations. The strongest fluctuations were found for trehalose. With an intracellular concentration of 1.6 mM in the dark, this disaccharide was six times more abundant at night than during the day. This fluctuation pattern of trehalose may be a consequence of starch degradation or of the synchronized cell cycle. On the other hand, maltose (and also sucrose) was below the detection limit (~10 µM). Accumulation of glycine in the light is in agreement with the presence of a classical glycolate pathway of photorespiration. We also provide evidence for the presence of fatty acid methyl and ethyl esters in O. tauri. Conclusions: This study shows how the metabolism of O. tauri adapts to day and night and gives new insights into the configuration of the carbon metabolism. In addition, several less common metabolites were identified.

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Publication

The role of oxygen in yeast metabolism during high cell density brewery fermentations.

Verbelen, P. J., Saerens, S. M. G., Van Mulders, S. E., Delvaux, F. & Delvaux, F. R. (2009). Applied Microbiology and Biotechnology, 82(6), 1143-1156.

The volumetric productivity of the beer fermentation process can be increased by using a higher pitching rate (i.e., higher inoculum size). However, the decreased yeast net growth observed in these high cell density fermentations can have a negative impact on the physiological stability throughout subsequent yeast generations. The use of different oxygen conditions (wort aeration, wort oxygenation, yeast preoxygenation) was investigated to improve the growth yield during high cell density fermentations and yeast metabolic and physiological parameters were assessed systematically. Together with a higher extent of growth (dependent on the applied oxygen conditions), the fermentation power and the formation of unsaturated fatty acids were also affected. Wort oxygenation had a significant decreasing effect on the formation of esters, which was caused by a decreased expression of the alcohol acetyl transferase gene ATF1, compared with the other conditions. Lower glycogen and trehalose levels at the end of fermentation were observed in case of the high cell density fermentations with oxygenated wort and the reference fermentation. The expression levels of BAP2 (encoding the branched chain amino acid permease), ERG1 (encoding squalene epoxidase), and the stress responsive gene HSP12 were predominantly influenced by the high cell concentrations, while OLE1 (encoding the fatty acid desaturase) and the oxidative stress responsive genes SOD1 and CTT1 were mainly affected by the oxygen availability per cell. These results demonstrate that optimisation of high cell density fermentations could be achieved by improving the oxygen conditions, without drastically affecting the physiological condition of the yeast and beer quality.

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Safety Information
Symbol : GHS08
Signal Word : Danger
Hazard Statements : H334
Precautionary Statements : P261, P284, P304+P340, P342+P311, P501
Safety Data Sheet
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