[(1R,4S)-(+)-3-Benzoyl-1,7,7-trimethyl­bicyclo­[2.2.1]heptan-2-olato-κ2 O 2,O 3](η4-norbornadiene)rhodium(I)

In the title complex mol­ecule, [Rh(C17H19O2)(C7H8)], the rhodium(I) metal centre is coordinated by the O atoms of a benzoyl­camphorate anion and the C=C bonds of the norbornadiene mol­ecule into a slightly distorted square-planar coordination geometry. The six-membered chelate ring is essentially planar (r.m.s. deviation = 0.0378 Å) and forms a dihedral angle of 31.67 (11)° with the phenyl ring

Nuclear delivery of NFκB-assisted DNA/polymer complexes: plasmid DNA quantitation by confocal laser scanning microscopy and evidence of nuclear polyplexes by FRET imaging

Quantification of a plasmid DNA (pDNA) and investigation of its polymer-associated state in the nucleus are crucial to evaluate the effectiveness of a gene-delivery system. This study was conducted with p3NF-luc-3NF, a pDNA-bearing optimized κB motif to favour NFκB-driven nuclear import. Here, a quantification of pDNA copies in the nucleus was performed by real-time confocal laser scanning microscopy in HeLa and C2C12 cells transfected with linear polyethylenimine or histidylated polylysine. Förster Resonance Energy Transfer (FRET) from the fluorescein-p3NF-luc-3NF donor to the co-localized rhodamine-polymer acceptor was carried out to investigate whether the pDNA was still condensed with the polymer in the nucleus. Upon 5 h of transfection, the nuclear amount of p3NF-luc3NF was ∼1500 copies in both cell lines whereas that of pTAL-luc, a 3NF-free counterpart pDNA, was less than 250. This quantity of p3NF-luc-3NF dropped dramatically to that of pTAL-luc in the presence of the BAY 11-7085, an inhibitor of NFκB activation. These data strongly support a nuclear import of p3NF-luc3NF mediated by NFκB. Moreover, FRET experiments clearly revealed that most of nuclear pDNA were still condensed with the polymer raising the question of their passage through the nuclear pore complex and their impact on the gene-expression efficiency

Tau Interaction with Tubulin and Microtubules: From Purified Proteins to Cells

International audienceMicrotubules (MTs) play an important role in many cellular processes and are dynamic structures regulated by an important network of microtubules-associated proteins, MAPs, such as Tau. Tau has been discovered as an essential factor for MTs formation in vitro, and its region implicated in binding to MTs has been identified. By contrast, the affinity, the stoichiometry, and the topology of Tau-MTs interaction remain controversial. Indeed, depending on the experiment conditions a wide range of values have been obtained. In this chapter, we focus on three biophysical methods, turbidimetry, cosedimentation assay, and Förster Resonance Energy Transfer to study Tau-tubulin interaction both in vitro and in cell. We highlight precautions that must be taken in order to avoid pitfalls and we detail the nature of the conclusions that can be drawn from these methods about Tau-tubulin interaction

The histone deacetylase inhibitor trichostatin A downregulates human MDR1 (ABCB1) gene expression by a transcription-dependent mechanism in a drug-resistant small cell lung carcinoma cell line model

Tumour drug-resistant ABCB1 gene expression is regulated at the chromatin level through epigenetic mechanisms. We examined the effects of the histone deacetylase inhibitor trichostatin A (TSA) on ABCB1 gene expression in small cell lung carcinoma (SCLC) drug-sensitive (H69WT) or etoposide-resistant (H69VP) cells. We found that TSA induced an increase in ABCB1 expression in drug-sensitive cells, but strongly decreased it in drug-resistant cells. These up- and downregulations occurred at the transcriptional level. Protein synthesis inhibition reduced these modulations, but did not completely suppress them. Differential temporal patterns of histone acetylation were observed at the ABCB1 promoter: increase in H4 acetylation in both cell lines, but different H3 acetylation with a progressive increase in H69WT cells but a transient one in H69VP cells. ABCB1 regulations were not related with the methylation status of the promoter −50GC, −110GC, and Inr sites, and did not result in further changes to these methylation profiles. Trichostatin A treatment did not modify MBD1 binding to the ABCB1 promoter and similarly increased PCAF binding in both H69 cell lines. Our results suggest that in H69 drug-resistant SCLC cell line TSA induces downregulation of ABCB1 expression through a transcriptional mechanism, independently of promoter methylation, and MBD1 or PCAF recruitment

Mise en évidence de l'intégration membranaire de la mitoxantrone à l'échelle de la cellule vivante par spectroscopie Raman SERS et transfert d'énergie de fluorescence

REIMS-BU Santé (514542104) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF

OGM détruits à Colmar : l’incompréhension

Entretien paru dans Savoir(s). Le magazine d’information de l’Unistra Numéro 5En 2005, l’Inra de Colmar lance un programme de recherche pour protéger la vigne de la virose du court-noué. Soixante-dix pieds de vigne avec porte-greffes OGM(2) sont plantés. L’Inra constitue au préalable un comité local de suivi d’une dizaine de personnes – un chercheur, des viticulteurs, des représentants d’Alsace nature, de la Confédération paysanne, d’une association de consommateurs, etc. – pour “co-construire” les conditions d’acceptation de cette expérience. Le 7 septembre 2009, tous les pieds de vigne sont coupés s par un opposant auxOGM. Le 30 septembre, le tribunal administratif de Strasbourg annule l’autorisation de planter des porte-greffes génétiquement modifiés. Des explications sur cette rocambolesque histoire avec Jean Masson, président de l’INRA de Colmar et Michel Breuzard, président d’Alsace nature Haut-Rhin et membre du comité de suivi

Phosphite and thiourea ligand synergy for rhodium catalyzed enantioselective hydroformylation of styrene

International audienc