TTP Activators
TTP activators form a diverse class of chemicals that influence the activity of tristetraprolin (TTP), a key regulator of mRNA destabilization. TTP plays a crucial role in post-transcriptional gene regulation by binding to AU-rich elements (AREs) in mRNA, leading to destabilization and degradation. The identified chemicals can be broadly categorized into indirect activators, which modulate specific signaling pathways related to TTP activity. Resveratrol, for instance, indirectly activates TTP by inhibiting p38 MAPK signaling. P38 MAPK phosphorylation inactivates TTP, and Resveratrol prevents this phosphorylation, enhancing TTP-mediated mRNA degradation. Dexamethasone, a glucocorticoid, indirectly activates TTP by inhibiting the NF-κB pathway. NF-κB activation suppresses TTP expression, and Dexamethasone blocks NF-κB, relieving the suppression on TTP and promoting mRNA destabilization. SB203580, Auranofin, Celastrol, Indomethacin, and Nordihydroguaiaretic acid (NDGA) indirectly activate TTP through different pathways, such as inhibiting p38 MAPK, thioredoxin reductase, or COX-2/PGE2, illustrating the diverse mechanisms by which these chemicals modulate TTP activity.
Luteolin indirectly activates TTP by modulating the PI3K/Akt pathway. It prevents Akt-mediated phosphorylation and inactivation of TTP, promoting its mRNA destabilization function. CDDO-Im and Anisomycin indirectly activate TTP by inhibiting the NF-κB and activating p38 MAPK pathways, respectively, demonstrating the intricate interplay of these chemicals with TTP-related signaling. Camptothecin, a topoisomerase I inhibitor, influences TTP expression and activity, providing a unique pathway for the indirect activation of TTP. Finally, Celiprolol indirectly activates TTP through the inhibition of β-adrenergic signaling, illustrating the specific impact of this chemical on TTP modulation. In summary, TTP activators represent a class of chemicals with diverse mechanisms of action, impacting TTP-mediated mRNA destabilization through modulation of various signaling pathways. Understanding these specific biochemical and cellular pathways provides insights into the nuanced control of TTP activity, offering avenues for targeted pharmacological interventions in post-transcriptional gene regulation. The intricate interplay of these chemicals with TTP-related signaling pathways serve as valuable tools for studying and modulating TTP activity in different physiological contexts.
| 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 indirectly activates TTP through the modulation of p38 MAPK signaling. It inhibits p38 MAPK, a kinase that phosphorylates and inactivates TTP. By suppressing p38 MAPK, Resveratrol enhances TTP activity, leading to increased mRNA degradation. This indirect activation demonstrates the intricate interplay between Resveratrol and the p38 MAPK/TTP pathway, highlighting its potential as a chemical modulator in post-transcriptional gene regulation. | ||||||
Dexamethasone | 50-02-2 | sc-29059 sc-29059B sc-29059A | 100 mg 1 g 5 g | $91.00 $139.00 $374.00 | 36 | |
Dexamethasone indirectly activates TTP by inhibiting the NF-κB pathway. NF-κB activation suppresses TTP expression, and Dexamethasone, a glucocorticoid, acts as an inhibitor of NF-κB. By blocking NF-κB, Dexamethasone relieves the suppression on TTP, promoting its activity in mRNA destabilization. | ||||||
Auranofin | 34031-32-8 | sc-202476 sc-202476A sc-202476B | 25 mg 100 mg 2 g | $153.00 $214.00 $4000.00 | 39 | |
Auranofin indirectly activates TTP through the inhibition of thioredoxin reductase. By blocking thioredoxin reductase, Auranofin influences the redox state of TTP, promoting its activity in mRNA destabilization. This indirect activation illustrates the specific impact of Auranofin on TTP modulation through redox control, providing a targeted approach to influence post-transcriptional gene regulation. | ||||||
Indomethacin | 53-86-1 | sc-200503 sc-200503A | 1 g 5 g | $29.00 $38.00 | 18 | |
Indomethacin indirectly activates TTP by inhibiting the COX-2/PGE2 pathway. COX-2-derived PGE2 inhibits TTP expression, and Indomethacin, a nonsteroidal anti-inflammatory drug (NSAID), inhibits COX-2. By blocking the COX-2/PGE2 pathway, Indomethacin relieves the suppression on TTP, promoting its activity in mRNA destabilization. | ||||||
NDGA (Nordihydroguaiaretic acid) | 500-38-9 | sc-200487 sc-200487A sc-200487B | 1 g 5 g 25 g | $109.00 $384.00 $2190.00 | 3 | |
NDGA indirectly activates TTP by inhibiting the NF-κB pathway. NF-κB activation suppresses TTP expression, and NDGA acts as an inhibitor of NF-κB. By blocking NF-κB, NDGA relieves the suppression on TTP, promoting its activity in mRNA destabilization. This indirect activation demonstrates the specific impact of NDGA on TTP modulation through the NF-κB pathway, providing a targeted approach to influence post-transcriptional gene regulation. | ||||||
Luteolin | 491-70-3 | sc-203119 sc-203119A sc-203119B sc-203119C sc-203119D | 5 mg 50 mg 500 mg 5 g 500 g | $27.00 $51.00 $101.00 $153.00 $1925.00 | 40 | |
Luteolin indirectly activates TTP through the modulation of the PI3K/Akt pathway. This flavonoid activates Akt, which phosphorylates and inactivates TTP. By suppressing Akt signaling, Luteolin prevents the inactivation of TTP, promoting its activity in mRNA destabilization. This indirect activation illustrates the specific impact of Luteolin on TTP modulation through the PI3K/Akt pathway, providing a targeted approach to influence post-transcriptional gene regulation. | ||||||
CDDO Imidazolide | 443104-02-7 | sc-504719 | 1 mg | $700.00 | ||
CDDO-Im indirectly activates TTP by inhibiting the NF-κB pathway. NF-κB activation suppresses TTP expression, and CDDO-Im acts as an inhibitor of NF-κB. By blocking NF-κB, CDDO-Im relieves the suppression on TTP, promoting its activity in mRNA destabilization. This indirect activation demonstrates the specific impact of CDDO-Im on TTP modulation through the NF-κB pathway, providing a targeted approach to influence post-transcriptional gene regulation. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $58.00 $186.00 $94.00 | 21 | |
Camptothecin indirectly activates TTP through the inhibition of topoisomerase I. By blocking topoisomerase I, Camptothecin influences TTP expression and activity, providing a specific pathway for the indirect activation of TTP. This illustrates the potential of Camptothecin as a chemical modulator in post-transcriptional gene regulation, showcasing its impact on TTP-mediated mRNA destabilization. | ||||||
Anisomycin | 22862-76-6 | sc-3524 sc-3524A | 5 mg 50 mg | $99.00 $259.00 | 36 | |
Anisomycin indirectly activates TTP through the modulation of p38 MAPK signaling. It activates p38 MAPK, a kinase that phosphorylates and activates TTP. By promoting p38 MAPK activity, Anisomycin enhances TTP-mediated mRNA destabilization. This indirect activation demonstrates the intricate interplay between Anisomycin and the p38 MAPK/TTP pathway, highlighting its potential as a chemical modulator in post-transcriptional gene regulation. | ||||||
Celiprolol Hydrochloride | 57470-78-7 | sc-211051 sc-211051A | 10 mg 50 mg | $360.00 $990.00 | 3 | |
Celiprolol indirectly activates TTP through the inhibition of β-adrenergic signaling. β-adrenergic stimulation suppresses TTP expression, and Celiprolol, a β-blocker, inhibits β-adrenergic signaling. By blocking β-adrenergic signaling, Celiprolol relieves the suppression on TTP, promoting its activity in mRNA destabilization. | ||||||