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2-(2-Aminobenzoyl)-benzoic acid

$64

  • Brand : BIOFRON

  • Catalogue Number : BN-O1055

  • Specification : 98%(HPLC)

  • CAS number : 1147-43-9

  • Formula : C14H11NO3

  • Molecular Weight : 241.24

  • PUBCHEM ID : 70847

  • Volume : 5mg

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Catalogue Number

BN-O1055

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

241.24

Appearance

Botanical Source

Structure Type

Category

SMILES

C1=CC=C(C(=C1)C(=O)C2=CC=CC=C2N)C(=O)O

Synonyms

2-Aminobenzophenone-2′-carboxylic acid/2-Anthraniloylbenzoic Acid/2-Aminobenzophenone-2'-carboxylic acid/2-(2-aminobenzoyl)benzoic acid/2'-Aminobenzophenone-2-carboxylic Acid

IUPAC Name

2-(2-aminobenzoyl)benzoic acid

Density

1.322 g/cm3

Solubility

Flash Point

268.8ºC

Boiling Point

520.9ºC at 760 mmHg

Melting Point

196-199 °C (dec.)(lit.)

InChl

InChl Key

KORKIRUGUNPQML-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#:1147-43-9) 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

29352099

Abstract

Objective
To investigate whether cigarette smoking interacts with genes involved in individual susceptibility to xenobiotics for the risk of Parkinson disease (PD).

Methods
Two French population-based case-control studies (513 patients, 1,147 controls) were included as a discovery sample to examine gene-smoking interactions based on 3,179 single nucleotide polymorphisms (SNPs) in 289 genes involved in individual susceptibility to xenobiotics. SNP-by-cigarette smoking interactions were tested in the discovery sample through an empirical Bayes (EB) approach. Nine SNPs were selected for replication in a population-based case-control study from California (410 patients, 845 controls) with standard logistic regression and the EB approach. For SNPs that replicated, we performed pooled analyses including the discovery and replication datasets and computed pooled odds ratios and confidence intervals (CIs) using random-effects meta-analysis.

Results
Nine SNPs interacted with smoking in the discovery dataset and were selected for replication. Interactions of smoking with rs4240705 in the RXRA gene and rs1900586 in the SLC17A6 gene were replicated. In pooled analyses (logistic regression), the interactions between smoking and rs4240705-G and rs1900586-G were 1.66 (95% CI 1.28-2.14, p = 1.1 × 10−4, p for heterogeneity = 0.366) and 1.61 (95% CI 1.17-2.21, p = 0.003, p for heterogeneity = 0.616), respectively. For both SNPs, while smoking was significantly less frequent in patients than controls in AA homozygotes, this inverse association disappeared in G allele carriers.

Conclusions
We identified and replicated suggestive gene-by-smoking interactions in PD. The inverse association of smoking with PD was less pronounced in carriers of minor alleles of both RXRA-rs4240705 and SLC17A6-rs1900586. These findings may help identify biological pathways involved in the inverse association between smoking and PD.

Title

Smoking and Parkinson disease: Evidence for gene-by-smoking interactions

Author

Pei-Chen Lee, PhD,* Ismaïl Ahmed, PhD,* Marie-Anne Loriot, PhD, Claire Mulot, PhD, Kimberly C. Paul, PhD, Jeff M. Bronstein, MD, PhD, Beate Ritz, MD, PhD, and Alexis Elbaz, MD, PhDcorresponding author

Publish date

2018 Feb 13

PMID

5874536

Abstract

kushner, D. J. (National Research Council, Ottawa, Ontario, Canada). Lysis and dissolution of cells and envelopes of an extremely halophilic bacterium. J. Bacteriol. 87:1147-1156. 1964.—Envelopes of the extremely halophilic bacterium, Halobacterium cutirubrum, disintegrate in the absence of salt to form much smaller particles. Extensive proteolytic breakdown to compounds of low molecular weight is not involved in this process or in the lysis of cells in the absence of salt. NaCl is much more effective than KCl or NH4Cl in preserving the integrity of intact cells, but is only slightly more effective in preserving the integrity of mechanically prepared envelopes, of cells made permeable by treatment with acid, and of cells made permeable by formalin fixation followed by exposure to water. MgCl2 is much more effective in preserving the integrity of these preparations than of intact cells. The results suggest that the exterior cell surface has sites specifically requiring Na+ to maintain their integrity, whereas the interior surface has sites whose integrity is maintained at least as well by K+ or NH4+ as by Na+.

Title

LYSIS AND DISSOLUTION OF CELLS AND ENVELOPES OF AN EXTREMELY HALOPHILIC BACTERIUM

Author

D. J. Kushner

Publish date

1964 May;

PMID

20857860

Abstract

Study Objectives:
The sleep-deprivation-induced changes in delta power, an electroencephalographical correlate of sleep need, and brain transcriptome profiles have importantly contributed to current hypotheses on sleep function. Because sleep deprivation also induces stress, we here determined the contribution of the corticosterone component of the stress response to the electrophysiological and molecular markers of sleep need in mice.

Design:
N/A

Settings:
Mouse sleep facility.

Participants:
C57BL/6J, AKR/J, DBA/2J mice.

Interventions:
Sleep deprivation, adrenalectomy (ADX).

Measurements and Results:
Sleep deprivation elevated corticosterone levels in 3 inbred strains, but this increase was larger in DBA/2J mice; i.e., the strain for which the rebound in delta power after sleep deprivation failed to reach significance. Elimination of the sleep-deprivation-associated corticosterone surge through ADX in DBA/2J mice did not, however, rescue the delta power rebound but did greatly reduce the number of transcripts affected by sleep deprivation. Genes no longer affected by sleep deprivation cover pathways previously implicated in sleep homeostasis, such as lipid, cholesterol (e.g., Ldlr, Hmgcs1, Dhcr7, −24, Fkbp5), energy and carbohydrate metabolism (e.g., Eno3, G6pc3, Mpdu1, Ugdh, Man1b1), protein biosynthesis (e.g., Sgk1, Alad, Fads3, Eif2c2, −3, Mat2a), and some circadian genes (Per1, −3), whereas others, such as Homer1a, remained unchanged. Moreover, several microRNAs were affected both by sleep deprivation and ADX.

Conclusions:
Our findings indicate that corticosterone contributes to the sleep-deprivation-induced changes in brain transcriptome that have been attributed to wakefulness per se. The study identified 78 transcripts that respond to sleep loss independent of corticosterone and time of day, among which genes involved in neuroprotection prominently feature, pointing to a molecular pathway directly relevant for sleep function.

Citation:
Mongrain V; Hernandez SA; Pradervand S; Dorsaz S; Curie T; Hagiwara G; Gip P; Heller HC; Franken P. Separating the contribution of glucocorticoids and wakefulness to the molecular and electrophysiological correlates of sleep homeostasis. SLEEP 2010;33(9):1147-1157.

KEYWORDS

Sleep regulation, corticosterone, neuroprotection, microarray, microRNA

Title

Separating the Contribution of Glucocorticoids and Wakefulness to the Molecular and Electrophysiological Correlates of Sleep Homeostasis

Author

Valerie Mongrain, Susana A. Hernandez, Sylvain Pradervand, Stephane Dorsaz, Thomas Curie, Grace Hagiwara, Phung Gip, H. Craig Heller, Paul Franken

Publish date

2010 Sep 1


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