PMID- 10644740
OWN - NLM
STAT- MEDLINE
DCOM- 20000229
LR  - 20190508
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 275
IP  - 4
DP  - 2000 Jan 28
TI  - Nuclear orphan receptors regulate transcription of the gene for the human
      luteinizing hormone receptor.
PG  - 2763-70
AB  - An imperfect estrogen receptor half-site response element direct-repeat, located 
      within the TATA-less promoter of the human luteinizing hormone receptor (hLHR),
      was identified as an inhibitory site for Sp1/Sp3-driven basal transcription.
      Isolation of proteins recognizing this site by yeast one-hybrid screening of a
      human placenta cDNA library revealed three nuclear orphan receptors, EAR2,
      EAR3/COUP-TFI, and TR4. Electrophoresis mobility shift assays demonstrated that
      the in vitro translated nuclear orphan receptors specifically bound the
      direct-repeat motif of the hLHR promoter. Also, endogenous EAR2 and EAR3/COUP-TFI
      from JAR cell and human testis and TR4 from testes bound this motif in
      electrophoresis mobility shift assays. Functional analyses in CV-1 cells showed
      that EAR2 and EAR3/COUP-TFI repressed the hLHR promoter activity by up to 70% in 
      a dose-dependent and sequence-specific manner. Conversely, TR4 activated the hLHR
      promoter activity up to 2.5-fold through binding to the same cis-element. The
      stimulation was reversed by coexpression of EAR2 or EAR3/COUP-TFI, indicating
      their competitive binding for this site. Such recognition of a common cognate
      site by the proteins with antagonistic functions implies that a net regulation of
      the hLHR gene may result from the relative availability of repressors and
      activator in a physiological state. This also may contribute to the differential 
      expression of the hLHR gene in gonadal and non-gonadal tissues.
FAU - Zhang, Y
AU  - Zhang Y
AD  - Section on Molecular Endocrinology, NICHD, National Institutes of Health,
      Bethesda, Maryland 20892, USA.
FAU - Dufau, M L
AU  - Dufau ML
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (COUP Transcription Factor I)
RN  - 0 (DNA, Complementary)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (NR2C2 protein, human)
RN  - 0 (NR2F1 protein, human)
RN  - 0 (NR2F6 protein, human)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Nr2f6 protein, rat)
RN  - 0 (Receptors, LH)
RN  - 0 (Receptors, Steroid)
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Base Sequence
MH  - COUP Transcription Factor I
MH  - Cell Line
MH  - DNA, Complementary
MH  - DNA-Binding Proteins/*physiology
MH  - Humans
MH  - Molecular Sequence Data
MH  - Nerve Tissue Proteins/*physiology
MH  - Promoter Regions, Genetic
MH  - Receptors, LH/*genetics
MH  - Receptors, Steroid/*physiology
MH  - *Receptors, Thyroid Hormone
MH  - Transcription Factors/*physiology
MH  - Transcription, Genetic/*physiology
EDAT- 2000/01/25 09:00
MHDA- 2000/03/04 09:00
CRDT- 2000/01/25 09:00
PHST- 2000/01/25 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/01/25 09:00 [entrez]
AID - 10.1074/jbc.275.4.2763 [doi]
PST - ppublish
SO  - J Biol Chem. 2000 Jan 28;275(4):2763-70. doi: 10.1074/jbc.275.4.2763.