How the genome is controlling metabolism and how fatty signaling molecules via nuclear hormone receptors change cell fate and function.
M.D. University of Debrecen, School of Medicine 1991 Ph.D. University of Debrecen 1995
Live-cell fluorescence correlation spectroscopy dissects the role of coregulator exchange and chromatin binding in retinoic acid receptor mobility.
Brazda P, Szekeres T, Bravics B, Tóth K, Vámosi G, Nagy L
J Cell Sci. 2011 Nov 1;124(Pt 21):3631-42
Gene expression profiles in peripheral blood for the diagnosis of autoimmune diseases.
Mesko B, Poliska S, Nagy L
Trends Mol Med. 2011 Apr;17(4):223-33
STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.
Szanto A, Balint BL, Nagy ZS, Barta E, Dezso B, Pap A, Szeles L, Poliska S, Oros M, Evans RM, Barak Y, Schwabe J, Nagy L
Immunity. 2010 Nov 24;33(5):699-712
Research resource: transcriptome profiling of genes regulated by RXR and its permissive and nonpermissive partners in differentiating monocyte-derived dendritic cells.
Széles L, Póliska S, Nagy G, Szatmari I, Szanto A, Pap A, Lindstedt M, Santegoets SJ, Rühl R, Dezsö B, Nagy L
Mol Endocrinol. 2010 Nov;24(11):2218-31
1,25-dihydroxyvitamin D3 is an autonomous regulator of the transcriptional changes leading to a tolerogenic dendritic cell phenotype.
Széles L, Keresztes G, Töröcsik D, Balajthy Z, Krenács L, Póliska S, Steinmeyer A, Zuegel U, Pruenster M, Rot A, Nagy L
J Immunol. 2009 Feb 15;182(4):2074-83
Nuclear receptor signalling in dendritic cells connects lipids, the genome and immune function.
Szatmari I, Nagy L
EMBO J. 2008 Sep 17;27(18):2353-62
PPARgamma regulates the function of human dendritic cells primarily by altering lipid metabolism.
Szatmari I, Töröcsik D, Agostini M, Nagy T, Gurnell M, Barta E, Chatterjee K, Nagy L
Blood. 2007 Nov 1;110(9):3271-80
PPARgamma controls CD1d expression by turning on retinoic acid synthesis in developing human dendritic cells.
Szatmari I, Pap A, Rühl R, Ma JX, Illarionov PA, Besra GS, Rajnavolgyi E, Dezso B, Nagy L
J Exp Med. 2006 Oct 2;203(10):2351-62
Arginine methylation provides epigenetic transcription memory for retinoid-induced differentiation in myeloid cells.
Balint BL, Szanto A, Madi A, Bauer UM, Gabor P, Benko S, Puskás LG, Davies PJ, Nagy L
Mol Cell Biol. 2005 Jul;25(13):5648-63
Activation of PPARgamma specifies a dendritic cell subtype capable of enhanced induction of iNKT cell expansion.
Szatmari I, Gogolak P, Im JS, Dezso B, Rajnavolgyi E, Nagy L
Immunity. 2004 Jul;21(1):95-106
Transcriptional regulation of human CYP27 integrates retinoid, peroxisome proliferator-activated receptor, and liver X receptor signaling in macrophages.
Szanto A, Benko S, Szatmari I, Balint BL, Furtos I, Rühl R, Molnar S, Csiba L, Garuti R, Calandra S, Larsson H, Diczfalusy U, Nagy L
Mol Cell Biol. 2004 Sep;24(18):8154-66
Mechanism of corepressor binding and release from nuclear hormone receptors.
Nagy L, Kao HY, Love JD, Li C, Banayo E, Gooch JT, Krishna V, Chatterjee K, Evans RM, Schwabe JW
Genes Dev. 1999 Dec 15;13(24):3209-16
PPARgamma promotes monocyte/macrophage differentiation and uptake of oxidized LDL.
Tontonoz P, Nagy L, Alvarez JG, Thomazy VA, Evans RM
Cell. 1998 Apr 17;93(2):241-52
Oxidized LDL regulates macrophage gene expression through ligand activation of PPARgamma.
Nagy L, Tontonoz P, Alvarez JG, Chen H, Evans RM
Cell. 1998 Apr 17;93(2):229-40
Nuclear receptor repression mediated by a complex containing SMRT, mSin3A, and histone deacetylase.
Nagy L, Kao HY, Chakravarti D, Lin RJ, Hassig CA, Ayer DE, Schreiber SL, Evans RM
Cell. 1997 May 2;89(3):373-80
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Pro-inflammatory cytokines negatively regulate PPARγ mediated gene expression in both human and murine macrophages via multiple mechanisms.
Nagy ZS, Czimmerer Z, Szanto A, Nagy L
Immunobiology. 2013 Nov;218(11):1336-44
RDH10, RALDH2, and CRABP2 are required components of PPARγ-directed ATRA synthesis and signaling in human dendritic cells.
Gyöngyösi A, Szatmari I, Pap A, Dezso B, Pos Z, Széles L, Varga T, Nagy L
J Lipid Res. 2013 Sep;54(9):2458-74
Laszlo Nagy's Research Focus
Dr. Nagy is a physician by training and a molecular and cell biologist with a long standing research interest in the biology of gene expression regulation, cellular differentiation and their contribution to human diseases. The fundamental question he raises in his research is how lipid signaling regulates gene expression and how a changing extra- and intracellular lipid environment impacts the expression of the genome and contributes to changing cellular phenotypes. He uses the paradigm of nuclear hormone receptor activation/ signaling and the contribution of this process to myeloid cell differentiation, function and to diseases, involving these cells, such as atherosclerosis, tissue regeneration, metabolic and various inflammatory disorders, as his model systems. He uses genome-wide and epigenomic approaches along with bioinformatics and data integration.
About Laszlo Nagy
Dr Nagy is a physician scientist and a cell and molecular biologist. He obtained an M.D. and subsequently a Ph.D. from the University of Debrecen, Hungary. He has carried out two post-doctoral training periods at the UNiversity of Texas-Houston and later at the Salk Institute in San Diego.