CDK3/CycE2 Kinase TR-FRET Detection Kit
Item | Cat# | Price |
TR-FRET Detection Kit | SNB-B-0010 | 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 3 (CDK3) is a serine/threonine kinase belonging to the cyclin-dependent kinase family, which orchestrates orderly cell-cycle progression. Although less extensively studied than CDK1 or CDK2, CDK3 plays a distinct regulatory role in the transition from the G0 quiescent state to the G1 phase and in the progression from G1 to S phase. CDK3 exerts its activity primarily through association with Cyclin C, forming the CDK3/Cyclin C complex that phosphorylates key substrates to promote cell-cycle re-entry.
One of the best-characterized substrates of CDK3 is the retinoblastoma protein (Rb). Phosphorylation of Rb by CDK3 leads to the release of E2F transcription factors, thereby activating genes necessary for DNA synthesis and cell-cycle initiation. Through this mechanism, CDK3 facilitates the reactivation of quiescent cells and supports the onset of proliferation.
CDK3 also participates in transcriptional regulation and DNA damage response, linking growth signals to cell-cycle control. Aberrant CDK3 expression or activation has been observed in certain cancers, including glioblastoma and colorectal carcinoma, where it contributes to enhanced cell proliferation and tumor progression. Due to its unique position at the G0/G1 transition, CDK3 represents a potential therapeutic target for controlling abnormal cell-cycle reactivation in proliferative diseases.