Deapi-platycoside ECAS# 849758-42-5 |
2D Structure
Quality Control & MSDS
3D structure
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Number of papers citing our products
Cas No. | 849758-42-5 | SDF | Download SDF |
PubChem ID | 70698289 | Appearance | Powder |
Formula | C64H104O34 | M.Wt | 1417.5 |
Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | [(2S,3R,4S,5S)-3-[(2S,3R,4S,5R,6S)-3,4-dihydroxy-6-methyl-5-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxyoxan-2-yl]oxy-4,5-dihydroxyoxan-2-yl] (4aR,5R,6aR,6aS,6bR,8aR,10R,11S,12aR,14bS)-5,11-dihydroxy-9,9-bis(hydroxymethyl)-2,2,6a,6b,12a-pentamethyl-10-[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxymethyl]oxan-2-yl]oxymethyl]oxan-2-yl]oxy-1,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylate | ||
SMILES | CC1C(C(C(C(O1)OC2C(C(COC2OC(=O)C34CCC(CC3C5=CCC6C(C5(CC4O)C)(CCC7C6(CC(C(C7(CO)CO)OC8C(C(C(C(O8)COC9C(C(C(C(O9)COC1C(C(C(C(O1)CO)O)O)O)O)O)O)O)O)O)O)C)C)(C)C)O)O)O)O)OC1C(C(C(CO1)O)O)O | ||
Standard InChIKey | UTBMWMLXRNXHHQ-ONYRRNLVSA-N | ||
Standard InChI | InChI=1S/C64H104O34/c1-23-49(95-54-44(81)35(72)27(69)17-87-54)43(80)48(85)55(91-23)96-50-36(73)28(70)18-88-57(50)98-58(86)64-12-11-59(2,3)13-25(64)24-7-8-32-60(4)14-26(68)51(63(21-66,22-67)33(60)9-10-61(32,5)62(24,6)15-34(64)71)97-56-47(84)42(79)39(76)31(94-56)20-90-53-46(83)41(78)38(75)30(93-53)19-89-52-45(82)40(77)37(74)29(16-65)92-52/h7,23,25-57,65-85H,8-22H2,1-6H3/t23-,25-,26-,27+,28-,29+,30+,31+,32+,33+,34+,35-,36-,37+,38+,39+,40-,41-,42-,43-,44+,45+,46+,47+,48+,49-,50+,51-,52+,53+,54-,55-,56-,57-,60+,61+,62+,64+/m0/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | 1. Deapi-platycoside E maybe have anti-HCV activity. |
Targets | HCV |
Deapi-platycoside E Dilution Calculator
Deapi-platycoside E Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 0.7055 mL | 3.5273 mL | 7.0547 mL | 14.1093 mL | 17.6367 mL |
5 mM | 0.1411 mL | 0.7055 mL | 1.4109 mL | 2.8219 mL | 3.5273 mL |
10 mM | 0.0705 mL | 0.3527 mL | 0.7055 mL | 1.4109 mL | 1.7637 mL |
50 mM | 0.0141 mL | 0.0705 mL | 0.1411 mL | 0.2822 mL | 0.3527 mL |
100 mM | 0.0071 mL | 0.0353 mL | 0.0705 mL | 0.1411 mL | 0.1764 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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'MCC' protein interacts with E-cadherin and beta-catenin strengthening cell-cell adhesion of HCT116 colon cancer cells.[Pubmed:29035389]
Oncogene. 2018 Feb 1;37(5):663-672.
E-cadherin and beta-catenin are key proteins that are essential in the formation of the epithelial cell layer in the colon but their regulatory pathways that are disrupted in cancer metastasis are not completely understood. Mutated in colorectal cancer (MCC) is a tumour suppressor gene that is silenced by promoter methylation in colorectal cancer and particularly in patients with increased lymph node metastasis. Here, we show that MCC methylation is found in 45% of colon and 24% of rectal cancers and is associated with proximal colon, poorly differentiated, circumferential and mucinous tumours as well as increasing T stage and larger tumour size. Knockdown of MCC in HCT116 colon cancer cells caused a reduction in E-cadherin protein level, which is a hallmark of epithelial-mesenchymal transition in cancer, and consequently diminished the E-cadherin/beta-catenin complex. MCC knockdown disrupted cell-cell adhesive strength and integrity in the dispase and transepithelial electrical resistance assays, enhanced hepatocyte growth factor-induced cell scatter and increased tumour cell invasiveness in an organotypic assay. The Src/Abl inhibitor dasatinib, a candidate anti-invasive drug, abrogated the invasive properties induced by MCC deficiency. Mechanistically, we establish that MCC interacts with the E-cadherin/beta-catenin complex. These data provide a significant advance in the current understanding of cell-cell adhesion in colon cancer cells.
Analysis of transient hypermorphic activity of E(spl)D during R8 specification.[Pubmed:29036187]
PLoS One. 2017 Oct 16;12(10):e0186439.
Drosophila atonal (ato) is required for the specification of founding R8 photoreceptors during retinal development. ato is regulated via dual eye-specific enhancers; ato-3' is subject to initial induction whereas 5'-ato facilitates Notch-mediated autoregulation. Notch is further utilized to induce bHLH repressors of the E(spl) locus to restrict Ato from its initial broad expression to individual cells. Although Notch operates in two, distinct phases, it has remained unclear how the two phases maintain independence from one another. The difference in these two phases has attributed to the hypothesized delayed expression of E(spl). However, immunofluorescence data indicate that E(spl) are expressed during early Ato patterning, suggesting a more sophisticated underlying mechanism. To probe this mechanism, we provide evidence that although E(spl) exert no influence on ato-3', E(spl) repress 5'-ato and deletion of the E(spl) locus elicits precocious 5'-ato activity. Thus, E(spl) imposes a delay to the timing in which Ato initiates autoregulation. We next sought to understand this finding in the context of E(spl)D, which encodes a dysregulated variant of E(spl)M8 that perturbs R8 patterning, though, as previously reported, only in conjunction with the mutant receptor Nspl. We established a genetic interaction between E(spl)D and roughened eye (roe), a known modulator of Notch signaling in retinogenesis. This link further suggests a dosage-dependence between E(spl) and the proneural activators Ato and Sens, as indicated via interaction assays in which E(spl)D renders aberrant R8 patterning in conjunction with reduced proneural dosage. In total, the biphasicity of Notch signaling relies, to some degree, on the post-translational regulation of individual E(spl) members and, importantly, that post-translational regulation is likely necessary to modulate the level of E(spl) activity throughout the progression of Ato expression.
Botulinum Toxins A and E Inflict Dynamic Destabilization on t-SNARE to Impair SNARE Assembly and Membrane Fusion.[Pubmed:29033286]
Structure. 2017 Nov 7;25(11):1679-1686.e5.
Botulinum toxins (BoNTs) A and E block neurotransmitter release by specifically cleaving the C- terminal ends of SNAP-25, a plasma membrane SNARE protein. Here, we find that SNAP-25A and E, the cleavage products of BoNT A and E, respectively, terminate membrane fusion via completely different mechanisms. Combined studies of single-molecule FRET and single-vesicle fusion assays reveal that SNAP-25E is incapable of supporting SNARE pairing and thus, vesicle docking. In contrast, SNAP-25A facilitates robust SNARE pairing and vesicle docking with somewhat reduced SNARE zippering, which leads to severe impairment of fusion pore opening. The electron paramagnetic resonance results show that the discrepancy between SNAP-25A and E might stem from the extent of the dynamic destabilization of the t-SNARE core at the N-terminal half, which plays a pivotal role in nucleating SNARE complex formation. Thus, the results provide insights into the structure/dynamics-based mechanism by which BoNT A and E impair membrane fusion.