Analytical Data
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Gene name
PPT1
- Application
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Alternative Names
PPT; CLN1; INCL; Ceroid-Lipofuscinosis,Neuronal 1,Infantile; Palmitoyl-protein hydrolase 1
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Species
Mouse
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Source
E. coli
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Tag
N-His
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Purity
Greater than 95% as determined by SDS-PAGE.
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Uniprot
O88531
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Expression Region
Asp28~Lys279
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Molecular Weight
32kDa
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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 PPT1 (palmitoyl-protein thioesterase 1) has gained significant attention due to its critical role in the pathogenesis of neurodegenerative disorders, particularly Batten disease, a severe childhood neurodegeneration caused by genetic mutations in the PPT1 gene. PPT1 is an enzyme responsible for the removal of palmitate from proteins, a post-translational modification that influences membrane localization, protein stability, and cellular signaling. Deficiencies in PPT1 activity lead to the accumulation of palmitoylated proteins in neuronal cells, contributing to cellular dysfunction and neurodegeneration. Research into PPT1 has focused on understanding its enzymatic mechanisms, substrate specificity, and the biochemical pathways affected by its deficiency. Additionally, therapeutic strategies, including gene therapy, small molecule compounds, and enzyme replacement therapies, are being explored to restore PPT1 function and mitigate the progression of associated neurodegenerative diseases. As advances are made in elucidating PPT1's biological roles and interactions, the findings hold promise for developing novel approaches to treat or even prevent the onset of disorders linked to PPT1 deficiency, underscoring the importance of continued research in this field.
