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CDKN2A, also known as cyclin-dependent kinase inhibitor 2A, is a gene which in humans is located at chromosome 9, band p21.3. [5] It is ubiquitously expressed in many tissues and cell types. [ 6 ] The gene codes for two proteins , including the INK4 family member p16 (or p16INK4a) and p14arf . [ 7 ]
The p21 protein binds directly to cyclin-CDK complexes that drive forward the cell cycle and inhibits their kinase activity, thereby causing cell cycle arrest to allow repair to take place. p21 can also mediate growth arrest associated with differentiation and a more permanent growth arrest associated with cellular senescence. The p21 gene ...
p16 (also known as p16 INK4a, cyclin-dependent kinase inhibitor 2A, CDKN2A, multiple tumor suppressor 1 and numerous other synonyms), is a protein that slows cell division by slowing the progression of the cell cycle from the G1 phase to the S phase, thereby acting as a tumor suppressor. It is encoded by the CDKN2A gene.
More specifically p16INK4a-pRb tumor suppressor and p53 are known effectors of senescence. Most cancer cells have a mutated p53 and p16INK4a-pRb, which allows the cancer cells to escape a senescent fate. [41] The p16 protein is a cyclin dependent kinase (CDK) inhibitor and it activates Rb tumor suppressor.
p21 is a potent cyclin-dependent kinase inhibitor (CKI). The p21 (CIP1/WAF1) protein binds to and inhibits the activity of cyclin-CDK2, -CDK1, and -CDK4 /6 complexes, and thus functions as a regulator of cell cycle progression at G 1 and S phase.
AMPK/p53 senescence produces a completely different SASP than IL-1 (p16 INK4a) senescence, which is primarily responsible for intervertebral disc degeneration (IVDD). [51] In IVDD, SASP is secreted by nucleus pulposus and annulus fibrosus cells, resulting in extracellular matrix degradation and extracellular inflammation. [51]
Human cells contain many different cyclins that bind to different CDKs. CDKs and cyclins appear and activate at specific cell cycle phases. Seven cyclin-dependent kinase inhibitor proteins have been identified. They are p15, p16, p18, p19, p21, p27, and p57. [7]
Senescence-associated beta-galactosidase, along with p16 Ink4A, is regarded to be a biomarker of cellular senescence. [1] [2] Its existence was proposed in 1995 by Dimri et al. [3] following the observation that when beta-galactosidase assays were carried out at pH 6.0, only cells in senescence state develop staining.