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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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