|Source:||The roots of Cyanotis arachnoidea C. B. Clarke|
|Biological Activity or Inhibitors:||1. 20-Hydroxyecdysone has immunomodulatory, hepatoprotective, anti-arrythmic, and cholesterol-lowering properties.
2. 20-Hydroxyecdysone as ingredients in nutritional supplements for various sports, particularly bodybuilding.
3. 20-Hydroxyecdysone induces autophagy and caspase activity, predominantly transduced by E93 in the remodeling fat body of Drosophila.
4. 20-Hydroxyecdysone (via GPCR activation and calcium signaling) activates CaMKII phosphorylation and nuclear translocation, which regulate USP1 lysine acetylation to form an EcRB1-USP1 complex for 20E response gene transcription.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.0807 mL||10.4037 mL||20.8073 mL||41.6146 mL||52.0183 mL|
|5 mM||0.4161 mL||2.0807 mL||4.1615 mL||8.3229 mL||10.4037 mL|
|10 mM||0.2081 mL||1.0404 mL||2.0807 mL||4.1615 mL||5.2018 mL|
|50 mM||0.0416 mL||0.2081 mL||0.4161 mL||0.8323 mL||1.0404 mL|
|100 mM||0.0208 mL||0.104 mL||0.2081 mL||0.4161 mL||0.5202 mL|
J Biol Chem. 2015 Mar 27;290(13):8469-81.
|The steroid hormone 20-hydroxyecdysone via nongenomic pathway activates Ca2+/calmodulin-dependent protein kinase II to regulate gene expression.[Pubmed: 25670853 ]|
|The steroid hormone 20-Hydroxyecdysone (20E) triggers calcium signaling pathway to regulate 20-Hydroxyecdysone response gene expression, but the mechanism underlying this process remains unclear. We propose that the 20-Hydroxyecdysone-induced phosphorylation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) serves an important function in 20-Hydroxyecdysone response gene transcription in the lepidopteran insect Helicoverpa armigera. CaMKII showed increased expression and phosphorylation during metamorphosis. 20-Hydroxyecdysone elevated CaMKII phosphorylation. However, the G protein-coupled receptor (GPCR) and ryanodine receptor inhibitor suramin, the phospholipase C inhibitor U73122, and the inositol 1,4,5-triphosphate receptor inhibitor xestospongin C suppressed 20-Hydroxyecdysone-induced CaMKII phosphorylation. Two ecdysone-responsible GPCRs and Gαq protein were involved in 20-Hydroxyecdysone-induced CaMKII phosphorylation by RNA interference analysis. 20-Hydroxyecdysone regulated CaMKII threonine phosphorylation at amino acid 290, thereby inducing CaMKII nuclear translocation. CaMKII knockdown by dsCaMKII injection into the larvae prevented the occurrence of larval-pupal transition and suppressed 20-Hydroxyecdysone response gene expression. CaMKII phosphorylation and nuclear translocation maintained USP1 lysine acetylation at amino acid 303 by inducing histone deacetylase 3 phosphorylation and nuclear export. The lysine acetylation of USP1 was necessary for the interaction of USP1 with EcRB1 and their binding to the ecdysone response element. Results suggest that 20-Hydroxyecdysone (via GPCR activation and calcium signaling) activates CaMKII phosphorylation and nuclear translocation, which regulate USP1 lysine acetylation to form an EcRB1-USP1 complex for 20-Hydroxyecdysone response gene transcription.|
Insect Mol Biol. 2014 Aug;23(4):407-16.
|20-hydroxyecdysone mediates non-canonical regulation of mosquito vitellogenins through alternative splicing.[Pubmed: 24720618]|
|We demonstrate that the hormone 20-Hydroxyecdysone (20E) is responsible for regulating post-transcriptional splicing of vitellogenin. After exposure of previtellogenic fat bodies to 20-Hydroxyecdysone, vitellogenin expression switches from a non-productive intron-retaining transcript to a spliced protein-coding transcript. This effect is independent of factors classically known to influence transcription, such as juvenile hormone-mediated competence and amino acid signalling through the target of rapamycin pathway. Non-canonical regulation of vitellogenesis through RUST is a novel role for the multifunctional hormone 20-Hydroxyecdysone, and may have important implications for general patterns of gene regulation in mosquitoes.|
Insect Biochem Mol Biol. 2014 Feb;45:30-9.
|E93 predominantly transduces 20-hydroxyecdysone signaling to induce autophagy and caspase activity in Drosophila fat body.[Pubmed: 24316411]|
|Both autophagy and caspase activity are induced by a pulse of molting hormone (20-Hydroxyecdysone, 20E) via the 20E nuclear receptor complex, EcR-USP. We here demonstrate that E93, a 20-Hydroxyecdysone primary-response gene encoding an HTH transcription factor, predominantly transduces 20-Hydroxyecdysone signaling to induce autophagy and caspase activity in the remodeling fat body. Taken together, we conclude that autophagy and caspase activity are induced by 20-Hydroxyecdysone and predominantly transduced by E93 in the remodeling fat body of Drosophila.|
Insect Biochem Mol Biol. 2013 Nov;43(11):1068-78.
|Balancing crosstalk between 20-hydroxyecdysone-induced autophagy and caspase activity in the fat body during Drosophila larval-prepupal transition.[Pubmed: 24036278]|
|Both autophagy and caspase activity progressively increase in the remodeling fat body, and they are induced by a pulse of the molting hormone (20-Hydroxyecdysone, 20E) during the larval-prepupal transition. Inhibition of autophagy and/or caspase activity in the remodeling fat body results in 25-40% pupal lethality, depending on the genotypes. Interestingly, a balancing crosstalk occurs between autophagy and caspase activity in this tissue: the inhibition of autophagy induces caspase activity and the inhibition of caspases induces autophagy. The Drosophila remodeling fat body provides an in vivo model for understanding the molecular mechanism of the balancing crosstalk between autophagy and caspase activity, which oppose with each other and are induced by the common stimulus 20-Hydroxyecdysone, and blockage of either path reinforces the other path.|