1500002O20Rik Activators
ECI2 Activators are a diverse array of chemical compounds that indirectly increase the functional activity of ECI2 through a variety of signaling pathways and cellular processes. Compounds such as Forskolin and Sphingosine-1-phosphate work by raising intracellular levels of cAMP and activating S1P receptors, respectively, both of which are crucial for the modulation of peroxisomal dynamics. The activation of PKA by Forskolin and subsequent phosphorylation of associated proteins can lead to enhanced lipid metabolism processes involving ECI2, while S1P receptor signaling promotes peroxisome proliferation, which is key for ECI2's role in peroxisomal β-oxidation. Similarly, PMA, through its PKC activating properties, and LY294002, as an inhibitor of PI3K, bring about changes in phosphorylation patterns and peroxisomal biogenesis that could indirectly enhance ECI2 activity. ECI2 activators are chemical compounds that indirectly augment the functional activity of ECI2 by modulating specific signaling pathways and cellular processes within which ECI2 operates.
This cascade results in enhanced lipid metabolism and peroxisomal proliferation-a key area of ECI2 activity. Forskolin's PKA-mediated phosphorylation of proteins, and the receptor-mediated actions of Sphingosine-1-phosphate, play significant roles in upregulating processes central to ECI2's function in peroxisomal β-oxidation. PMA and LY294002, by activating PKC and inhibiting PI3K respectively, further influence the phosphorylation of proteins and peroxisome biogenesis, which are pivotal to the functional enhancement of ECI2. In addition to the above, U0126's inhibition of MEK impacts MAPK/ERK pathway activity, which in turn can modulate peroxisomal dynamics and function, indirectly promoting ECI2 activity. Peroxisomal proliferators like Fibrates, and PPAR agonists such as Oleoylethanolamide, Bezafibrate, and GW7647, directly stimulate the peroxisome proliferation receptor, leading to an increased number and function of peroxisomes and thereby enhancing ECI2's role in fatty acid β-oxidation.
SEE ALSO...
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Insulin | 11061-68-0 | sc-29062 sc-29062A sc-29062B | 100 mg 1 g 10 g | $153.00 $1224.00 $12239.00 | 82 | |
Insulin engages the PI3K/AKT pathway by binding to its receptor, leading to the phosphorylation and activation of AKT. RICTOR, as a critical component of the mTORC2 complex, is required for the full activation of AKT by phosphorylating its hydrophobic motif. Thus, insulin indirectly enhances RICTOR activity by facilitating AKT activation, which is a downstream event reliant on RICTOR function. | ||||||
17-AAG | 75747-14-7 | sc-200641 sc-200641A | 1 mg 5 mg | $66.00 $153.00 | 16 | |
17-AAG is an HSP90 inhibitor that stabilizes its client proteins, including AKT. By inhibiting HSP90, 17-AAG can increase the level of active AKT, which requires RICTOR-mediated phosphorylation for full activation. Therefore, 17-AAG indirectly enhances RICTOR function by increasing the pool of AKT that RICTOR can act on. | ||||||
A-443654 | 552325-16-3 | sc-507339 | 1 mg | $140.00 | ||
A-443654 is an AKT activator that directly increases AKT phosphorylation and activity. Since RICTOR is necessary for the phosphorylation of AKT at Ser473, the activation of AKT by A-443654 logically leads to an enhanced requirement for RICTOR function, thereby indirectly increasing RICTOR activity. | ||||||
C2 Ceramide | 3102-57-6 | sc-201375 sc-201375A | 5 mg 25 mg | $77.00 $316.00 | 12 | |
Ceramide activates protein phosphatase 2A (PP2A), which can dephosphorylate AKT at its threonine 308 residue. This action indirectly necessitates the re-phosphorylation and activation of AKT, in which RICTOR plays a crucial role as part of mTORC2. Thus, ceramide can indirectly lead to enhanced RICTOR activity through its effects on AKT. | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Resveratrol activates SIRT1, which can deacetylate and activate LKB1, leading to the activation of AMPK. AMPK can inhibit mTORC1, which, due to the complex interplay between mTORC1 and mTORC2, may relieve negative feedback on RICTOR-containing mTORC2, indirectly enhancing RICTOR activity. | ||||||
Metformin | 657-24-9 | sc-507370 | 10 mg | $77.00 | 2 | |
Metformin activates AMPK, which has an inhibitory effect on mTORC1. This inhibition can reduce the negative feedback on the insulin/IGF-1 signaling pathway, potentially enhancing the activity of RICTOR through increased AKT phosphorylation as a result of its action in the mTORC2 complex. | ||||||
Palmitic Acid | 57-10-3 | sc-203175 sc-203175A | 25 g 100 g | $112.00 $280.00 | 2 | |
Palmitic acid has been shown to activate mTOR signaling. As part of the mTORC2 complex, RICTOR is involved in the phosphorylation of AKT. Thus, palmitic acid may indirectly enhance RICTOR activity by increasing mTORC2-dependent AKT phosphorylation. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
LY294002 is a PI3K inhibitor that leads to decreased AKT phosphorylation. Paradoxically, the inhibition of PI3K can result in compensatory feedback mechanisms that enhance signaling through alternative pathways, potentially increasing the demand for RICTOR's function in mTORC2-mediated AKT phosphorylation under certain contexts. | ||||||