CDK2/CycD1 Kinase TR-FRET Detection Kit
Item | Cat# | Price |
TR-FRET Detection Kit | SNB-B-0006 | 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 2 (CDK2) is a serine/threonine protein kinase that plays a pivotal role in regulating the eukaryotic cell cycle, particularly the transitions between the G1/S and S/G2 phases. CDK2 activity is dependent on its association with regulatory cyclins—Cyclin E during the G1/S transition and Cyclin A during S phase progression. Upon activation through cyclin binding and phosphorylation at threonine 160, CDK2 phosphorylates multiple substrates involved in DNA replication initiation, centrosome duplication, and cell-cycle checkpoint control.
Functionally, CDK2 ensures the orderly initiation of DNA synthesis and prevents re-replication by phosphorylating key replication factors such as CDC6, NPAT, and MCM proteins. It also contributes to chromatin remodeling and histone modification, thereby coordinating replication with transcriptional regulation.
CDK2 activity is tightly regulated by cyclin-dependent kinase inhibitors (CKIs) such as p21^Cip1 and p27^Kip1, which block its activation under stress or DNA damage conditions. Dysregulation or overactivation of CDK2 has been implicated in various cancers, promoting uncontrolled cell proliferation and genomic instability. Consequently, CDK2 is an important target in oncology research, and selective CDK2 inhibitors are being developed to suppress aberrant cell-cycle progression in tumor cells.