A synthetic peptide corresponding to residues on the N-terminus of human CDK4 was used as an immunogen.
Buffer
50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.
Clone Name
EPR2513Y
Isotype
IgG
Species Reactivity
Human
Concentration
Purification
Guaranteed Application *
WB
Suggested Dilutions
WB (1:500); Flow Cytometry (1:60); IP (1:30)
Background
Cyclin dependent kinases (CDK's) are kinases that interact with cyclins and regulate cell division. There is evidence that phosphorylation of the C-terminal region of Rb by Cdk4/6 initiates successive intramolecular interactions between the C-terminal region and the central pocket. The initial interaction displaces histone deacetylase from the pocket, blocking active transcriptional repression by Rb. These intramolecular interactions provide a molecular basis for sequential phosphorylation of Rb by Cdk4/6 and Cdk2. Cdk4/6 is activated early in G1, blocking active repression by Rb (1). In primary epidermal cells, it has been found that oncogenic Ras transiently decreases cyclin-dependent kinase (CDK) 4 expression in association with cell cycle arrest in G1 phase. CDK4 co-expression circumvents Ras growth suppression and induces invasive human neoplasia resembling squamous cell carcinoma. Tumorigenesis is dependent on CDK4 kinase function, with cyclin D1 required but not sufficient for this process. These data identify a new role for oncogenic Ras in CDK4 regulation and highlight the functional importance of CDK4 suppression in preventing uncontrolled growth (2).
Related Pathway
Cell cycle
TGF Beta Signaling Pathway
* Shipping is in business days
* OriGene provides validated application data and protocol, with money back guarantee.
