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1.

001-es BibID:BIBFORM077161
Első szerző:Chowdhury, P.
Cím:Bexarotene : a Novel Modulator of AURKA and the Primary Cilium in VHL-deficient Cells / Chowdhury P., Powell R. T., Stephan C., Uray I. P., Talley T., Karki M., Tripathi D. N., Park Y. S., Mancini M. A., Davies P. J. A., Dere R.
Dátum:2018
ISSN:0021-9533
Megjegyzések:Loss of the gene von Hippel?Lindau (VHL) is associated with loss of primary cilia and is causally linked to elevated levels of Aurora kinase A (AURKA). We developed an image-based high-throughput screening (HTS) assay using a dual-labeling image analysis strategy that identifies both the cilium and the basal body. By using this strategy, we screened small-molecule compounds for the targeted rescue of cilia defects associated with VHL deficiency with high accuracy and reproducibility. Bexarotene was identified and validated as a positive regulator of the primary cilium. Importantly, the inability of an alternative retinoid X receptor (RXR) agonist to rescue ciliogenesis, in contrast to bexarotene, suggested that multiple bexarotene-driven mechanisms were responsible for the rescue. We found that bexarotene decreased AURKA expression in VHL-deficient cells, thereby restoring the ability of these cells to ciliate in the absence of VHL. Finally, bexarotene treatment reduced the propensity of subcutaneous lesions to develop into tumors in a mouse xenograft model of renal cell carcinoma (RCC), with a concomitant decrease in activated AURKA, highlighting the potential of bexarotene treatment as an intervention strategy in the clinic to manage renal cystogenesis associated with VHL deficiency and elevated AURKA expression.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Cell Science. - 131 (2018), p. 1-12. -
További szerzők:Powell, R. T. Stephan, C. Uray Iván Péter (1970-) (kutatóorvos) Talley, T. Karki, M. Tripathi, D. N. Park, Y. S. Mancini, Michael A. Davies, Peter J. A. Dere, Ruhee
Pályázati támogatás:GINOP-2.3.2-15-2016-00020
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2.

001-es BibID:BIBFORM061539
Első szerző:Piredda, Lucia
Cím:Lack of 'tissue' transglutaminase protein cross-linking leads to leakage of macromolecules from dying cells : relationship to development of autoimmunity in MRLIpr/Ipr mice / Lucia Piredda, Alessandra Amendola, Vittorio Colizzi, Peter J. A. Davies, Maria Grazia Farrace, Maurizio Fraziano, Vittorio Gentile, Ivan Uray, Mauro Piacentini, Laszlo Fesus
Dátum:1997
ISSN:1350-9047
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cell Death and Differentiation 4 : 6 (1997), p. 463-472. -
További szerzők:Amendola, Alessandra Colizzi, Vittorio Davies, Peter J. A. Farrace, Maria Grazia Fraziano, Maurizio Gentile, Vittorio Uray Iván Péter (1970-) (kutatóorvos) Piacentini, Mauro Fésüs László (1947-) (orvos biokémikus)
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3.

001-es BibID:BIBFORM061542
Első szerző:Razeghi, Peter
Cím:Downregulation of metabolic gene expression in failing human heart before and after mechanical unloading / Razeghi P., Young M. E., Ying J., Depre C., Uray I. P., Kolesar J., Shipley G. L., Moravec C. S., Davies P. J. A., Frazier O. H., Taegtmeyer H.
Dátum:2002
ISSN:0008-6312
Megjegyzések:Background: We have previously shown that several metabolic genes are downregulated in the failing human heart. We now tested the hypothesis that mechanical unloading might reverse this process. Methods: Clinical data and myocardial tissue were collected from 14 failing hearts paired for the time of implantation and explantation of a left ventricular assist device (LVAD) and compared to 10 non-failing hearts. Transcript levels for key regulators of energy metabolism and for atrial natriuretic factor (ANF) were measured by real-time quantitative RT-PCR. Results: The expression of the glucose transporter 1 and 4 (GLUT1, GLUT4), muscle carnitine palmitoyl transferase-1 (mCPT-1), and uncoupling protein 3 (UCP3) were downregulated by up to 80% in the failing heart. Although LVAD treatment improved clinical markers of heart failure (decrease of left ventricular diastolic dimension and normalization of serum sodium), only UCP3 expression reversed to non-failing transcript levels following mechanical unloading. Conclusions: LVAD treatment only partially reverses depressed metabolic gene expression in the failing human heart. Reversal of depressed UCP3 expression may be an important mechanism for reducing the formation of oxygen-derived free radicals. Further studies are necessary to define the effects of mechanical unloading on post-transcriptional mechanisms.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiology. - 97 : 4 (2002), p. 203-209. -
További szerzők:Young, Martin E. Ying, Jun Depre, Christophe Uray Iván Péter (1970-) (kutatóorvos) Kolesar, June Shipley, Gregory L. Moravec, Christine S. Davies, Peter J. A. Frazier, O. Howard Taegtmeyer, Heinrich
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4.

001-es BibID:BIBFORM061543
Első szerző:Szántó Attila (orvos, biokémikus)
Cím:Retinoid X receptors : x-ploring their (patho)physiological functions / A. Szanto, V. Narkar, Q. Shen, I. P. Uray, P. J. A. Davies, L. Nagy
Dátum:2004
ISSN:1350-9047
Megjegyzések:Retinoid X receptor (RXR) belongs to a family of ligandactivated transcription factors that regulate many aspects of metazoan life. A class of nuclear receptors requires RXR as heterodimerization partner for their function. This places RXR in the crossroad of multiple distinct biological pathways. This and the fact that the debate on the endogenous ligand requirement for RXR is not yet settled make RXR still an enigmatic transcription factor. Here, we review some of the biology of RXR. We place RXR into the evolution of nuclear receptors, review structural details and ligands of the receptor. Then processes regulated by RXR are discussed focusing on the developmental roles deduced from studies on knockout animals and metabolic roles in diseases such as diabetes and atherosclerosis deduced from pharmacological studies. Finally, aspects of RXR's involvement in myeloid differentiation and apoptosis are summarized along with issues on RXR's suitability as a therapeutic target.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
nuclear receptor
RXR
transcription
retinoid
rexinoid
Megjelenés:Cell Death And Differentiation. - 11 (2004), p. 126-143. -
További szerzők:Narkar, Vihang Shen, Qiang Uray Iván Péter (1970-) (kutatóorvos) Davies, Peter J. A. Nagy László (1966-) (molekuláris sejtbiológus, biokémikus)
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5.

001-es BibID:BIBFORM061540
Első szerző:Uray Iván Péter (1970-)
Cím:Left ventricular unloading alters receptor tyrosine kinase expression in the failing human heart / Iván P. Uray, John H. Connelly, Vilmos Thomázy, Gregory L. Shipley, William K. Vaughn, O. Howard Frazier, Heinrich Taegtmeyer, Peter J. A. Davies
Dátum:2002
ISSN:1053-2498
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Heart And Lung Transplantation. - 21 : 7 (2002), p. 771-782. -
További szerzők:Connelly, John H. Thomázy Vilmos Shipley, Gregory L. Vaughn, William K. Frazier, O. Howard Taegtmeyer, Heinrich Davies, Peter J. A.
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6.

001-es BibID:BIBFORM061568
Első szerző:Uray Iván Péter (1970-)
Cím:Altered expression of tyrosine kinase receptors Her2/neu and GP130 following left ventricular assist device (LVAD) placement in patients with heart failure / I. P. Uray, J. H. Connelly, O. Frazier, H. Taegtmeyer, P. J. Davies
Dátum:2001
ISSN:1053-2498
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:Journal Of Heart And Lung Transplantation. - 20 : 2 (2001), p. 210. -
További szerzők:Connelly, John H. Frazier, O. Howard Taegtmeyer, Heinrich Davies, Peter J. A.
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7.

001-es BibID:BIBFORM061541
Első szerző:Uray Iván Péter (1970-)
Cím:Mechanical unloading increases caveolin expression in the failing human heart / Ivan P. Uray, John H. Connelly, O. Howard Frazier, Heinrich Taegtmeyer, Peter J. A. Davies
Dátum:2003
ISSN:0008-6363
Megjegyzések:Objective: Implantation of a left ventricular assist device (LVAD) in the failing human heart initiates structural and functional changes termed reverse remodeling. Mechanical unloading improves cardiac adrenergic responsiveness and lipid metabolism, processes regulated by caveolar function. We tested the hypothesis that mechanical unloading alters the expression of caveolins and these changes are linked to altered expression of markers of reverse remodeling. Methods: Paired human myocardial samples were obtained from patients who received an LVAD as a bridge to cardiac transplantation. Transcript levels were measured using real-time Q-RT-PCR in RNA prepared from 34 pairs of formalin-fixed myocardial tissue blocks. Caveolin-1 and -3 protein levels were determined from frozen tissue (n55) by Western blots. Caveolin-3 localization was demonstrated by immunohistochemistry. Results: Caveolin-1 protein levels were upregulated in all LVAD-patients after mechanical unloading (P50.002). Caveolin-1 mRNA was increased in 76% of the patients (n534, P,0.001). Larger induction of caveolin-1 was associated with greater suppression of ANF. Caveolin-3 transcript levels increased in 82% of the cohort, along with a 2.5-fold induction of caveolin-2. Sarcolemmal caveolin-3 staining was increased after LVAD-support, although no change in total caveolin-3 protein was detected. The mRNA levels of the caveolin-associated CD36 also increased with unloading. Patients with ischemic cardiomyopathy showed greater induction of CD36 (P,0.05) than non-ischemic cases, as well as highly correlated changes in the expression of caveolin isoforms. Conclusion: Mechanical unloading induces the expression of caveolins and CD36. The induction of caveolin-1 and the reciprocal suppression of ANF suggest that the changes in the expression of both genes are linked to decreased hemodynamic load. Enhanced caveolin expression during mechanical unloading of failing human hearts may be a part of the reverse remodeling of lipid metabolism, nitric oxide production and adrenergic signaling.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cardiomyopathy
Heart failure
Gene expression
Remodeling
Transplantation
Megjelenés:Cardiovascular Research. - 59 : 1 (2003), p. 57-66. -
További szerzők:Connelly, John H. Frazier, O. Howard Taegtmeyer, Heinrich Davies, Peter J. A.
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8.

001-es BibID:BIBFORM060605
Első szerző:Uray Iván Péter (1970-)
Cím:Pharmacological separation of the expression of tissue transglutaminase and apoptosis after chemotherapeutic treatment of HepG2 cells / Iván P. Uray, Peter J. A. Davies, László Fésüs
Dátum:2001
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular pharmacology. - 59 : 6 (2001), p. 1388-1394. -
További szerzők:Davies, Peter J. A. Fésüs László (1947-) (orvos biokémikus)
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