Product Name: CDK4 (169-175) pT172
Product Number: PE-04AJN99
Size: 200 µg      Price:42.00
1 mg      $US84.00
Peptide Name: CDK4 (169-175) pT172

Product Use: Services as a blocking peptide for use with the CDK4-pT172 rabbit polyclonal antibody (Cat. No.: AB-PK569) that is also available from Kinexus. This phosphopeptide may also be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the protein kinase catalytic domain activation T-loop between subdomains VII and VIII. T172 stimulates phosphotransferase activity.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: MAL-pT-PVV

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys
Peptide Modifications Other: Phosphorylated

Peptide Molecular Mass Calculated: 984.12 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Related Product 1: CDK4 - pT172 phosphosite-specific antibody (Cat. No.: AB-PK569)

Scientific Background: CDK4 is a protein-serine/threonine kinase of the CMGC group and CDK family. It functions as a component of the cyclin D-CDK4 complex that inhibits retinoblastoma (RB) family members (e.g. RB1) and regulates the G1/S phase transtion of the cell cycle. Phosphorylation of T172 increases phosphotransferase activity, whereas Y17 phosphorylation is inhibitory. Phosphorylation of RB1 by CDK4 releases the transcription factor E2F from the RB-E2F complex, which then translocates to the nucleus and stimulates transcription of genes involved in the progression of the cell through the G1 phase. In addition, cyclin D-CDK4 complexes are central integrators of mitogenic and anti-mitogenic signals. The ability of CDK4 to phosphorylate the RB protein is directly inhibited by the p16, p15, and p18 proteins. CDK4 appears to be an oncoprotein (OP). It has a key role in the promotion of tumourigenesis, either due to a mutation that prevents p16-mediated inhibition of the CDK4 protein or resulting from the elevated expression of CDK4 that effectively overwhelms the inhibitory capacity of the normal levels of p16 protein. Several mutations in the CDK4 gene sequence have been identified in melanoma patients, including a somatic R24C substitution and a germline R24H substitution. CDK4 activity is necessary for Ras-mediated transformation in a variety of cancer types. Furthermore, over-expression of both the CDK4 gene and protein are observed in a significant proportion of human breast cancer specimens, corresponding with elevated levels of the cyclin D1 protein. Additionally, elevated expression of CDK4 is also commonly observed in sarcoma and glioma cancer cells. In general, CDK4 levels are up-regulated 1.6-fold in human tumours compared to most other protein kinases.