Analytical Data
-
Gene name
CLN5
- Application
-
Alternative Names
CLN5；BMPS；Bis(monoacylglycero)phosphate synthase CLN5
-
Species
Human
-
Source
E. coli
-
Tag
His tag N-Terminus
-
Purity
Greater than 90% as determined by SDS-PAGE.
-
Uniprot
O75503
-
Expression Region
47-358aa
-
AA Sequence
IPSRRHWPVPYKRFDFRPKPDPYCQAKYTFCPTGSPIPVMEGDDDIEVFRLQAPVWEFKYGDLLGHLKIMHDAIGFRSTLTGKNYTMEWYELFQLGNCTFPHLRPEMDAPFWCNQGAACFFEGIDDVHWKENGTLVQVATISGNMFNQMAKWVKQDNETGIYYETWNVKASPEKGAETWFDSYDCSKFVLRTFNKLAEFGAEFKNIETNYTRIFLYSGEPTYLGNETSVFGPTGNKTLGLAIKRFYYPFKPHLPTKEFLLSLLQIFDAVIVHKQFYLFYNFEYWFLPMKFPFIKITYEEIPLPIRNKTLSGL
-
Molecular Weight
44.1 kDa
-
Endotoxin
< 1.0 EU per μg protein as determined by the LAL method.
-
Form
Freeze-dried powder
-
Buffer formulation
PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300.
-
Reconstitution
Reconstitute in ddH2O to a concentration of 0.1-0.5 mg/mL. Do not vortex.
- Customization
-
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.
-
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.
-
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
CLN5, or ceroid-lipofuscinosis neuronal protein 5, is linked to Batten disease, a neurodegenerative disorder characterized by lysosomal dysfunction and the accumulation of lipopigments in neurons. This disorder primarily affects children, leading to severe cognitive and motor decline, and ultimately, premature death. CLN5 mutations disrupt normal cellular processes, highlighting the importance of this protein in neuronal health. Recent studies have focused on the recombinant expression of CLN5 to better understand its structure, function, and interactions within the lysosomal milieu. By generating this recombinant protein, researchers aim to investigate the underlying mechanisms of CLN5’s role in lysosomal storage pathways and its impact on neurodegeneration. The knowledge gained from such studies is crucial for developing therapeutic interventions, including gene therapy and small molecule drugs, aimed at alleviating the symptoms of Batten disease and improving patient outcomes. Moreover, understanding CLN5's function at a molecular level could provide insights not only into Batten disease but also into related neurodegenerative disorders with lysosomal dysfunction, thus broadening the implications of this research beyond a single condition.
