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5,7-Dihydroxy-6,8-dimethoxyflavone

$1,120

  • Brand : BIOFRON

  • Catalogue Number : BN-O1452

  • Specification : 98%(HPLC)

  • CAS number : 3162-45-6

  • Formula : C17H14O6

  • Molecular Weight : 314.3

  • PUBCHEM ID : 11609345

  • Volume : 5mg

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Catalogue Number

BN-O1452

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

314.3

Appearance

Yellow powder

Botanical Source

This product is isolated and purified from the roots of Sophora flavescens Ait.

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=C(C(=C2C(=C1O)C(=O)C=C(O2)C3=CC=CC=C3)OC)O

Synonyms

4H-1-Benzopyran-4-one, 5,7-dihydroxy-6,8-dimethoxy-2-phenyl-/6-Methoxywogonin/5,7-Dihydroxy-6,8-dimethoxyflavone/5,7-Dihydroxy-6,8-dimethoxyflavon/5,7-Dihydroxy-6,8-dimethoxy-2-phenyl-4H-chromen-4-one/5,7-dihydroxy-6,8-dimethoxy-2-phenyl-chromen-4-one

IUPAC Name

5,7-dihydroxy-6,8-dimethoxy-2-phenylchromen-4-one

Density

1.4±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

223.0±23.6 °C

Boiling Point

592.4±50.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

RBVYFSLWUBLPMG-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2914500000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:3162-45-6) 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.

PMID

17681284

Abstract

Apoptosis may be regulated by oxidants such as peroxynitrite (ONOO−). The tumour suppressor, p53, has been reported to play a crucial role in apoptosis induced by oxidants, therefore we assessed the ability of a ONOO− donor, GEA 3162, to activate caspases and induce mitochondrial permeability in a p53-deficient murine bone marrow cell line, Jaws II. Furthermore, these cells were stably transfected with Bcl-2, in order to investigate the impact of this survival protein on ONOO−-induced apoptosis. GEA 3162 activated caspases and induced loss of mitochondrial membrane potential in Jaws II cells. In particular, caspases 3 and 2 were activated, alongside minor activation of caspases 8 and 9, and apoptosis was partially dependent upon p38 MAP kinase activation, with little or no role for JNK. Overexpression of Bcl-2 abolished activation of all caspases and reduced the change in mitochondrial membrane potential. Thus, we have demonstrated that the ONOO− donor, GEA 3162, induces apoptosis in Jaws II murine myeloid cells despite lacking functional p53, via a pathway that principally involves caspases 2 and 3 and mitochondrial changes. This is blocked by overexpression of Bcl-2 via a mechanism that does not appear to merely reflect stabilisation of the mitochondrial membrane.

KEYWORDS

Peroxynitrite, Apoptosis, Caspase, p53, Bcl-2, Myeloid

Title

GEA 3162, a peroxynitrite donor, induces Bcl-2-sensitive, p53-independent apoptosis in murine bone marrow cells

Author

Emma L. Taylor,a,* John T. Li,b Joan C. Tupper,c Adriano G. Rossi,d Robert K. Winn,e and John M. Harlanc

Publish date

2007 Oct 1.

PMID

25691096

Abstract

Prostate cancer is the second most common malignancy among men worldwide. Genome-wide association studies (GWAS) have identified 100 risk variants for prostate cancer, which can explain ~33% of the familial risk of the disease. We hypothesized that a comprehensive analysis of genetic variations found within the 3′ UTR of genes predicted to affect miRNA binding (miRSNPs) can identify additional prostate cancer risk variants. We investigated the association between 2,169 miRSNPs and prostate cancer risk in a large-scale analysis of 22,301 cases and 22,320 controls of European ancestry from 23 participating studies. Twenty-two miRSNPs were associated (p<2.3×10−5) with risk of prostate cancer, 10 of which were within the 7 genes previously not mapped by GWASs. Further, using miRNA mimics and reporter gene assays, we showed that miR-3162-5p has specific affinity for the KLK3 rs1058205 miRSNP T-allele whilst miR-370 has greater affinity for the VAMP8 rs1010 miRSNP A-allele, validating their functional role. Significance Findings from this large association study suggest that a focus on miRSNPs, including functional evaluation, can identify candidate risk loci below currently accepted statistical levels of genome-wide significance. Studies of miRNAs and their interactions with SNPs could provide further insights into the mechanisms of prostate cancer risk.

Title

A large scale analysis of genetic variants within putative miRNA binding sites in prostate cancer

Author

Shane Stegeman, Ernest Amankwah, Kerenaftali Klein, Tracy A. O’Mara, Donghwa Kim, Hui-Yi Lin, Jennifer Permuth-Wey, Thomas A. Sellers, Srilakshmi Srinivasan, Rosalind Eeles, Doug Easton, Zsofia Kote-Jarai, Ali Amin Al Olama, Sara Benlloch, Kenneth Muir, Graham G. Giles, Fredrik Wiklund, Henrik Gronberg, Christopher A. Haiman, Johanna Schleutker, Børge G. Nordestgaard, Ruth C. Travis, David Neal, Paul Pharoah, Kay-Tee Khaw, Janet L. Stanford, William J. Blot, Stephen Thibodeau, Christiane Maier, Adam S. Kibel, Cezary Cybulski, Lisa Cannon-Albright, Hermann Brenner, Radka Kaneva, Manuel R. Teixeira, PRACTICAL Consortium, Australian Prostate Cancer BioResource, Amanda B. Spurdle, Judith A. Clements, Jong Y. Park, Jyotsna Batra

Publish date

2015 Oct 1.

PMID

6285339

Abstract

Anthrax toxin is composed of three proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). These proteins individually cause no known physiological effects in animals but in pairs produce two toxic actions. Injection of PA with LF causes death of rats in 60 min, whereas PA with EF causes edema in the skin of rabbits and guinea pigs. The mechanisms of action of these proteins have not been determined. It is shown here that EF is an adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] produced by Bacillus anthracis in an inactive form. Activation occurs upon contact with a heat-stable eukaryotic cell material. The specific activity of the resulting adenylate cyclase nearly equals that of the most active known cyclase. In Chinese hamster ovary cells exposed to PA and EF, cAMP concentrations increase without a lag to values about 200-fold above normal, remain high in the continued presence of toxin, and decrease rapidly after its removal. The increase in cAMP is completely blocked by excess LF. It is suggested that PA interacts with cells to form a receptor system by which EF and perhaps LF gain access to the cytoplasm.

Title

Anthrax toxin edema factor: a bacterial adenylate cyclase that increases cyclic AMP concentrations of eukaryotic cells.

Author

S H Leppla

Publish date

1982 May;


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