Impact of Mdm2-p53 on the proteasome assembly and disassembly Role of the ubiquitination of some 19S subunits

The ubiquitin proteasome system is a fundamental actor for the proteolysis of cellular proteins. My results demonstrated that the E3 ligase Mdm2 and its substrate p53 might be implied in the formation of the fully-assembled proteasome. Mdm2 promotes also the ubiquitination of some 19S subunits of the proteasome via a non-conventional chain and it is not a signal for self-degradation. Moreover, this ubiqitination seemed to play a role in the formation of the proteasome

Comparative study of super-resolution algorithms

Cet article propose une étude expérimentale comparative entre des algorithmes de super-résolution basés sur une reconstruction régularisée et sur une interpolation non uniforme dans le cas plus général que la translation. Les performances de méthodes à bas coût sont évaluées dans le but de quantifier la perte de qualité des reconstructions SR. Un classement entre les méthodes comparées est établi à partir de résultats expérimentaux réalisés sur des données de synthèse

3-(R)-[3-(2 methoxyphenylthio-2-(S)-methylpropyl] alubi-3,4-dihydro-2H-1,5-benzoxathiepine bromhydrate (F 15845) prevents ischemia-induced heart remodeling by reduction of the intracellular Na+ overload.

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Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning

Ischemic postconditioning (IPOC) could be ineffective or even detrimental if the index ischemic duration is either too short or too long. The present study is to demonstrate that oxygen supply and metabolism defines a salvageable ischemic time window of IPOC in mice. C57BL/6 mice underwent coronary artery occlusion followed by reperfusion (I/R), with or without IPOC by three cycles of 10 s/10 s R/I. In vivo myocardial tissue oxygenation was monitored with electron paramagnetic resonance oximetry. Regional blood flow (RBF) was measured with a laser Doppler monitor. At the end of 60 min reperfusion, tissue from the risk area was collected, and mitochondrial enzyme activities were assayed. Tissue oximetry demonstrated that I/R induced a reperfusion hyperoxygenation state in the 30- and 45-min but not 15- and 60-min ischemia groups. IPOC attenuated the hyperoxygenation with 45 but not 30 min ischemia. RBF, eNOS phosphorylation, and mitochondrial enzyme activities were suppressed after I/R with different ischemic time, and IPOC afforded protection with 30 and 45 but not 60 min ischemia. Infarct size measurement indicated that IPOC reduced infarction with 30 and 45 min but not 60 min ischemia. Clearly, IPOC protected mouse heart with a defined ischemic time window between 30 and 45 min. This salvageable time window was accompanied by the improvement of RBF due to increased phosphorylated eNOS and the preservation of mitochondrial oxygen consumption due to conserved mitochondrial enzyme activities. Interestingly, this salvageable ischemic time window was mirrored by tissue hyperoxygenation status in the postischemic heart

Protease-Activated Receptor-1 Antagonist F 16618 Reduces Arterial Restenosis by Down-Regulation of Tumor Necrosis Factor α and Matrix Metalloproteinase 7 Expression, Migration, and Proliferation of Vascular Smooth Muscle Cells

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