Peptide Library / Detail
P21 (CDKN1A)
Half-life
Variable, protein stability regulated by ubiquitin-proteasome degradation (minutes to hours)
Delivery
Gene therapy, epigenetic modulators, or peptide-based inhibitors targeting P21 pathways
Dosage
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Research Use Only
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Description
P21 is a cyclin-dependent kinase inhibitor protein that plays a critical role in cell cycle regulation, cellular senescence, and tumor suppression. As a key mediator of the p53 pathway, P21 controls cell proliferation and has become a therapeutic target for age-related diseases and cancer. Research focuses on modulating P21 expression to balance between preventing uncontrolled cell growth and avoiding premature cellular senescence.
Usage
P21 is primarily studied as a therapeutic target rather than administered directly. Research protocols investigate P21 pathway modulation through epigenetic regulators, peptide inhibitors, or gene therapy approaches. Studies examine tissue-specific P21 expression levels and downstream effects on cellular senescence markers in various pathologies including cancer, cardiovascular disease, and kidney aging.
Mechanism of Action
P21 functions by binding to and inhibiting cyclin-CDK complexes, thereby blocking cell cycle progression at G1/S and G2/M checkpoints. It is upregulated by p53 in response to cellular stress, DNA damage, or oncogenic signals. The EZH2-H3K27me3-p21 axis regulates expression through histone methylation, while P21 accumulation triggers cellular senescence pathways. P21 also modulates apoptosis, DNA repair, and inflammatory responses through interactions with multiple signaling cascades including PGC-1α and YAP pathways.
Benefits(7)
- Tumor suppression through cell cycle arrest in cancer cells
- Prevention of uncontrolled cellular proliferation
- Protection against premature cellular senescence when appropriately regulated
- Reduction of age-related tissue dysfunction through senescence modulation
- Kidney protection via suppression of mesangial cell senescence (PMID: 41674011)
- Cardiovascular protection through regulation of vascular smooth muscle cell aging
- Potential therapeutic target for osteoarthritis through chondrocyte senescence regulation (PMID: 41620554)
Side Effects(6)
- Excessive P21 activation may promote cellular senescence and tissue aging
- Impaired wound healing and tissue regeneration when overexpressed
- Potential for therapeutic resistance in cancer treatment
- Cell cycle arrest in healthy proliferating tissues
- Contribution to senescence-associated secretory phenotype (SASP) in chronic conditions
- Dysregulation associated with actinic keratosis and keratinocyte cancers (PMID: 41683940)