Analytical Data
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Gene name
FMR1
- Application
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Alternative Names
FMRP; FRAXA
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Species
Human
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Source
E. coli
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Tag
N-His
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Purity
Greater than 90% as determined by SDS-PAGE.
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Uniprot
Q06787
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Expression Region
Met1~Val314
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Molecular Weight
42&40kDa
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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 FMR1 gene, located on the X chromosome, encodes the Fragile X Mental Retardation Protein (FMRP), which is crucial for neural development and synaptic plasticity. Mutations or expansions in the FMR1 gene lead to Fragile X syndrome (FXS), a common hereditary form of intellectual disability and a major cause of autism spectrum disorders. In FXS patients, the hypermethylation of the FMR1 promoter typically results in the silencing of the gene, leading to the loss of FMRP. Research on recombinant FMR1 protein focuses on understanding the structure and function of FMRP, which plays a significant role in mRNA transport and translation regulation. Through techniques such as protein expression and purification, scientists aim to investigate the molecular mechanisms underlying FMRP's role in synaptic function and neurodevelopmental processes. This research not only enhances our understanding of the pathophysiology of FXS but also opens avenues for potential therapeutic interventions targeting synaptic malfunctions associated with the absence of FMRP. By studying the FMR1 recombinant protein, researchers hope to identify critical interactions and pathways that could be modulated to restore normal function in affected individuals, thereby providing insights into strategies for treatment and management of FXS-related symptoms.











