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4-(4-Aminophenoxy)-N-methyl-2-pyridinecarboxamide

$63

  • Brand : BIOFRON

  • Catalogue Number : BN-O1187

  • Specification : 98%(HPLC)

  • CAS number : 284462-37-9

  • Formula : C13H13N3O2

  • Molecular Weight : 243.26

  • PUBCHEM ID : 16655129

  • Volume : 5mg

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Catalogue Number

BN-O1187

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

243.26

Appearance

Botanical Source

Structure Type

Category

SMILES

CNC(=O)C1=NC=CC(=C1)OC2=CC=C(C=C2)N

Synonyms

THIOPHENE 2-CARBONITRILE/2-Pyridinecarboxamide, 4-(4-aminophenoxy)-N-methyl-/[4-(4-aminophenoxy)(2-pyridyl)]-n-methylcarboxamide/4-(4-Aminophenoxy)-N-methylpyridine-2-carboxamide/4-(4-Aminophenoxy)-N-methylpicolinamide/4-(4-Aminophenoxy)-N-methyl-2-pyridinecarboxamide/4-[(4-aminomethyl)phenoxy]-2-pyridine carbonic acid methylamide/4-[(4-aminophenoxy)(2-pyridyl)]-N-methylcarboxamide/4-(2-(N-methylcarbamoyl)-4-pyridyloxy)aniline/4-(4-amino-phenoxy)-pyridine-2-carboxylic acid methylamide

IUPAC Name

4-(4-aminophenoxy)-N-methylpyridine-2-carboxamide

Density

1.2±0.1 g/cm3

Solubility

Flash Point

242.2±27.3 °C

Boiling Point

476.8±40.0 °C at 760 mmHg

Melting Point

110-112ºC

InChl

InChl Key

RXZZBPYPZLAEFC-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#:284462-37-9) 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

25319637

Abstract

Adenosine is an endogenous molecule that regulates many physiological processes via the activation of four specific G-protein-coupled ADORA receptors. Extracellular adenosine may originate either from the hydrolysis of released ATP by the ectonucleotidases or from cellular exit via the equilibrative nucleoside transporters (SLC29A). Adenosine extracellular concentration is also regulated by its successive hydrolysis into uric acid by membrane-bound enzymes or by cell influx via the concentrative nucleoside transporters (SLC28A). All of these members constitute the adenosine signaling pathway and regulate adenosine functions. Although the roles of this pathway are quite well understood in adults, little is known regarding its functions during vertebrate embryogenesis. We have used Xenopus laevis as a model system to provide a comparative expression map of the different members of this pathway during vertebrate development. We report the characterization of the different enzymes, receptors, and nucleoside transporters in both X. laevis and X. tropicalis, and we demonstrate by phylogenetic analyses the high level of conservation of these members between amphibians and mammals. A thorough expression analysis of these members during development and in the adult frog reveals that each member displays distinct specific expression patterns. These data suggest potentially different developmental roles for these proteins and therefore for extracellular adenosine. In addition, we show that adenosine levels during amphibian embryogenesis are very low, confirming that they must be tightly controlled for normal development.

Electronic supplementary material
The online version of this article (doi:10.1007/s11302-014-9431-6) contains supplementary material, which is available to authorized users.

KEYWORDS

Comparative genomic and expression analysis of the adenosine signaling pathway members in Xenopus

Title

Comparative genomic and expression analysis of the adenosine signaling pathway members in Xenopus

Author

Alice Tocco, Benoît Pinson, Pierre Thiebaud, Nadine Theze, and Karine Massecorresponding author

Publish date

2015 Mar

PMID

25755278

Abstract

Growth-associated protein 43 (GAP43) is known to regulate axon growth, but whether it also plays a role in synaptogenesis remains unclear. Here, we found that GAP43 regulates the aggregation of gephyrin, a pivotal protein for clustering postsynaptic GABAA receptors (GABAARs), in developing cortical neurons. Pharmacological blockade of either protein kinase C (PKC) or neuronal activity increased both GAP43-gephyrin association and gephyrin misfolding-induced aggregation, suggesting the importance of PKC-dependent regulation of GABAergic synapses. Furthermore, we found that PKC phosphorylation-resistant GAP43S41A, but not PKC phosphorylation-mimicking GAP43S41D, interacted with cytosolic gephyrin to trigger gephyrin misfolding and its sequestration into aggresomes. In contrast, GAP43S41D, but not GAP43S41A, inhibited the physiological aggregation/clustering of gephyrin, reduced surface GABAARs under physiological conditions, and attenuated gephyrin misfolding under transient oxygen-glucose deprivation (tOGD) that mimics pathological neonatal hypoxia. Calcineurin-mediated GAP43 dephosphorylation that accompanied tOGD also led to GAP43-gephyrin association and gephyrin misfolding. Thus, PKC-dependent phosphorylation of GAP43 plays a critical role in regulating postsynaptic gephyrin aggregation in developing GABAergic synapses.

Title

Protein Kinase C-Dependent Growth-Associated Protein 43 Phosphorylation Regulates Gephyrin Aggregation at Developing GABAergic Synapses

Author

Chen-Yu Wang,a,b,g Hui-Ching Lin,a Yi-Ping Song,b Yu-Ting Hsu,b Shu-Yu Lin,c Pei-Chien Hsu,a Chun-Hua Lin,d Chia-Chi Hung,a,b Min-Ching Hsu,b Yi-Min Kuo,a,e Yih-Jing Lee,f Chung Y. Hsu,g and Yi-Hsuan Leecorresponding authora,b

Publish date

2015 May;


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