41 research outputs found
Commentarii Petri Tatareti in libros philosophie naturalis et metaphysice Aristotelis. Annotatur in marginibus si quando author/ ut plerumque solet/ in hisce commentariis ex Scoto quippiam desumpserit. Venundantur Parisius In vico sancti Johannis lateranensis e regione collegii Cameracensis. Gilles de Gourmont.
No full textAncien possesseur : Percevault, MathurinAncien possesseur : Blazonneau, Constantincollation : [1], ii-xix, xviii (=xx), xxi-xlix, xlii (=l), li-cxviii, [6] f. (sig. A-P8 XX4
PPARalpha inhibits vascular smooth muscle cell proliferation underlying intimal hyperplasia by inducing the tumor suppressor gene p16INK4a
No full textVascular SMC proliferation is a crucial event in occlusive cardiovascular diseases. PPAR alpha is a nuclear receptor controlling lipid metabolism and inflammation, but its role in the regulation of SMC growth remains to be established. Here, we show that PPARa. controls SMC cell-cycle progression at the G(1)/S transition by targeting the cyclin-dependent kinase inhibitor and tumor suppressor p16(INK4a) (p16), resulting in an inhibition of retinoblastoma protein phosphorylation. PPARa activates p16 gene transcription by both binding to a canonical PPAR-response element and interacting with the transcription factor Sp1 at specific proximal Sp1-binding sites of the p16 promoter. In a carotid arterial-injury mouse model, p16 deficiency results in an enhanced SMC proliferation underlying intimal hyperplasia.. Moreover, PPAR alpha activation inhibits SMC growth in vivo, and this effect requires p 16 expression. These results identify an unexpected role for p16 in SMC cell-cycle control and demonstrate that PPARa. inhibits SMC proliferation through p16. Thus, the PPAR alpha/p16 pathway may be a potential pharmacological target for the prevention of cardiovascular occlusive complications of atherosclerosis
Multi-Ion Deposition Modelling: Copper and Zinc Layers Production Application
No full textInternational audienc
Two-Phase Electrolysis Modelling : Two Scales Numerical and Experimental Investigation
No full text218th ECS Meeting - Las Vegas, Nevada, USA - October 10-15 201
Two-Phase Electrolysis Modelling : Two Scales Numerical and Experimental Investigation
No full textInternational audienc
Multi-Ion Deposition Modelling: Copper and Zinc Layers Production Application
No full text218th ECS Meeting - Las Vegas, Nevada, USA - October 10-15 201
Multi-Ion Deposition Modelling: Copper and Zinc Layers Production Application
No full textInternational audienc
Two-Phase Electrolysis Modelling : Two Scales Numerical and Experimental Investigation
No full textInternational audienc
Intrinsic and Extrinsic Connections of Tet3 Dioxygenase with CXXC Zinc Finger Modules.
No full textTet proteins are emerging as major epigenetic modulators of cell fate and plasticity. However, little is known about how Tet proteins are targeted to selected genomic loci in distinct biological contexts. Previously, a CXXC-type zinc finger domain in Tet1 was shown to bind CpG-rich DNA sequences. Interestingly, in human and mouse the Tet2 and Tet3 genes are adjacent to Cxxc4 and Cxxc10-1, respectively. The CXXC domains encoded by these loci, together with those in Tet1 and Cxxc5, identify a distinct homology group within the CXXC domain family. Here we provide evidence for alternative mouse Tet3 transcripts including the Cxxc10-1 sequence (Tet3(CXXC)) and for an interaction between Tet3 and Cxxc4. In vitro Cxxc4 and the isolated CXXC domains of Tet1 and Tet3(CXXC) bind DNA substrates with similar preference towards the modification state of cytosine at a single CpG site. In vivo Tet1 and Tet3 isoforms with and without CXXC domain hydroxylate genomic 5-methylcytosine with similar activity. Relative transcript levels suggest that distinct ratios of Tet3(CXXC) isoforms and Tet3-Cxxc4 complex may be present in adult tissues. Our data suggest that variable association with CXXC modules may contribute to context specific functions of Tet proteins
Glucose regulates the expression of the farnesoid X receptor in liver
No full textAn increased prevalence of hypertriglyceridemia and gallbladder disease occurs in patients with diabetes or insulin resistance. Hypertriglyceridemia is positively associated to gall bladder disease risk. The farnesoid X receptor (FXR) is a bile acid-activated nuclear receptor that plays a key role in bile acid and triglyceride homeostasis. The mechanisms controlling FXR gene expression are poorly understood. This study evaluated whether FXR gene expression is regulated by alterations in glucose homeostasis. FXR expression was decreased in livers of streptozotocin-induced diabetic rats and normalized upon insulin supplementation. Concomitantly with diabetes progression, FXR expression also decreased in aging diabetic Zucker rats. In primary rat hepatocytes, D-glucose increased FXR mRNA in a dose- and time-dependent manner, whereas insulin counteracted this effect. Addition of xylitol, a precursor of xylulose-5-phosphate, to primary rat hepatocytes increased FXR expression to a comparable level as D-glucose. Finally, expression of the FXR target genes, SHP and apolipoprotein C-III, were additively regulated by D-glucose and FXR ligands. This study demonstrates that FXR is decreased in animal models of diabetes. In addition, FXR is regulated by glucose likely via the pentose phosphate pathway. Dysregulation of FXR expression may contribute to alterations in lipid and bile acid metabolism in patients with diabetes or insulin resistance
