PMID- 20861222
OWN - NLM
STAT- MEDLINE
DCOM- 20110202
LR  - 20211028
IS  - 1944-9917 (Electronic)
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 24
IP  - 11
DP  - 2010 Nov
TI  - Research resource: transcriptome profiling of genes regulated by RXR and its 
      permissive and nonpermissive partners in differentiating monocyte-derived 
      dendritic cells.
PG  - 2218-31
LID - 10.1210/me.2010-0215 [doi]
AB  - Retinoid X receptors (RXRs) are heterodimerization partners for many nuclear 
      receptors and also act as homodimers. Heterodimers formed by RXR and a 
      nonpermissive partner, e.g. retinoic acid receptor (RAR) and vitamin D receptor 
      (VDR), can be activated only by the agonist of the partner receptor. In contrast, 
      heterodimers that contain permissive partners, e.g. liver X receptor (LXR) and 
      peroxisome proliferator-activated receptor (PPAR), can be activated by agonists 
      for either the partner receptor or RXR, raising the possibility of pleiotropic 
      RXR signaling. However, it is not known to what extent the receptor's activation 
      results in triggering mechanisms dependent or independent of permissive 
      heterodimers. In this study, we systematically and quantitatively characterized 
      all probable RXR-signaling pathways in differentiating human monocyte-derived 
      dendritic cells (Mo-DCs). Using pharmacological, microarray and quantitative 
      RT-PCR techniques, we identified and characterized gene sets regulated by RXR 
      agonists (LG100268 and 9-cis retinoic acid) and agonists for LXRs, PPARs, RARalpha, 
      and VDR. Our results demonstrated that permissiveness was partially impaired in 
      Mo-DCs, because a large number of genes regulated by PPAR or LXR agonists was not 
      affected by RXR-specific agonists or was regulated to a lesser extent. As 
      expected, we found that RXR agonists regulated only small portions of RARalpha or VDR 
      targets. Importantly, we could identify and characterize PPAR- and 
      LXR-independent pathways in Mo-DCs most likely mediated by RXR homodimers. These 
      data suggested that RXR signaling in Mo-DCs was mediated via multiple permissive 
      heterodimers and also by mechanism(s) independent of permissive heterodimers, and 
      it was controlled in a cell-type and gene-specific manner.
FAU - Szeles, Lajos
AU  - Szeles L
AD  - Department of Biochemistry and Molecular Biology, Medical and Health Science 
      Center, University of Debrecen, Egyetem Ter 1, H-4010 Debrecen, Hungary.
FAU - Poliska, Szilard
AU  - Poliska S
FAU - Nagy, Gergely
AU  - Nagy G
FAU - Szatmari, Istvan
AU  - Szatmari I
FAU - Szanto, Attila
AU  - Szanto A
FAU - Pap, Attila
AU  - Pap A
FAU - Lindstedt, Malin
AU  - Lindstedt M
FAU - Santegoets, Saskia J A M
AU  - Santegoets SJ
FAU - Ruhl, Ralph
AU  - Ruhl R
FAU - Dezso, Balazs
AU  - Dezso B
FAU - Nagy, Laszlo
AU  - Nagy L
LA  - eng
GR  - WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100922
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Benzoates)
RN  - 0 (FABP4 protein, human)
RN  - 0 (Fatty Acid-Binding Proteins)
RN  - 0 (Ligands)
RN  - 0 (Liver X Receptors)
RN  - 0 (Nicotinic Acids)
RN  - 0 (Orphan Nuclear Receptors)
RN  - 0 (PPAR delta)
RN  - 0 (PPAR gamma)
RN  - 0 (Receptors, Calcitriol)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Tetrahydronaphthalenes)
RN  - 102121-60-8 (Am 580)
RN  - 5688UTC01R (Tretinoin)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
RN  - UVU4X1103P (LG 100268)
SB  - IM
MH  - Benzoates/pharmacology
MH  - Cell Differentiation/drug effects/*genetics
MH  - Cell Line
MH  - Dendritic Cells/*cytology/drug effects/metabolism
MH  - Fatty Acid-Binding Proteins/metabolism
MH  - *Gene Expression Profiling
MH  - *Gene Expression Regulation/drug effects
MH  - Humans
MH  - Ligands
MH  - Liver X Receptors
MH  - Monocytes/*cytology/drug effects/metabolism
MH  - Nicotinic Acids/pharmacology
MH  - Orphan Nuclear Receptors/agonists/metabolism
MH  - PPAR delta/agonists/metabolism
MH  - PPAR gamma/agonists/metabolism
MH  - Phenotype
MH  - Receptors, Calcitriol/agonists/metabolism
MH  - Receptors, Retinoic Acid/agonists/*metabolism
MH  - Signal Transduction/drug effects
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tetrahydronaphthalenes/pharmacology
MH  - Tretinoin/pharmacology
MH  - Up-Regulation/drug effects
PMC - PMC3051201
EDAT- 2010/09/24 06:00
MHDA- 2011/02/03 06:00
PMCR- 2010/11/01
CRDT- 2010/09/24 06:00
PHST- 2010/09/24 06:00 [entrez]
PHST- 2010/09/24 06:00 [pubmed]
PHST- 2011/02/03 06:00 [medline]
PHST- 2010/11/01 00:00 [pmc-release]
AID - me.2010-0215 [pii]
AID - 4736 [pii]
AID - 10.1210/me.2010-0215 [doi]
PST - ppublish
SO  - Mol Endocrinol. 2010 Nov;24(11):2218-31. doi: 10.1210/me.2010-0215. Epub 2010 Sep 
      22.