CDK6/CycD3 Kinase TR-FRET Detection Kit
Item | Cat# | Price |
TR-FRET Detection Kit | SNB-B-0019 | Inquiry |
Compound Test Services | CT-001 | $1,050 per 384w plate (Up To 16 cpds Dose) |
Product Description
Cyclin-dependent kinases (CDKs) are a family of serine/threonine kinases that play central roles in regulating the eukaryotic cell cycle. Their activity depends on association with specific cyclins, which control CDK activation at distinct cell cycle phases. For example, CDK4/6–cyclin D complexes drive G1 phase progression, while CDK1–cyclin B controls entry into mitosis. CDKs function by phosphorylating key substrates that govern DNA replication, mitotic entry, and transcriptional regulation. Beyond cell cycle control, several CDKs (e.g., CDK7, CDK9) are involved in transcriptional regulation via phosphorylation of RNA polymerase II. Dysregulation of CDK activity is frequently observed in cancer, leading to uncontrolled proliferation. Consequently, selective CDK inhibitors such as palbociclib, ribociclib, and abemaciclib have been developed as targeted therapies, particularly for breast cancer, underscoring the critical role of CDKs in both normal cellular homeostasis and oncogenesis.
Screeningbio’s TR-FRET CDKs kinase assay kit is designed to measure the relative activity levels of kinases. The kit uses a specific CDKs kinase substrate and detection reagents to evaluate kinase activity. Cyclin-dependent kinases (CDKs) constitute a large family, including CDK1/3/4/6/7/9/10/12/13/15–18, which specifically recognize and phosphorylate the Retinoblastoma-associated protein (Rb) at serine residue 780 (S780). Therefore, this kit employs an optimized Rb (S780) peptide as a substrate, coupled with TR-FRET LA(TR-FRET Acceptor) and TR-FRET Solar Eu conjugates(TR-FRET Donor), together with a phospho-Rb (S780)–specific antibody. This allows kinase activity to be quantified by detecting the level of phosphorylated substrate.
Data
Target Background
Cyclin-dependent kinase 6 (CDK6) is a serine/threonine kinase that plays a central role in regulating the G1 to S phase transition of the cell cycle. Functionally similar to CDK4, CDK6 forms active complexes with D-type cyclins (Cyclin D1, D2, or D3) in response to mitogenic and growth signals. The CDK6/Cyclin D complex phosphorylates the retinoblastoma protein (Rb), leading to the release of E2F transcription factors and activation of genes necessary for DNA replication and cell-cycle progression.
Beyond its canonical cell-cycle function, CDK6 also contributes to cell differentiation, hematopoiesis, and tumorigenesis. In hematopoietic and neuronal cells, CDK6 has been shown to act as a transcriptional regulator independent of its kinase activity, influencing gene expression related to proliferation and differentiation.
Dysregulation of CDK6—through overexpression, amplification, or loss of upstream inhibitors such as p16^INK4a—has been implicated in various malignancies, including leukemia, lymphoma, glioblastoma, and breast cancer. Its oncogenic role makes CDK6 a critical target for cancer therapy.
Clinically, selective CDK4/6 inhibitors such as palbociclib, ribociclib, and abemaciclib effectively block CDK6-mediated Rb phosphorylation, inducing G1 cell-cycle arrest and suppressing tumor growth. These inhibitors have revolutionized the treatment of hormone receptor–positive breast cancer and are being investigated for broader oncologic applications.