Cyclin-dependent kinase inhibitor protein

A cyclin-dependent kinase inhibitor protein (also known as CKIs, CDIs, or CDKIs) is a protein that inhibits the enzyme cyclin-dependent kinase (CDK) and Cyclin activity by stopping the cell cycle if there are unfavorable conditions, therefore, acting as tumor suppressors.

Cell cycle progression is stopped by Cyclin-dependent kinase inhibitor protein at the G1 phase.

Cyclin-dependent kinase inhibitor proteins use ATP as a phosphate contributor to phosphorylate serine and threonine residues.

[7] These cyclin-dependent kinase inhibitor proteins emerge only in their specific cell cycle phase.

The discovery of Cyclin-dependent kinase inhibitor proteins in 1990 opened the door in how we think about cell cycle control.

[8] Further research has demonstrates that Cdks, cyclins and CKIs play essential roles in processes such as transcription, epigenetic regulation, metabolism, stem cell self-renewal, neuronal functions and spermatogenesis.

[2] In mammals, p27, a cyclin-dependent kinase inhibitor protein, helps control CDK activity in G1.

The carboxyl-terminal end of the p27 fragment interacts with the beta sheet of CDKs, causing interference with the structure; p27 slides into the ATP-binding site of CDK2 and inhibits ATP binding.

The typical inactivation mechanism of the CDK/ Cyclin complex is based on binding a CDK inhibitor to the CDK cyclin complex and a partial conformational rotation. The cyclin is thus forced to release the T loop and detach from the CDK. The CDK attaches its loop to the CKI stopping the activation of CDK/ Cyclin complex.