p14 ARF/p16 Activators
The chemical class known as p14 ARF/p16 Activators encompasses a group of molecules designed to modulate the activity of the p14 ARF and p16 INK4a tumor suppressor proteins. These proteins are integral components of the cell cycle regulation machinery, playing crucial roles in controlling cellular proliferation and maintaining genomic integrity. The p14 ARF (Alternate Reading Frame) protein, also known as p19 ARF in mice, operates primarily through the p53 signaling pathway; it stabilizes the p53 protein by sequestering the MDM2 ubiquitin ligase, which targets p53 for degradation. On the other hand, p16 INK4a (Inhibitor of Cyclin-Dependent Kinase 4a) directly inhibits cyclin-dependent kinases CDK4 and CDK6, thus preventing the phosphorylation and inactivation of the retinoblastoma (Rb) protein, leading to cell cycle arrest at the G1 phase. Together, these proteins act as a crucial barrier against uncontrolled cell division and oncogenesis.
The p14 ARF/p16 Activators are characterized by their ability to increase the levels or enhance the functions of the p14 ARF and p16 INK4a proteins. As molecules influencing the ARF-MDM2-p53 and INK4a-CDK4/6-Rb pathways, they are involved in the intricate network of signaling cascades that dictate cell fate decisions, including cell cycle progression and senescence. The regulation of these pathways is fundamental to the maintenance of normal cellular function and to the prevention of aberrant growth. By activating p14 ARF and p16 INK4a, these molecules can influence the expression patterns of a wide array of genes involved in cell cycle control, apoptosis, and senescence.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $80.00 $220.00 $460.00 | 64 | |
Resveratrol is a natural polyphenol found in various plants. It activates p14 ARF/p16 indirectly by modulating the SIRT1 pathway. Resveratrol functions as a SIRT1 activator, leading to deacetylation of p53. This deacetylation enhances p14 ARF expression, promoting cell cycle arrest and inhibiting the cyclin-dependent kinase activity associated with p16. | ||||||
Roscovitine | 186692-46-6 | sc-24002 sc-24002A | 1 mg 5 mg | $94.00 $265.00 | 42 | |
Roscovitine, a purine derivative, is a CDK inhibitor affecting the cell cycle. By inhibiting CDKs, especially CDK2 and CDK7, it indirectly activates p14 ARF/p16. This inhibition prevents phosphorylation events critical for p16 degradation, stabilizing p16 levels. Consequently, there is increased binding of p16 to cyclin D-CDK4/6 complexes, leading to cell cycle arrest and tumor suppression. | ||||||
A-769662 | 844499-71-4 | sc-203790 sc-203790A sc-203790B sc-203790C sc-203790D | 10 mg 50 mg 100 mg 500 mg 1 g | $184.00 $741.00 $1076.00 $3417.00 $5304.00 | 23 | |
A769662, an AMP-activated protein kinase (AMPK) activator, indirectly activates p14 ARF/p16. It triggers AMPK phosphorylation, leading to downstream effects on mTOR and p53. Activated p53 upregulates p14 ARF, reinforcing the cell cycle inhibitory effects of p16. | ||||||
Trichostatin A | 58880-19-6 | sc-3511 sc-3511A sc-3511B sc-3511C sc-3511D | 1 mg 5 mg 10 mg 25 mg 50 mg | $152.00 $479.00 $632.00 $1223.00 $2132.00 | 33 | |
Trichostatin A, a histone deacetylase (HDAC) inhibitor, influences epigenetic regulation. By inhibiting HDACs, it increases acetylation of histones associated with the p14 ARF/p16 locus. This enhanced acetylation promotes an open chromatin structure, facilitating transcription factor binding and thereby activating p14 ARF/p16 expression. | ||||||
Suberoylanilide Hydroxamic Acid | 149647-78-9 | sc-220139 sc-220139A | 100 mg 500 mg | $133.00 $275.00 | 37 | |
Vorinostat, another HDAC inhibitor, acts similarly to trichostatin A. It induces hyperacetylation of histones at the p14 ARF/p16 locus, favoring transcription. This epigenetic modulation results in increased p14 ARF and p16 expression, contributing to the suppression of cell cycle progression and tumor growth. | ||||||
1,1-Dimethylbiguanide, Hydrochloride | 1115-70-4 | sc-202000F sc-202000A sc-202000B sc-202000C sc-202000D sc-202000E sc-202000 | 10 mg 5 g 10 g 50 g 100 g 250 g 1 g | $20.00 $43.00 $63.00 $156.00 $260.00 $510.00 $31.00 | 37 | |
Metformin, an anti-diabetic drug, activates AMPK, leading to downstream effects on the mTOR pathway. This indirect activation of p14 ARF/p16 occurs through p53 upregulation. Metformin-induced AMPK activation enhances p53 stability, resulting in increased transcription of p14 ARF, reinforcing the anti-proliferative effects mediated by p16. | ||||||
5-Azacytidine | 320-67-2 | sc-221003 | 500 mg | $280.00 | 4 | |
5-Azacytidine, a DNA methyltransferase inhibitor, influences DNA methylation patterns. By demethylating the p14 ARF/p16 promoter region, it removes epigenetic silencing marks, promoting transcription. This demethylation-induced reactivation enhances the expression of p14 ARF and p16, contributing to their tumor-suppressive functions. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $90.00 $349.00 | 284 | |
SB203580, a p38 MAPK inhibitor, indirectly activates p14 ARF/p16 by modulating the MAPK pathway. Inhibition of p38 MAPK alters the balance of downstream signaling, leading to increased p53 activity. Activated p53 upregulates p14 ARF, reinforcing the cell cycle inhibitory effects of p16 and contributing to the suppression of tumorigenesis. | ||||||
(–)-Nutlin-3 | 675576-98-4 | sc-222086 sc-222086A | 1 mg 5 mg | $122.00 $219.00 | 2 | |
Nutlin-3 is a small molecule that disrupts the interaction between MDM2 and p53, leading to p53 stabilization and activation. This indirect activation of p14 ARF/p16 occurs through p53-dependent mechanisms. Activated p53 upregulates p14 ARF, reinforcing the cell cycle inhibitory effects of p16 and contributing to the suppression of tumor growth. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $123.00 $400.00 | 148 | |
LY294002, a PI3K inhibitor, indirectly activates p14 ARF/p16 by influencing the PI3K/AKT pathway. Inhibition of PI3K leads to decreased AKT activity, resulting in the stabilization and activation of p53. Activated p53 upregulates p14 ARF, reinforcing the cell cycle inhibitory effects of p16 and contributing to the suppression of tumorigenesis. | ||||||