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001-es BibID:	BIBFORM080522
035-os BibID:	(WOS)000480733000011 (Scopus)85071351221 (PMID)31337666
Első szerző:	Diszházi Gyula (gyógyszerész)
Cím:	Dantrolene Requires Mg2+ and ATP To Inhibit the Ryanodine Receptor / Gyula Diszházi, Zsuzsanna Édua Magyar, János András Mótyán, László Csernoch, István Jóna, Péter Pál Nánási, János Almássy
Dátum:	2019
ISSN:	0026-895X
Megjegyzések:	Dantrolene is a ryanodine receptor (RyR) inhibitor, which is used to relax muscles in malignant hyperthermia syndrome. Although dantrolene binds to the RyR protein, its mechanism of action is unknown, mainly because of the controversial results showing that dantrolene inhibited Ca2+ release from intact fibers and sarcoplasmic reticulum (SR) vesicles, but failed to inhibit single RyR channel currents in bilayers. Accordingly, it was concluded that an important factor for dantrolene's action was lost during the purification procedure of RyR. Recently, Mg2+ was demonstrated to be the essential factor for dantrolene to inhibit Ca2+ release in skinned muscle fibers. The aim of the present study was confirm these results in Ca2+ release and bilayer experiments, using SR vesicles and solubilized channels, respectively. Our Ca2+ release experiments demonstrated that the effect of dantrolene and Mg2+ was cooperative and that ATP enhanced the inhibiting effect of dantrolene. Namely, 10 mu M dantrolene reduced RyR channel open probability by similar to 50% in the presence of 3 mM free Mg2+ and 1 mMATP, whereas channel activity further decreased to similar to 20% of control when [ATP] was increased to 2 mM. Our data provide important complementary information that supports the direct, Mg2+-dependent mechanism of dantrolene's action and suggests that dantrolene also requires ATP to inhibit RyR.
Tárgyszavak:	idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Molecular Pharmacology. - 96 : 3 (2019), p. 401-407. -
További szerzők:	Magyar Zsuzsanna Édua (1993-) (molekuláris biológus) Mótyán János András (1981-) (biokémikus, molekuláris biológus) Csernoch László (1961-) (élettanász) Jóna István (1948-) (élettanász, fizikus) Nánási Péter Pál (1956-) (élettanász) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító)
Pályázati támogatás:	PD112199 OTKA K115397 OTKA GINOP-2.3.2-15-2016-00040 GINOP EFOP-3.6.2-16-2017-00006 EFOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM085619
Első szerző:	Nagy László (molekuláris sejtbiológus, biokémikus)
Cím:	Retinoids potentiate peroxisome proliferator-activated receptor [gamma] action in differentiation, gene expression, and lipid metabolic processes in developing myeloid cells / Szántó Attila, Nagy László
Dátum:	2005
ISSN:	0026-895X
Megjegyzések:	Nuclear hormone receptors have been shown to be important transcription factors for regulating lipid metabolism in myeloid cells and were also implicated in differentiation processes of the myeloid lineage and macrophages. Peroxisome proliferator-activated receptor gamma (PPARgamma) seems to be a key component of lipid uptake by inducing the scavenger receptor CD36 that mediates oxidized low-density lipoprotein uptake in macrophages. Retinoic acid receptors, on the other hand, were also shown to play important roles in myeloid cell differentiation. In this study, we present evidence for a cross-talk between these two nuclear receptor pathways in myeloid cells. We show that expression level of PPARgamma increases with the degree of monocyte/macrophage commitment during maturation. Activation of PPARgamma leads to the increased expression of maturation markers (e.g., CD14, CD36). It is interesting that retinoid treatment potentiates PPARgamma's ability to induce transcription of its target genes. Retinoid-increased PPARgamma response is sufficient for enhancing lipid uptake. Our data, taken together, indicate that the expression level of PPARgamma increases during monocyte/macrophage development. PPARgamma activity can be enhanced by retinoids at least in part via increasing PPARgamma expression level. These observations can be exploited to enhance therapeutically beneficial PPAR responses in myeloid cells.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk RAR DOUBLE MUTANTS PPAR-GAMMA ACID RECEPTORS IN-VITRO TRANSCRIPTIONAL REGULATION HEMATOPOIETIC-CELLS OXIDIZED LDL C/EBP-BETA ALPHA ADIPOGENESIS
Megjelenés:	Molecular Pharmacology. - 67 : 6 (2005), p. 1935-1943. -
További szerzők:	Szántó Attila (1976-) (orvos, biokémikus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM028733
Első szerző:	Szondy Zsuzsanna (molekuláris sejtbiológus, biokémikus)
Cím:	Induction of apoptosis by retinoids and retinoic acid receptor gamma-selective compounds in mouse thymocytes through a novel apoptosis pathway / Zsuzsa Szondy, Uwe Reichert, Jean-Michel Bernardon, Serge Michel, Réka Tóth, Philippe Ancian, Eva Ajzner, Laszlo Fesus
Dátum:	1997
ISSN:	0026-895X
Megjegyzések:	Retinoic acids are morphogenic signaling molecules that are derived from vitamin A and involved in a variety of tissue functions. Two groups of their nuclear receptors have been identified: retinoic acid receptors (RARs) and retinoic acid X receptors (RXRs). All-trans retinoic acid is the high affinity ligand for RARs, and 9-cis retinoic acid also binds to RXRs with high affinity. In cells at high concentrations, all-trans retinoic acid can be converted to 9-cis retinoic acid via unknown mechanisms. It was previously shown that retinoic acids prevents activation-induced death of thymocytes. Here, we report that both all-trans and 9-cis retinoic acid induce apoptosis of mouse thymocytes and purified CD4+CD8+ cells in ex vivo cultures, with 9-cis retinoic acid being 50 times more effective. The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. In vivo administration of an RARgamma analog resulted in thymus involution with the concomitant activation of the apoptosis-related endonuclease and induction of tissue transglutaminase. The RARgamma pathway of apoptosis is RNA and protein synthesis dependent, affects the CD4+CD8+ double positive thymocytes, and can be inhibited by the addition of either Ca2+ chelators or protease inhibitors. Using various RAR- and RXR-specific analogs and antagonists, it was demonstrated that stimulation of RAR alpha inhibits the RARgamma-specific death pathway (which explains the lack of apoptosis stimulatory effects of all-trans retinoic acid at physiological concentrations) and that costimulation of the RXR receptors (in the case of 9-cis retinoic acid) can neutralize this inhibitory effect. It is suggested that formation of 9-cis retinoic acid may be a critical element in regulating both the positive selection and the "default cell death pathway" of thymocytes.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Molecular Pharmacology. - 51 : 6 (1997), p. 972-982. -
További szerzők:	Reichert, Uwe Bernardon, Jean Michel Michel, Serge Révészné Tóth Réka (1969-) (molekuláris biológus, biokémikus) Ancian, Philippe Ajzner Éva (1968-) (laboratóriumi szakorvos) Fésüs László (1947-) (orvos biokémikus)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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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)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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