Analytical Data
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Gene name
ETHE1
- Application
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Alternative Names
ETHE1；HSCO;Persulfide dioxygenase ETHE1. mitochondrial
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Species
Human
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Source
E. coli
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Tag
His tag N-Terminus
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Purity
Greater than 90% as determined by SDS-PAGE.
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Uniprot
O95571
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Expression Region
13-254aa
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AA Sequence
MGSSHHHHHH SSGLVPRGSH MGSHMLSQRG GSGAPILLRQ MFEPVSCTFT YLLGDRESRE AVLIDPVLET APRDAQLIKE LGLRLLYAVN THCHADHITG SGLLRSLLPG CQSVISRLSG AQADLHIEDG DSIRFGRFAL ETRASPGHTP GCVTFVLNDH SMAFTGDALL IRGCGRTDFQ QGCAKTLYHS VHEKIFTLPG DCLIYPAHDY HGFTVSTVEE ERTLNPRLTL SCEEFVKIMG NLNLPKPQQI DFAVPANMRC GVQTPTA
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Molecular Weight
29 kDa
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Endotoxin
< 1.0 EU per μg protein as determined by the LAL method.
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Form
Freeze-dried powder
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Buffer formulation
PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300.
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Reconstitution
Reconstitute in ddH2O to a concentration of 0.1-0.5 mg/mL. Do not vortex.
- Customization
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Stability Test
The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37℃ for 48h, and no obvious degradation and precipitation were observed. The loss rate isless than 8% within the expiration date under appropriate storage condition.
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Storage & Shelf Life
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
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Shipping
In general, recombinant proteins are supplied as lyophilized powder and shipped at ambient temperature. For bulk packages, the proteins are provided as frozen liquid and shipped with blue ice, unless otherwise requested by the customer.
Quality inspection process
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Protein Description
ETHE1 is a crucial protein implicated in the cellular response to sulfide toxicity and the maintenance of mitochondrial function. Research into ETHE1 has gained significance due to its role in various biological processes and its association with specific human diseases, particularly ethylmalonic encephalopathy (EE), a rare metabolic disorder caused by mutations in the ETHE1 gene. This condition is characterized by neurological abnormalities, growth retardation, and metabolic dysfunctions. Understanding ETHE1's structure and function is vital for elucidating its mechanisms in sulfur metabolism and mitochondrial homeostasis. Studies have shown that ETHE1 acts as a sulfur dioxygenase, playing a pivotal role in detoxifying harmful sulfide compounds, thereby protecting cells from oxidative stress and mitochondrial damage. Moreover, disruptions in ETHE1 function can lead to an accumulation of sulfide, exacerbating cellular toxicity and contributing to disease pathology. Consequently, investigating the molecular dynamics of ETHE1, including its interactions with other cellular components and pathways, is essential for developing therapeutic strategies to manage diseases linked to ETHE1 dysfunction. Insights gained from ETHE1 research may not only enhance our understanding of sulfide metabolism but also pave the way for novel approaches in treating related metabolic disorders and improving mitochondrial health.
