PMID- 15591535
OWN - NLM
STAT- MEDLINE
DCOM- 20050831
LR  - 20091119
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 19
IP  - 4
DP  - 2005 Apr
TI  - Protein-protein interactions and transcriptional antagonism between the subfamily 
      of NGFI-B/Nur77 orphan nuclear receptors and glucocorticoid receptor.
PG  - 885-97
AB  - Glucocorticoids (Gc) act through the glucocorticoid receptor (GR) to enhance or 
      repress transcription of glucocorticoid-responsive genes depending on the 
      promoter and cellular context. Repression of proopiomelanocortin (POMC) gene 
      expression by Gc was proposed to use different mechanisms. We described the POMC 
      promoter Nur response element (NurRE) as a target for Gc repression. NGFI-B 
      (Nur77), an orphan nuclear receptor, and two related factors, Nurr1 and NOR1, 
      bind the NurRE as homo- or heterodimers to enhance POMC gene expression in 
      response to CRH. Gc antagonize CRH-stimulated as well as NGFI-B-dependent 
      transcription. We now show that GR antagonizes NurRE-dependent transcription 
      induced by all members of the Nur77 subfamily and that these nuclear receptors 
      can all interact directly with GR. Transcriptional antagonism as well as direct 
      protein-protein interaction between NGFI-B and GR take place primarily via their 
      respective DNA binding domains, although DNA binding itself and the GR 
      homodimerization interface are not involved. In vivo, GR and Nur factors can be 
      coimmunoprecipitated whereas GR is recruited to the POMC promoter upon 
      glucocorticoid action. Thus, our data suggest a mechanism for transrepression 
      between two nuclear receptors, GR and NGFI-B, that is unique, although quite 
      similar to that proposed for transrepression between GR and activator protein 1 
      (AP-1) or nuclear factor-kappaB (NFkappaB).
FAU - Martens, Christine
AU  - Martens C
AD  - Laboratoire de genetique moleculaire, Institut de Recherches Cliniques de 
      Montreal (IRCM), 110, Avenue des Pins Ouest, Montreal, Quebec, Canada H2W 1R7.
FAU - Bilodeau, Steve
AU  - Bilodeau S
FAU - Maira, Mario
AU  - Maira M
FAU - Gauthier, Yves
AU  - Gauthier Y
FAU - Drouin, Jacques
AU  - Drouin J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20041209
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Glucocorticoids)
RN  - 0 (NR4A1 protein, human)
RN  - 0 (Nuclear Receptor Subfamily 4, Group A, Member 1)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Receptors, Steroid)
RN  - 0 (Repressor Proteins)
RN  - 0 (Transcription Factors)
RN  - 66796-54-1 (Pro-Opiomelanocortin)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Cells, Cultured
MH  - DNA-Binding Proteins/*antagonists & inhibitors/metabolism
MH  - *Down-Regulation
MH  - Glucocorticoids/pharmacology
MH  - Humans
MH  - Immunoprecipitation
MH  - Molecular Sequence Data
MH  - Mutation
MH  - Nuclear Receptor Subfamily 4, Group A, Member 1
MH  - Pro-Opiomelanocortin/*genetics
MH  - Promoter Regions, Genetic
MH  - Protein Structure, Tertiary
MH  - Receptors, Cytoplasmic and Nuclear/*antagonists & inhibitors/metabolism
MH  - Receptors, Glucocorticoid/genetics/*metabolism
MH  - Receptors, Steroid/*antagonists & inhibitors/metabolism
MH  - Repressor Proteins/genetics/*metabolism
MH  - Transcription Factors/*antagonists & inhibitors/metabolism
MH  - Transcription, Genetic
EDAT- 2004/12/14 09:00
MHDA- 2005/09/01 09:00
CRDT- 2004/12/14 09:00
PHST- 2004/12/14 09:00 [pubmed]
PHST- 2005/09/01 09:00 [medline]
PHST- 2004/12/14 09:00 [entrez]
AID - me.2004-0333 [pii]
AID - 10.1210/me.2004-0333 [doi]
PST - ppublish
SO  - Mol Endocrinol. 2005 Apr;19(4):885-97. doi: 10.1210/me.2004-0333. Epub 2004 Dec 
      9.