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Neodiosmin

$143

  • Brand : BIOFRON

  • Catalogue Number : BF-N2012

  • Specification : 98%

  • CAS number : 38665-01-9

  • Formula : C28H32O15

  • Molecular Weight : 608.54

  • PUBCHEM ID : 69964214

  • Volume : 20mg

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Catalogue Number

BF-N2012

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

608.54

Appearance

White crystal

Botanical Source

synthesis

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1C(C(C(C(O1)OC2C(C(C(OC2OC3=CC(=C4C(=C3)OC(=CC4=O)C5=CC(=C(C=C5)OC)O)O)CO)O)O)O)O)O

Synonyms

Diosmetin-7-neohesperidoside/Neodiosmin/Diosmetin-7-O-neohesperidoside/4'-O-methylluteolin-7-O-rhamnoglucoside/4H-1-Benzopyran-4-one, 7-[[2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl]oxy]-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-/Neohesperidin dihydrochalcone impurity B/5-Hydroxy-2-(3-hydroxy-4-methoxyphenyl)-4-oxo-4H-chromen-7-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside/diosmetin 7-O-neohesperidoside

IUPAC Name

7-[(2S,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxyoxan-2-yl]oxy-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)chromen-4-one

Density

1.7±0.1 g/cm3

Solubility

Methanol; Water; DMF

Flash Point

306.4±27.8 °C

Boiling Point

930.4±65.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C28H32O15/c1-10-21(33)23(35)25(37)27(39-10)43-26-24(36)22(34)19(9-29)42-28(26)40-12-6-14(31)20-15(32)8-17(41-18(20)7-12)11-3-4-16(38-2)13(30)5-11/h3-8,10,19,21-31,33-37H,9H2,1-2H3/t10-,19+,21-,22+,23+,24-,25+,26+,27-,28+/m0/s1

InChl Key

VCCNKWWXYVWTLT-CYZBKYQRSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:38665-01-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

27924849

Abstract

Notch1 signaling plays a critical role in maintaining and determining neural stem/progenitor cell (NSPC) fate, yet the transcriptional mechanism controlling Notch1 specific expression in NSPCs remains incomplete. Here, we show transcription factor Nkx6.1 interacts with a cis-element (CR2, an evolutionarily conserved non-coding fragment in the second intron of Notch1 locus) and regulates the expression of Notch1 in ventral NSPCs of the developing spinal cord. We show that the Notch1 expression is modulated by the interaction of Nkx6.1 with a 139 bp enhancer sequence within CR2. Knockdown or overexpression of Nkx6.1 leads to down- or up-regulated Notch1 expression, respectively. In CR2-GFP transgenic mouse, GFP expression was found prominent in the ventricular zone and neural progenitor cells from embryonic day 9.5 to postnatal day 7. GFP+ cells were mainly neural progenitors for interneurons and not for motoneurons or glial cells. Moreover, GFP expression persisted in a subset of ependymal cells in the adult spinal cord, suggesting that CR2 is active in both embryonic and adult NSPCs. Together our data reveal a novel mechanism of Notch1 transcriptional regulation in the ventral spinal cord by Nkx6.1 via its binding with Notch1 enhancer CR2 during embryonic development.

Notch1 is a member of the Notch protein family which encodes a single-pass trans-membrane receptor. Notch1 signaling plays a critical role in the development of the central nervous system (CNS) by inhibiting neuronal progenitor differentiation, maintaining radial glia identity, specifying glial cell type, promoting apoptotic cell death and regulating axonal guidance of post-mitotic neurons1,2,3,4,5,6,7. In the spinal cord, in additional to its role in neural stem cells, Notch1 is involved in fate determination of dorsal interneurons and V2b interneurons8,9,10. Notch1 deficiency results in a premature neuronal differentiation in the ventral spinal cord and a gradual depletion of the ventral central canal5. However, despite the importance of Notch1 pathway, transcriptional regulation of Notch1 expression is not completely understood. Usually, transcription factors function by binding to gene regulatory DNA elements, e.g., promoters, enhancers. Often these cis-elements are evolutionarily conserved11,12. We have previously identified an evolutionarily conserved cis-element in the second intron of Notch1 gene (Notch1CR2, or CR2, a 399 bp non-coding DNA fragment)13. CR2 regulates gene expression in neural stem/progenitor cells (NSPCs) and was predominantly active in the GABAergic interneuron progenitors in the ganglionic eminence during neocortical development13.

In the spinal cord, differentiation of neurons and glial cells are regulated by a transcription factor network including Notch1, Nkx6.1, Pax6, Foxn4 and Dll4, etc.14. Nkx6.1 in particular, is critical for the fate determination of progenitor cells in ventral interneuron layer 2 and 3 (V2, V3)15. Nkx6.1 deletion leads to the loss of V2 and motoneuron (MN) markers such as Lhx3, Isl1/2 and Hb915, while over-expression of Nkx6.1 leads to an increase of V2, MN markers and decrease of V1 marker16.

In this study, we investigated the Notch1 transcription regulation by CR2 in the developing mouse and chick spinal cord. We show that a 139 bp fragment within CR2 contains binding sites for transcription factor Nkx6.1. The interaction of this fragment with Nkx6.1 is essential for CR2 gene regulatory activity in regulating Notch1 in the NSPCs which develop into interneurons. Our study provides a novel mechanism of Notch1 gene regulation in NSPCs by Nkx6.1-CR2 interaction during the development of the spinal cord.

Title

Transcriptional Regulation of Notch1 Expression by Nkx6.1 in Neural Stem/Progenitor Cells during Ventral Spinal Cord Development

Author

Ying Li,1 Evangeline Tzatzalos,1,* Kelvin Y. Kwan,2 Martin Grumet,2 and Li Caia,1

Publish date

2016;

PMID

22984265

Abstract

Toll-like receptors (TLRs) are a group of pattern recognition receptors that play a crucial role in the induction of the innate immune response against bacterial and viral infections. TLR3 has emerged as a key sensor of viral double-stranded RNA. Thus, a clearer understanding of the biological processes that modulate TLR3 signaling is essential. Limited studies have applied proteomics toward understanding the dynamics of TLR signaling. Herein, a proteomics approach identified 14-3-3ϵ and 14-3-3σ proteins as new members of the TLR signaling complex. Toward the functional characterization of 14-3-3ϵ and 14-3-3σ in TLR signaling, we have shown that both of these proteins impair TLR2, TLR3, TLR4, TLR7/8, and TLR9 ligand-induced IL-6, TNFα, and IFN-β production. We also show that 14-3-3ϵ and 14-3-3σ impair TLR2-, TLR3-, TLR4-, TLR7/8-, and TLR9-mediated NF-κB and IFN-β reporter gene activity. Interestingly, although the 14-3-3 proteins inhibit poly(I:C)-mediated RANTES production, 14-3-3 proteins augment Pam3CSK4, LPS, R848, and CpG-mediated production of RANTES (regulated on activation normal T cell expressed and secreted) in a Mal (MyD88 adaptor-like)/MyD88-dependent manner. 14-3-3ϵ and 14-3-3σ also bind to the TLR adaptors and to both TRAF3 and TRAF6. Our study conclusively shows that 14-3-3ϵ and 14-3-3σ play a major regulatory role in balancing the host inflammatory response to viral and bacterial infections through modulation of the TLR signaling pathway. Thus, manipulation of 14-3-3 proteins may represent novel therapeutic targets for inflammatory conditions and infections.

KEYWORDS

TLR Signaling, 14-3-3 Protein, Cytokine, Negative Regulation

Title

14-3-3ϵ and 14-3-3σ Inhibit Toll-like Receptor (TLR)-mediated Proinflammatory Cytokine Induction*An external file that holds a picture, illustration, etc.Object name is sbox.jpg

Author

Aisha Qasim Butt, Suaad Ahmed, Ashwini Maratha, and Sinead M. Miggin1

Publish date

2012 Nov 9;

PMID

31709086

Abstract

The reactions of N-heterocyclic carbene CuI and AgI halides with potassium thio- or seleno­cyanate gave unexpected products. The attempted substitution reaction of bromido­(1,3-dibenzyl-4,5-di­phenyl­imidazol-2-yl­idene)silver (NHC*—Ag—Br) with KSCN yielded bis­[bis­(1,3-dibenzyl-4,5-di­phenyl­imidazol-2-yl­idene)silver(I)] tris­(thio­cyanato)­argentate(I) diethyl ether disolvate, [Ag(C29H24N2)2][Ag(NCS)3]·2C4H10O or [NHC*2Ag]2[Ag(SCN)3]·2Et2O, (1), while reaction with KSeCN led to bis­(μ-1,3-dibenzyl-4,5-diphenyl-2-seleno­imidazole-κ2 Se:Se)bis­[bromido­(1,3-dibenzyl-4,5-diphenyl-2-seleno­imid­azole-κSe)silver(I)] di­chloro­methane hexa­solvate, [Ag2Br2(C29H24N2Se)4]·6CH2Cl2 or (NHC*Se)4Ag2Br2·6CH2Cl2, (2), via oxidation of the NHC* fragment to 2-seleno­imidazole. This oxidation was observed again in the reaction of NHC*—Cu—Br with KSeCN, yielding catena-poly[[[(1,3-dibenzyl-4,5-diphenyl-2-seleno­imidazole-κSe)copper(I)]-μ-cyanido-κ2 C:N] aceto­nitrile monosolvate], {[Cu(CN)(C29H24N2Se)]·C2H3N}n or NHC*Se—CuCN·CH3CN, (3). Compound (1) represents an organic/inorganic salt with AgI in a linear coordination in each of the two cations and in a trigonal coordination in the anion, accompanied by diethyl ether solvent mol­ecules. The tri-blade boomerang-shaped complex anion [Ag(SCN)3]2− present in (1) is characterized by X-ray diffraction for the first time. Compound (2) comprises an isolated centrosymmetric mol­ecule with AgI in a distorted tetra­hedral BrSe3 coordination, together with di­chloro­methane solvent mol­ecules. Compound (3) exhibits a linear polymeric 1 ∞[Cu—C≡N—Cu—] chain structure with a seleno­imidazole moiety additionally coordinating to each CuI atom, and completed by aceto­nitrile solvent mol­ecules. Electron densities associated with an additional ether solvent mol­ecule in (1) and two additional di­chloro­methane solvent mol­ecules in (2) were removed with the SQUEEZE procedure [Spek (2015 ▸). Acta Cryst. C71, 9-18] in PLATON.

KEYWORDS

N-Heterocyclic carbene, copper(I), silver(I), thio­cyanate, seleno­cyanate, d10 electron configuration, crystal structure

Title

Unexpected reactions of NHC*—CuI and —AgI bromides with potassium thio- or seleno­cyanate

Author

Matthias Tacke,a Daniel Marhofer,a Hessah Althani,a and Helge Muller-Bunza,*

Publish date

2019 Nov 1;


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