Analytical Data
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Gene name
CDK18-CCNY
- Application
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Species
Human
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Source
Baculovirus
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Tag
GST;Flag
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Purity
Greater than 90% as determined by SDS-PAGE.
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Uniprot
Q07002-2 (M1-F474)&Q8ND76-1
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Expression Region
Q07002-2 (M1-F474)&Q8ND76-1 (M1-S341)
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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
CDK18-CCNY is a hybrid protein complex that plays a critical role in the regulation of cell cycle progression and gene expression. Cyclin-dependent kinases (CDKs) are key regulators of the cell cycle, and CDK18 has been identified as a member of this family that interacts specifically with the cyclin CCNY (Cyclin Y) to form a functional complex. This interaction is significant as it influences various signaling pathways related to cell proliferation, differentiation, and response to stress. Research into the CDK18-CCNY complex has gained attention due to its potential implications in cancer biology, where dysregulation of the cell cycle is a hallmark of tumorigenesis. Studies have suggested that aberrations in the expression or activity of CDK18 and CCNY may contribute to the progression of certain cancers, making this complex a potential therapeutic target. Understanding the molecular mechanisms governing the CDK18-CCNY interaction and its downstream effects could provide insights into novel strategies for cancer treatment and highlight the importance of targeted therapies in managing malignancies driven by cell cycle dysregulation. Furthermore, elucidating the precise roles of CDK18 and CCNY in various cellular contexts will enhance our understanding of their biological significance, opening avenues for future research aimed at exploiting this pathway for therapeutic interventions.
