Cyclin-dependent kinase inhibitor 2A_TAT, Human Recombinant
p16-INK4a, Cyclin-Dependent Kinase Inhibitor 2A, Cyclin-Dependent Kinase 4 Inhibitor A, CDK4I, p16IN
|Calculated MW||18 kDa|
|Other Names||p16-INK4a, Cyclin-Dependent Kinase Inhibitor 2A, Cyclin-Dependent Kinase 4 Inhibitor A, CDK4I, p16INK4A, p16-INK4, Multiple Tumor Suppressor 1, MTS-1|
|Sequence||Full-length human Cyclin-dependent kinase inhibitor 2A and a 12-residue C-terminal TAT peptide (GYGRKKRRQRRR)|
|Target/Specificity||Cyclin-dependent kinase inhibitor 2A-TAT|
|Application Notes||Reconstitute in sterile water to a concentration of 0.1-1.0 mg/ml. Do not vortex. Additional carrier protein (example 0.1% BSA) is recommended for long term storage.|
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Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein. This activity has the effect of suppressing tumor formation and growth, and of inducing replicative senescence in various normal cells, including stem cells. The expression of Cyclin-Dependent Kinase Inhibitor 2A steadily increases with age, and tends to accumulate in stem cell compartments. The deletion, rearrangement, or mutation of the Cyclin-Dependent Kinase Inhibitor 2A gene is frequently found in melanomas, as well as in certain other types of cancer. TAT is a cell penetrating peptides (CPPs) and was shown to enable the introduction of nucleic acids into cells.
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