Találati lista | Tudóstér

001-es BibID:	BIBFORM057165
Első szerző:	Kiss Beáta (biokémikus, molekuláris biológus)
Cím:	Retinoids induce Nur77-dependent apoptosis in mouse thymocytes / Beáta Kiss, Katalin Tóth, Zsolt Sarang, Éva Garabuczi, Zsuzsa Szondy
Dátum:	2015
ISSN:	0167-4889
Megjegyzések:	Nur77 is a transcription factor, which plays a determinant role in mediating T cell receptor-induced cell death of thymocytes. In addition to regulation of transcription, Nur77 contributes to apoptosis induction by targeting mitochondria, where it can convert Bcl-2, an anti-apoptotic protein into a proapoptotic molecule. Previous studies have demonstrated that retinoids are actively produced in the mouse thymus and can induce a transcription-dependent apoptosis in mouse thymocytes. Here we show that retinoic acids induce the expression of Nur77, and retinoid-induced apoptosis is completely dependent on Nur77, as retinoids were unable to induce apoptosis in Nur77 null thymocytes. In wild-type thymocytes retinoids induced enhanced expression of the apoptosis-related genes FasL, TRAIL, NDG-1, Gpr65 and Bid, all of them in a Nur77-dependent manner. The combined action of these proteins led to Caspase 8-dependent Bid cleavage in the mitochondria. In addition, we could demonstrate the Nur77-dependent induction of STAT1 leading to enhanced Bim expression, and the mitochondrial translocation of Nur77 leading to the exposure of the Bcl-2/BH3 domain. The retinoid-induced apoptosis was dependent on both Caspase 8 and STAT1. Our data together indicate that retinoids induce a Nur77-dependent cell death program in thymocytes activating the mitochondrial pathway of apoptosis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Apoptosis Nur77 Retinoid Thymocyte PPAR UCP2
Megjelenés:	Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. - 1853 : 3 (2015), p. 660-670. -
További szerzők:	Tóth Katalin Ágnes (1977-) (biokémikus, molekuláris biológus) Sarang Zsolt (1976-) (mikrobiológus) Garabuczi Éva (1982-) (biokémikus, molekuláris biológus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM037168
Első szerző:	Kiss Beáta (biokémikus, molekuláris biológus)
Cím:	Retinoids Induce A Nur77-Dependent Apoptosis In Mouse Thymocytes / Beata Kiss, Katalin Tóth, Zsolt Sarang, Éva Garabuczi, László Fésüs, Zsuzsa Szondy
Dátum:	2012
Megjegyzések:	Nur77 is a transcription factor, which plays a determinant role in mediating T cell receptor-induced cell death of thymocytes. In addition to regulation of transcription, Nur77 contributes to apoptosis induction by targeting mitochondria, where it can convert Bcl-2, an anti-apoptotic protein into a proapoptotic molecule. Previous studies have demonstrated that retinoids are actively produced in the mouse thymus and can induce a transcription-dependent apoptosis in mouse thymocytes. Here we show that similar to TCR stimulation, retinoic acids also induce the expression of Nur77 in a dose-dependent manner, 9-cis retinoic acid being more effective than all-trans retinoic acid. Retinoid-induced apoptosis was found to be completely dependent on Nur77, as retinoids were unable to induce apoptosis in Nur77 null thymocytes. In wild-type thymocytes retinoids induced the expression of five apoptosis-related genes, FasL, TRAIL, NDG-1, Gpr65 and Bid, all of them in a Nur77-dependent manner. The combined action of these proteins led to Caspase 8-dependent Bid cleavage in the mitochondria. In addition, we could demonstrate the mitochondrial translocation of Nur77 leading to the exposure of the Bcl-2/BH3 domain. The retinoid-induced apoptosis was dependent on both Caspase 8 and 9. Our data together indicate that retinoids induce a Nur77-dependent cell death program in thymocytes activating the mitochondrial pathway of apoptosis.
ISBN:	978-953-95551-4-4
Tárgyszavak:	Természettudományok Biológiai tudományok előadáskivonat Retinoids Nur77
Megjelenés:	FEBS3 + Meeting From molecules to life and back, Book of abstracts / eds. Jerka Dumic, Zrinka Kovarik, Jadranka Varljen. - p. 111. -
További szerzők:	Tóth Katalin Ágnes (1977-) (biokémikus, molekuláris biológus) Sarang Zsolt (1976-) (mikrobiológus) Garabuczi Éva (1982-) (biokémikus, molekuláris biológus) Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Pályázati támogatás:	TÁMOP-4.2.2/B-10/1-2010-0024 TÁMOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM054135
Első szerző:	Sarang Zsolt (mikrobiológus)
Cím:	Macrophages engulfing apoptotic thymocytes produce retinoids to promote selection, differentiation, removal and replacement of double positive thymocytes / Zsolt Sarang, Éva Garabuczi, Gergely Joós, Beáta Kiss, Katalin Tóth, Ralph Rühl, Zsuzsa Szondy
Dátum:	2013
ISSN:	0171-2985
Megjegyzések:	The thymus provides the microenvironment in which thymocytes develop into mature T-cells, and interactions with thymic stromal cells are thought to provide the necessary signals for thymocyte maturation. Recognition of self-MHC by T-cells is a basic requirement for mature T-cell functions, and those thymocytes that do not recognize or respond too strongly to the peptide-loaded self-MHC molecules found in the thymus undergo apoptosis. As a result, 95% of the thymocytes produced will die and be subsequently cleared by macrophages. This review describes a complex crosstalk between developing thymocytes and engulfing macrophages which is mediated by retinoids produced by engulfing macrophages. The interaction results in the harmonization of the rate of cell death of dying double positive cells with their clearance and replacement, and in promotion of the differentiation of the selected cells in the thymus.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Immunobiology. - 218 : 11 (2013), p. 1354-1360. -
További szerzők:	Garabuczi Éva (1982-) (biokémikus, molekuláris biológus) Joós Gergely Kiss Beáta (1984-) (biokémikus, molekuláris biológus) Tóth Katalin Ágnes (1977-) (biokémikus, molekuláris biológus) Rühl, Ralph (1969-) (vegyész) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM013470
Első szerző:	Tóth Katalin Ágnes (biokémikus, molekuláris biológus)
Cím:	Retinoids enhance glucocorticoid-induced apoptosis of T cells by facilitating glucocorticoid receptor-mediated transcription / K. Tóth, Z. Sarang, B. Scholtz, P. Brázda, N. Ghyselinck, P. Chambon, L. Fésüs, Z. Szondy
Dátum:	2011
ISSN:	1350-9047
Megjegyzések:	Glucocorticoid-induced apoptosis of thymocytes is one of the first recognized forms of programmed cell death. It was shown to require gene activation induced by the glucocorticoid receptor (GR) translocated into the nucleus following ligand binding. In addition, the necessity of the glucocorticoid-induced, but transcription-independent phosphorylation of phosphatidylinositol-specific phospholipase C (PI-PLC) has also been shown. Here we report that retinoic acids, physiological ligands for the nuclear retinoid receptors, enhance glucocorticoid-induced death of mouse thymocytes both in vitro and in vivo. The effect is mediated by retinoic acid receptor (RAR) alpha/retinoid X receptor (RXR) heterodimers, and occurs when both RAR? and RXR are ligated by retinoic acids. We show that the ligated RAR?/RXR interacts with the ligated GR, resulting in an enhanced transcriptional activity of the GR. The mechanism through which this interaction promotes GR-mediated transcription does not require DNA binding of the retinoid receptors and does not alter the phosphorylation status of Ser232, known to regulate the transcriptional activity of GR. Phosphorylation of PI-PLC was not affected. Besides thymocytes, retinoids also promoted glucocorticoid-induced apoptosis of various T-cell lines, suggesting that they could be used in the therapy of glucocorticoid-sensitive T-cell malignancies.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk apoptosis glucocorticoid retinoid T cells Molekuláris Medicina
Megjelenés:	Cell Death and Differentiation. - 18 : 5 (2011), p. 783-792. -
További szerzők:	Sarang Zsolt (1976-) (mikrobiológus) Scholtz Beáta (1967-) (biokémikus, molekuláris biológus) Brázda Péter (1980-) (biológus, angol-magyar szakfordító) Ghyselinck, N. Chambon, P. Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Pályázati támogatás:	T 049445 OTKA K 77587 OTKA NI 67877 OTKA TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Az apoptózis és a fagocitózis folyamatának összehangolása a szövetet tönkretevő gyulladási reakciók elkerülésére
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: