Analytical Data
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Gene name
FXN
- Application
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Alternative Names
FXN；FRDA；X25；;Frataxin. 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
Q16595
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Expression Region
1-210aa
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AA Sequence
MWTLGRRAVAGLLASPSPAQAQTLTRVPRPAELAPLCGRRGLRTDIDATCTPRRASSNQRGLNQIWNVKKQSVYLMNLRKSGTLGHPGSLDETTYERLAEETLDSLAEFFEDLADKPYTFEDYDVSFGSGVLTVKLGGDLGTYVINKQTPNKQIWLSSPSSGPKRYDWTGKNWVYSHDGVSLHELLAAELTKALKTKLDLSSLAYSG kDa
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Molecular Weight
28.1 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
Related Products
Protein Description
The study of FXN (Frataxin) recombinant protein has gained significant attention due to its critical role in mitochondrial function and iron-sulfur cluster biosynthesis. Frataxin is a small mitochondrial protein encoded by the FXN gene, and its deficiency is associated with Friedreich's ataxia, a debilitating neurodegenerative disorder that leads to progressive loss of motor coordination, sensory loss, and diabetes. Patients with Friedreich's ataxia suffer from impaired mitochondrial energy production and increased oxidative stress resulting from iron accumulation. In recent years, researchers have focused on the potential of FXN recombinant protein as a therapeutic strategy to restore function and alleviate symptoms in affected individuals. Advances in protein expression systems have enabled the production of high-purity recombinant FXN, facilitating studies that decipher its biochemical properties, interaction with other mitochondrial proteins, and overall role in cellular metabolism. Furthermore, these studies have led to explorations of gene therapy and small molecule drugs aimed at increasing FXN levels in patients. Understanding the mechanistic pathways involving FXN has the potential not only to advance treatments for Friedreich's ataxia but also to provide insights into other mitochondrial disorders, making FXN recombinant protein a focal point of contemporary biomedical research.
