Catalogue Number
BD-P0852
Analysis Method
HPLC,NMR,MS
Specification
98.5%(HPLC)
Storage
2-8°C
Molecular Weight
Appearance
White powder
Botanical Source
Resina Draconis/Dracaena cochinchinensis (Lour.) S. C. Chen
Structure Type
Chalcones
Category
Standards;Natural Pytochemical;API
SMILES
COC1=C(C=CC(=C1)O)CCC(=O)C2=CC=C(C=C2)O
Synonyms
3-(4-Hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)-1-propanone/1-Propanone, 3-(4-hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)-3-(4-hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)propan-1-one
IUPAC Name
3-(4-hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)propan-1-one
Density
1.2±0.1 g/cm3
Solubility
Methanol
Flash Point
189.6±22.2 °C
Boiling Point
503.4±45.0 °C at 760 mmHg
Melting Point
InChl
InChI=1S/C16H16O4/c1-20-16-10-14(18)8-4-12(16)5-9-15(19)11-2-6-13(17)7-3-11/h2-4,6-8,10,17-18H,5,9H2,1H3
InChl Key
LCKRZXFBCWYAKU-UHFFFAOYSA-N
WGK Germany
RID/ADR
HS Code Reference
2933990000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:116384-24-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
No Technical Documents Available For This Product.
18925509
Lysophosphatidic acid (LPA), a component of mildly-oxidized LDL and the lipid rich core of atherosclerotic plaques, elicits platelet activation. LPA is the ligand of G protein-coupled receptors (GPCR) of the EDG family (LPA1-3) and the newly identified LPA 4-7 subcluster. LPA4, LPA5 and LPA7 increase cellular cAMP levels that would induce platelet inhibition rather than activation. In the present study we quantified the mRNA levels of the LPA1-7 GPCR in human platelets and found a rank order LPA4=LPA5>LPA7>LPA6=LPA2>>LPA1>LPA3. We examined platelet shape change using a panel of LPA receptor subtype-selective agonists and antagonists and compared them with their pharmacological profiles obtained in heterologous LPA1-5 receptor expression systems. Responses to different natural acyl and alkyl species of LPA, and octyl phosphatidic acid analogs, alpha-substituted phosphonate analogs, N-palmitoyl-tyrosine phosphoric acid, N-palmitoyl-serine phosphoric acid were tested. All of these compounds elicited platelet activation and also inhibited LPA-induced platelet shape change after pre-incubation, suggesting that receptor desensitization is likely responsible for the inhibition of this response. Fatty acid free albumin (10 µM) lacking platelet activity completely inhibited platelet shape change induced by LPA with an IC50 of 1.1 µM but had no effect on the activation of LPA1,2,3,&5 expressed in endogenously non-LPA-responsive RH7777 cells. However, albumin reduced LPA4 activation and shifted the dose-response curve to the right. LPA5 transiently expressed in RH7777 cells showed preference to alkyl-LPA over acyl-LPA that is similar to that in platelets. LPA did not increase cAMP levels in platelets. In conclusion, our results with the pharmacological compounds and albumin demonstrate that LPA does not induce platelet shape change simply through activation of LPA1-5, and the receptor(s) mediating LPA-induced platelet activation remains elusive.
lysophosphatidic acid, G protein-coupled receptor, agonist, antagonist, albumin
Lysophosphatidic Acid-Induced Platelet Shape Change Revealed Through LPA1-5 Receptor-selective Probes and Albumin
A.L. Khandoga,1,# Y. Fujiwara,2,# P. Goyal,1 D. Pandey,1 R. Tsukahara,2 A. Bolen,2 H. Guo,2 N. Wilke,1 J. Liu,2 W.J. Valentine,2 G.G. Durgam,3 D.D. Miller,3 G. Jiang,4 G.D. Prestwich,4 G. Tigyi,2 and W. Siess1
2009 Oct 5.
18377664
Recent advances in pain research provide a clear picture for the molecular mechanisms of acute pain; substantial information concerning plasticity that occurs during neuropathic pain has also become available. The peripheral mechanisms responsible for neuropathic pain are found in the altered gene/protein expression of primary sensory neurons. With damage to peripheral sensory fibers, a variety of changes in pain-related gene expression take place in dorsal root ganglion neurons. These changes, or plasticity, might underlie unique neuropathic pain-specific phenotype modifications – decreased unmyelinated-fiber functions, but increased myelinated A-fiber functions. Another characteristic change is observed in allodynia, the functional change of tactile to nociceptive perception. Throughout a series of studies, using novel nociceptive tests to characterize sensory-fiber or pain modality-specific nociceptive behaviors, it was demonstrated that communication between innocuous and noxious sensory fibers might play a role in allodynia mechanisms. Because neuropathic pain in peripheral and central demyelinating diseases develops as a result of aberrant myelination in experimental animals, demyelination seems to be a key mechanism of plasticity in neuropathic pain. More recently, we discovered that lysophosphatidic acid receptor activation initiates neuropathic pain, as well as possible peripheral mechanims of demyelination after nerve injury. These results lead to further hypotheses of physical communication between innocuous Aβ- and noxious C- or Aδ-fibers to influence the molecular mechanisms of allodynia.
Peripheral mechanisms of neuropathic pain - involvement of lysophosphatidic acid receptor-mediated demyelination
Hiroshi Uedacorresponding author1
2008;
25489849
Sugarcane interacts with particular types of beneficial nitrogen-fixing bacteria that provide fixed-nitrogen and plant growth hormones to host plants, promoting an increase in plant biomass. Other benefits, as enhanced tolerance to abiotic stresses have been reported to some diazotrophs. Here we aim to study the effects of the association between the diazotroph Gluconacetobacter diazotrophicus PAL5 and sugarcane cv. SP70-1143 during water depletion by characterizing differential transcriptome profiles of sugarcane. RNA-seq libraries were generated from roots and shoots of sugarcane plants free of endophytes that were inoculated with G. diazotrophicus and subjected to water depletion for 3 days. A sugarcane reference transcriptome was constructed and used for the identification of differentially expressed transcripts. The differential profile of non-inoculated SP70-1143 suggests that it responds to water deficit stress by the activation of drought-responsive markers and hormone pathways, as ABA and Ethylene. qRT-PCR revealed that root samples had higher levels of G. diazotrophicus 3 days after water deficit, compared to roots of inoculated plants watered normally. With prolonged drought only inoculated plants survived, indicating that SP70-1143 plants colonized with G. diazotrophicus become more tolerant to drought stress than non-inoculated plants. Strengthening this hypothesis, several gene expression responses to drought were inactivated or regulated in an opposite manner, especially in roots, when plants were colonized by the bacteria. The data suggests that colonized roots would not be suffering from stress in the same way as non-inoculated plants. On the other hand, shoots specifically activate ABA-dependent signaling genes, which could act as key elements in the drought resistance conferred by G. diazotrophicus to SP70-1143. This work reports for the first time the involvement of G. diazotrophicus in the promotion of drought-tolerance to sugarcane cv. SP70-1143, and it describes the initial molecular events that may trigger the increased drought tolerance in the host plant.
Drought Tolerance Conferred to Sugarcane by Association with Gluconacetobacter diazotrophicus: A Transcriptomic View of Hormone Pathways
Livia Vargas, 1 Ailton B. Santa Brigida, 1 Jose P. Mota Filho, 1 Thais G. de Carvalho, 1 Cristian A. Rojas, 1 , 2 Dries Vaneechoutte, 3 , 4 Michiel Van Bel, 3 , 4 Laurent Farrinelli, 5 Paulo C. G. Ferreira, 1 Klaas Vandepoele, 3 , 4 and Adriana S. Hemerly 1 ,
2014
