Analytical Data
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Gene name
CLN6
- Application
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Alternative Names
CLN6; Ceroid-lipofuscinosis neuronal protein 6; Protein CLN6
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Species
Human
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Source
E. coli
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Tag
GST-tag at N-terminal
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Purity
Greater than 90% as determined by SDS-PAGE.
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Uniprot
Q9NWW5
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Expression Region
1-311aa
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AA Sequence
MEATRRRQHLGATGGPGAQLGASFLQARHGSVSADEAARTAPFHLDLWFY FTLQNWVLDFGRPIAMLVFPLEWFPLNKPSVGDYFHMAYNVITPFLLLKL IERSPRTLPRSITYVSIIIFIMGASIHLVGDSVNHRLLFSGYQHHLSVRE NPIIKNLKPETLIDSFELLYYYDEYLGHCMWYIPFFLILFMYFSGCFTAS KAESLIPGPALLLVAPSGLYYWYLVTEGQIFILFIFTFFAMLALVLHQKR KRLFLDSNGLFLFSSFALTLLLVALWVAWLWNDPVLRKKYPGVIYVPEPW AFYTLHVSSRH
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Molecular Weight
62.3 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
CLN6 is a protein associated with the neuronal ceroid lipofuscinoses (NCLs), a group of inherited neurodegenerative disorders predominantly affecting children. The CLN6 gene, located on chromosome 15, encodes a protein involved in lysosomal function and cellular homeostasis. Mutations in CLN6 lead to the accumulation of lipofuscins, indicative of lysosomal dysfunction, resulting in progressive neurodegeneration. Understanding the structure and function of CLN6 is crucial for elucidating the pathophysiological mechanisms underlying NCLs, which currently have no effective treatments. Research into recombinant CLN6 protein aims to facilitate the study of its interactions within cellular pathways and potential therapeutic interventions. By producing and characterizing this protein, scientists can explore its role in lysosomal signaling, investigate the effects of specific mutations, and develop targeted strategies to mitigate disease progression. Furthermore, recombinant CLN6 may serve as a valuable tool for high-throughput screening of drug candidates and for studying potential gene therapies. Overall, the investigation of CLN6 recombinant protein is pivotal for advancing our understanding of NCLs and for paving the way toward innovative treatments for affected individuals.
