CDK5/p25 Kinase TR-FRET Detection Kit
Item | Cat# | Price |
TR-FRET Detection Kit | SNB-B-0015 | 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 5 (CDK5) is an atypical member of the cyclin-dependent kinase family that plays essential roles in the nervous system rather than in classical cell-cycle regulation. Unlike other CDKs, CDK5 is not activated by cyclins but instead by neuron-specific activators such as p35 and p39. The CDK5/p35 or CDK5/p39 complexes are highly expressed in post-mitotic neurons, where they regulate diverse processes including neuronal migration, axonal guidance, synaptic plasticity, and neurotransmitter release.
Functionally, CDK5 phosphorylates a wide range of neuronal substrates, including tau, neurofilament proteins, synapsin, and dynamin I, thereby influencing cytoskeletal dynamics, vesicle trafficking, and synaptic function. Proper CDK5 activity is crucial for maintaining neuronal architecture and signaling. However, under pathological conditions such as oxidative stress or neurotoxic insult, cleavage of p35 into p25 leads to aberrant CDK5 hyperactivation and mislocalization, resulting in excessive phosphorylation of tau and other proteins. This process contributes to neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS).
Beyond the nervous system, CDK5 also participates in cell adhesion, migration, and apoptosis in non-neuronal cells. Because of its dual role in neuronal development and degeneration, CDK5 has emerged as a potential therapeutic target for neuroprotection and the treatment of neurodegenerative disorders.