We Offer Worldwide Shipping
Login Wishlist

4,6,7-Trihydroxycoumarin

$320

  • Brand : BIOFRON

  • Catalogue Number : BN-O1462

  • Specification : 98%(HPLC)

  • CAS number : 22649-24-7

  • Formula : C9H6O5

  • Molecular Weight : 194.14

  • PUBCHEM ID : 86597497

  • Volume : 20mg

Available on backorder

Quantity
Checkout Bulk Order?

Catalogue Number

BN-O1462

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

194.14

Appearance

Botanical Source

Structure Type

Category

SMILES

C1=C2C(=CC(=O)OC2=CC(=C1O)O)O

Synonyms

4,6,7-Trihydroxy-cumarin/4,6,7-Trihydroxy-chromen-2-one

IUPAC Name

4,6,7-trihydroxychromen-2-one

Density

Solubility

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

Flash Point

Boiling Point

Melting Point

InChl

InChl Key

FNYQCLTWIHHCQV-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:22649-24-7) 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

26229107

Abstract

MDM2 and p53 form a negative feedback loop, in which p53 as a transcription factor positively regulates MDM2 and MDM2 negatively regulates tumor suppressor p53 through promoting its degradation. However, the mechanism of the feedback loop is poorly understood in cancers. We had reported previously that the oncoprotein hepatitis B X-interacting protein (HBXIP) is a key oncoprotein in the development of cancer. Thus, we supposed that HBXIP might be involved in the event. Here, we observed that the expression levels of HBXIP were positively correlated to those of MDM2 in clinical breast cancer tissues. Interestingly, HBXIP was able to up-regulate MDM2 at the levels of mRNA and protein in MCF-7 breast cancer cells. Mechanically, HBXIP increased the promoter activities of MDM2 through directly binding to p53 in the P2 promoter of MDM2. Strikingly, we identified that the acetyltransferase p300 was recruited by HBXIP to p53 in the promoter of MDM2. Moreover, we validated that HBXIP enhanced the p53 degradation mediated by MDM2. Functionally, the knockdown of HBXIP or/and p300 inhibited the proliferation of breast cancer cells in vitro, and the depletion of MDM2 or overexpression of p53 significantly blocked the HBXIP-promoted growth of breast cancer in vitro and in vivo. Thus, we concluded that highly expressed HBXIP accelerates the MDM2-mediated degradation of p53 in breast cancer through modulating the feedback loop of MDM2/p53, resulting in the fast growth of breast cancer cells. Our findings provide new insights into the mechanism of the acceleration of the MDM2/p53 feedback loop in the development of cancer.

KEYWORDS

breast cancer, mouse double minute 2 homolog (MDM2), oncogene, p53, tumor, HBXIP, p300

Title

The Oncoprotein HBXIP Modulates the Feedback Loop of MDM2/p53 to Enhance the Growth of Breast Cancer

Author

Hang Li,‡ Qian Liu,‡ Zhen Wang,‡ Runping Fang,‡ Yu Shen,‡ Xiaoli Cai,‡ Yuen Gao,§ Yinghui Li,‡ Xiaodong Zhang,§,1 and Lihong Ye‡,2

Publish date

2015 Sep 11;

PMID

29340495

Abstract

Objective:
To validate the Portuguese-language version of the STOP-Bang (acronym for Snoring, Tiredness, Observed apnea, high blood Pressure, Body mass index, Age, Neck circumference, and Gender) questionnaire, culturally adapted for use in Brazil, as a means of screening for obstructive sleep apnea (OSA) in adults.

Methods:
In this validation study, we enrolled patients ≥ 18 years of age, recruited between May of 2015 and November of 2016. All patients completed the STOP-Bang questionnaire and underwent overnight polysomnography. To evaluate the performance of the questionnaire, we used contingency tables and areas under the (receiver operating characteristic) curve (AUCs).

Results:
We included 456 patients. The mean age was 43.7 ± 12.5 years, and 291 (63.8%) of the patients were male. On the basis of the apnea-hypopnea index (AHI), we categorized OSA as mild/moderate/severe (any OSA; AHI ≥ 5 events/h), moderate/severe (AHI ≥ 15 events/h), or severe (AHI ≥ 30 events/h). The overall prevalence of OSA was 78.3%, compared with 52.0%, and 28.5% for moderate/severe and severe OSA, respectively. The most common score on the STOP-Bang questionnaire was 4 points (n = 106), followed by 3 points (n = 85) and 5 points (n = 82). An increase in the score was paralleled by a reduction in sensitivity with a corresponding increase in specificity for all AHI cut-off points. The AUCs obtained for the identification of any, moderate/severe, and severe OSA were: 0.743, 0.731, and 0.779, respectively. For any OSA, the score on the questionnaire (cut-off, ≥ 3 points) presented sensitivity, specificity, and accuracy of 83.5%, 45.5%, and 75.2%, respectively.

Conclusions:
The STOP-Bang questionnaire performed adequately for OSA screening, indicating that it could be used as an effective screening tool for the disorder.

KEYWORDS

Sleep apnea, obstructive/diagnosis; Polysomnography; Diagnostic techniques and procedures; Surveys and questionnaires

Title

Validation of the STOP-Bang questionnaire as a means of screening for obstructive sleep apnea in adults in Brazil

Author

Ricardo Luiz de Menezes Duarte, 1 , 2 Lorena Barbosa de Moraes Fonseca, 3 , 4 , 5 Flavio Jose Magalhães-da-Silveira, 1 Erika Aparecida da Silveira, 3 and Marcelo Fouad Rabahi 3 , 4 , 5

Publish date

2017 Nov-Dec;

PMID

28186988

Abstract

Human malignant mesothelioma (MM) is an aggressive cancer linked to asbestos and erionite exposure. We previously reported that High-Mobility Group Box-1 protein (HMGB1), a prototypic damage-associated molecular pattern, drives MM development and sustains MM progression. Moreover, we demonstrated that targeting HMGB1 inhibited MM cell growth and motility in vitro, reduced tumor growth in vivo, and prolonged survival of MM-bearing mice. Ethyl pyruvate (EP), the ethyl ester of pyruvic acid, has been shown to be an effective HMGB1 inhibitor in inflammation-related diseases and several cancers. Here, we studied the effect of EP on the malignant phenotype of MM cells in tissue culture and on tumor growth in vivo using an orthotopic MM xenograft model. We found that EP impairs HMGB1 secretion by MM cells leading to reduced RAGE expression and NF-κB activation. As a consequence, EP impaired cell motility, cell proliferation, and anchorage-independent growth of MM cells. Moreover, EP reduced HMGB1 serum levels in mice and inhibited the growth of MM xenografts.

Our results indicate that EP effectively hampers the malignant phenotype of MM, offering a novel potential therapeutic approach to patients afflicted with this dismal disease.

KEYWORDS

HMGB1, RAGE, ethyl pyruvate, mesothelioma, therapeutic

Title

HMGB1 targeting by ethyl pyruvate suppresses malignant phenotype of human mesothelioma

Author

Laura Pellegrini,1 Jiaming Xue,1,3 David Larson,1 Sandra Pastorino,1 Sandro Jube,2 Kelly H. Forest,3 Zeyana Salim Saad-Jube,4 Andrea Napolitano,1,5 Ian Pagano,1 Vishal S. Negi,5 Marco E. Bianchi,6 Paul Morris,7 Harvey I. Pass,8 Giovanni Gaudino,1 Michele Carbone,1 and Haining Yang1

Publish date

2017 Apr 4;


Description :

Empty ...