PMID- 7476963
OWN - NLM
STAT- MEDLINE
DCOM- 19951212
LR  - 20220310
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 9
IP  - 7
DP  - 1995 Jul
TI  - Signaling cross-talk between peroxisome proliferator-activated receptor/retinoid 
      X receptor and estrogen receptor through estrogen response elements.
PG  - 794-804
AB  - Peroxisome proliferator-activated receptors (PPARs) and retinoid X receptors 
      (RXRs) are nuclear hormone receptors that are activated by fatty acids and 
      9-cis-retinoic acid, respectively. PPARs and RXRs form heterodimers that activate 
      transcription by binding to PPAR response elements (PPREs) in the promoter of 
      target genes. The PPREs described thus far consist of a direct tandem repeat of 
      the AGGTCA core element with one intervening nucleotide. We show here that the 
      vitellogenin A2 estrogen response element (ERE) can also function as a PPRE and 
      is bound by a PPAR/RXR heterodimer. Although this heterodimer can bind to several 
      other ERE-related palindromic response elements containing AGGTCA half-sites, 
      only the ERE is able to confer transactivation of test reporter plasmids, when 
      the ERE is placed either close to or at a distance from the transcription 
      initiation site. Examination of natural ERE-containing promoters, including the 
      pS2, very-low-density apolipoprotein II and vitellogenin A2 genes, revealed 
      considerable differences in the binding of PPAR/RXR heterodimers to these EREs. 
      In their natural promoter context, these EREs did not allow transcriptional 
      activation by PPARs/RXRs. Analysis of this lack of stimulation of the 
      vitellogenin A2 promoter demonstrated that PPARs/RXRs bind to the ERE but cannot 
      transactivate due to a nonpermissive promoter structure. As a consequence, 
      PPARs/RXRs inhibit transactivation by the estrogen receptor through competition 
      for ERE binding. This is the first example of signaling cross-talk between 
      PPAR/RXR and estrogen receptor.
FAU - Keller, H
AU  - Keller H
AD  - Institut de Biologie animale, Universite de Lausanne, Switzerland.
FAU - Givel, F
AU  - Givel F
FAU - Perroud, M
AU  - Perroud M
FAU - Wahli, W
AU  - Wahli W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Estrogens)
RN  - 0 (Fatty Acids)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Estrogen)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Transcription Factors)
RN  - 0 (Vitellogenins)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Base Sequence
MH  - Chromosome Mapping
MH  - Estrogens/metabolism
MH  - Fatty Acids/metabolism
MH  - HeLa Cells
MH  - Humans
MH  - Molecular Sequence Data
MH  - Promoter Regions, Genetic/genetics
MH  - Receptors, Cytoplasmic and Nuclear/*metabolism
MH  - Receptors, Estrogen/*metabolism
MH  - Receptors, Retinoic Acid/*metabolism
MH  - Retinoid X Receptors
MH  - *Signal Transduction
MH  - Transcription Factors/*metabolism
MH  - *Transcriptional Activation
MH  - Tretinoin/metabolism
MH  - Vitellogenins/genetics/*metabolism
EDAT- 1995/07/01 00:00
MHDA- 1995/07/01 00:01
CRDT- 1995/07/01 00:00
PHST- 1995/07/01 00:00 [pubmed]
PHST- 1995/07/01 00:01 [medline]
PHST- 1995/07/01 00:00 [entrez]
AID - 10.1210/mend.9.7.7476963 [doi]
PST - ppublish
SO  - Mol Endocrinol. 1995 Jul;9(7):794-804. doi: 10.1210/mend.9.7.7476963.