We Offer Worldwide Shipping
Login Wishlist

Glycyrrhisoflavone

$1,120

  • Brand : BIOFRON

  • Catalogue Number : BD-P0953

  • Specification : 98.0%(HPLC)

  • CAS number : 116709-70-7

  • Formula : C20H18O6

  • Molecular Weight : 354.36

  • PUBCHEM ID : 5317764

  • Volume : 25mg

Available on backorder

Quantity
Checkout Bulk Order?

Catalogue Number

BD-P0953

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC)

Storage

2-8°C

Molecular Weight

354.36

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

SMILES

CC(=CCC1=C(C(=CC(=C1)C2=COC3=CC(=CC(=C3C2=O)O)O)O)O)C

Synonyms

3-[3,4-dihydroxy-5-(3-methylbut-2-enyl)phenyl]-5,7-dihydroxychromen-4-one

IUPAC Name

3-[3,4-dihydroxy-5-(3-methylbut-2-enyl)phenyl]-5,7-dihydroxychromen-4-one

Applications

Density

1.4±0.1 g/cm3

Solubility

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

Flash Point

229.4±25.0 °C

Boiling Point

631.9±55.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C20H18O6/c1-10(2)3-4-11-5-12(6-16(23)19(11)24)14-9-26-17-8-13(21)7-15(22)18(17)20(14)25/h3,5-9,21-24H,4H2,1-2H3

InChl Key

JOQWUUJQWPZLAT-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#:116709-70-7) 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

22419826

Abstract

The syncytium is a unique plant root organ whose differentiation is induced by plant-parasitic cyst nematodes to create a source of nourishment. Syncytium formation involves the redifferentiation and fusion of hundreds of root cells. The underlying regulatory networks that control this unique change of plant cell fate are not understood. Here, we report that a strong down-regulation of Arabidopsis (Arabidopsis thaliana) microRNA396 (miR396) in cells giving rise to the syncytium coincides with the initiation of the syncytial induction/formation phase and that specific miR396 up-regulation in the developed syncytium marks the beginning of the maintenance phase, when no new cells are incorporated into the syncytium. In addition, our results show that miR396 in fact has a role in the transition from one phase to the other. Expression modulations of miR396 and its Growth-Regulating Factor (GRF) target genes resulted in reduced syncytium size and arrested nematode development. Furthermore, genome-wide expression profiling revealed that the miR396-GRF regulatory system can alter the expression of 44% of the more than 7,000 genes reported to change expression in the Arabidopsis syncytium. Thus, miR396 represents a key regulator for the reprogramming of root cells. As such, this regulatory unit represents a powerful molecular target for the parasitic animal to modulate plant cells and force them into novel developmental pathways.

Title

The Arabidopsis MicroRNA396-GRF1/GRF3 Regulatory Module Acts as a Developmental Regulator in the Reprogramming of Root Cells during Cyst Nematode Infection1,[W][OA]

Author

Tarek Hewezi, Tom R. Maier, Dan Nettleton, and Thomas J. Baum*

Publish date

2012 May

PMID

27903974

Abstract

Long non-coding RNAs (lncRNAs) have been implicated in pathogenesis of various cancers, including lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD). We used cBioPortal to analyze lncRNA alteration frequencies and their ability to predict overall survival (OS) using 504 LUSC and 522 LUAD samples from The Cancer Genome Atlas (TCGA) database. In LUSC, 624 lncRNAs had alteration rates > 1% and 64 > 10%. In LUAD 625 lncRNAs had alteration rates > 1% and 36 > 10%. Among those, 620 lncRNAs had alteration frequencies > 1% in both LUSC and LUAD, while 22 were LUSC-specific and 23 were LUAD-specific. Twenty lncRNAs had alteration frequencies > 10% in both LUSC and LUAD, while 44 were LUSC-specific and 16 were LUAD specific. Genome ontology and pathway analyses produced similar results for LUSC and LUAD. Two lncRNAs (IGF2BP2-AS1 and DGCR5) correlated with better OS in LUSC, and three (MIR31HG, CDKN2A-AS1 and LINC01600) predicted poor OS in LUAD. Chip-seq and luciferase reporter assays identified potential IGF2BP2-AS1, DGCR5 and LINC01600 promoters and enhancers. This study presented lncRNA landscapes and revealed differentially expressed, highly altered lncRNAs in LUSC and LUAD. LncRNAs that act as oncogenes and lncRNA-regulating transcription factors provide novel targets for anti-lung cancer therapeutics.

KEYWORDS

lung squamous cell carcinoma, lung adenocarcinoma, long non-coding RNA, overall survival, gene regulation

Title

LncRNAs are altered in lung squamous cell carcinoma and lung adenocarcinoma

Author

Bing Liu,#1 Yifei Chen,#1 and Jiong Yang1

Publish date

2017 Apr 11

PMID

27854420

Abstract

Introduction
Heart disease and cancer are the first and second leading causes of death in the United States. Age-standardized death rates (risk) have declined since the 1960s for heart disease and for cancer since the 1990s, whereas the overall number of heart disease deaths declined and cancer deaths increased. We analyzed mortality data to evaluate and project the effect of risk reduction, population growth, and aging on the number of heart disease and cancer deaths to the year 2020.

Methods
We used mortality data, population estimates, and population projections to estimate and predict heart disease and cancer deaths from 1969 through 2020 and to apportion changes in deaths resulting from population risk, growth, and aging.

Results
We predicted that from 1969 through 2020, the number of heart disease deaths would decrease 21.3% among men (-73.9% risk, 17.9% growth, 34.7% aging) and 13.4% among women (-73.3% risk, 17.1% growth, 42.8% aging) while the number of cancer deaths would increase 91.1% among men (-33.5% risk, 45.6% growth, 79.0% aging) and 101.1% among women (-23.8% risk, 48.8% growth, 76.0% aging). We predicted that cancer would become the leading cause of death around 2016, although sex-specific crossover years varied.

Conclusion
Risk of death declined more steeply for heart disease than cancer, offset the increase in heart disease deaths, and partially offset the increase in cancer deaths resulting from demographic changes over the past 4 decades. If current trends continue, cancer will become the leading cause of death by 2020.

Title

Heart Disease and Cancer Deaths — Trends and Projections in the United States, 1969-2020

Author

Hannah K. Weir, PhD,corresponding author Robert N. Anderson, PhD, Sallyann M. Coleman King, MD, MSc, Ashwini Soman, MPH, Trevor D. Thompson, BS, Yuling Hong, MD, MS, PhD, Bjorn Moller, PhD, and Steven Leadbetter, MS

Publish date

2016;