PMID- 10480874
OWN - NLM
STAT- MEDLINE
DCOM- 19991013
LR  - 20220318
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 38
DP  - 1999 Sep 17
TI  - Selective binding of steroid hormone receptors to octamer transcription factors 
      determines transcriptional synergism at the mouse mammary tumor virus promoter.
PG  - 26713-9
AB  - Transcriptional synergism between glucocorticoid receptor (GR) and octamer 
      transcription factors 1 and 2 (Oct-1 and Oct-2) in the induction of mouse mammary 
      tumor virus (MMTV) transcription has been proposed to be mediated through 
      directed recruitment of the octamer factors to their binding sites in the viral 
      long terminal repeat. This recruitment correlates with direct binding between the 
      GR DNA binding domain and the POU domain of the octamer factors. In present 
      study, in vitro experiments identified several nuclear hormone receptors to have 
      the potential to bind to the POU domains of Oct-1 and Oct-2 through their DNA 
      binding domains, suggesting that POU domain binding may be a property shared by 
      many nuclear hormone receptors. However, physiologically relevant binding to the 
      POU domain appeared to be a property restricted to only a few nuclear receptors 
      as only GR, progesterone receptor (PR), and androgen receptor (AR), were found to 
      interact physically and functionally with Oct-1 and Oct-2 in transfected cells. 
      Thus GR, PR, and AR efficiently promoted the recruitment of Oct-2 to adjacent 
      octamer motifs in the cell, whereas mineralocorticoid receptor (MR), estrogen 
      receptor alpha, and retinoid X receptor failed to facilitate octamer factor DNA 
      binding. For MMTV, although GR and MR both induced transcription efficiently, 
      mutation of the promoter proximal octamer motifs strongly decreased GR-induced 
      transcription without affecting the total level of reporter gene activity in 
      response to MR. These results suggest that the configuration of the hormone 
      response element within the MMTV long terminal repeat may promote a dependence 
      for the glucocorticoid response upon the recruitment of octamer transcription 
      factors to their response elements within the viral promoter.
FAU - Prefontaine, G G
AU  - Prefontaine GG
AD  - Graduate Program in Biochemistry, University of Ottawa, Loeb Institute for 
      Medical Research, Ottawa Civic Hospital, Ottawa K1Y 4E9, Ontario, Canada.
FAU - Walther, R
AU  - Walther R
FAU - Giffin, W
AU  - Giffin W
FAU - Lemieux, M E
AU  - Lemieux ME
FAU - Pope, L
AU  - Pope L
FAU - Hache, R J
AU  - Hache RJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (DNA, Viral)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Hcfc1 protein, mouse)
RN  - 0 (Host Cell Factor C1)
RN  - 0 (Octamer Transcription Factor-1)
RN  - 0 (Octamer Transcription Factor-2)
RN  - 0 (Pou2f1 protein, mouse)
RN  - 0 (Pou2f2 protein, mouse)
RN  - 0 (Rara protein, mouse)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Receptors, Mineralocorticoid)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoic Acid Receptor alpha)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - Binding Sites
MH  - DNA, Viral/metabolism
MH  - DNA-Binding Proteins/*metabolism
MH  - Drosophila
MH  - Fibroblasts/metabolism
MH  - Host Cell Factor C1
MH  - Mammary Tumor Virus, Mouse/*genetics
MH  - Mice
MH  - Octamer Transcription Factor-1
MH  - Octamer Transcription Factor-2
MH  - *Promoter Regions, Genetic
MH  - Protein Folding
MH  - Rabbits
MH  - Receptors, Glucocorticoid/*metabolism
MH  - Receptors, Mineralocorticoid/*metabolism
MH  - Receptors, Retinoic Acid/metabolism
MH  - Retinoic Acid Receptor alpha
MH  - Transcription Factors/*metabolism
MH  - *Transcription, Genetic
MH  - Transcriptional Activation
EDAT- 1999/09/10 00:00
MHDA- 1999/09/10 00:01
CRDT- 1999/09/10 00:00
PHST- 1999/09/10 00:00 [pubmed]
PHST- 1999/09/10 00:01 [medline]
PHST- 1999/09/10 00:00 [entrez]
AID - S0021-9258(19)55081-5 [pii]
AID - 10.1074/jbc.274.38.26713 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Sep 17;274(38):26713-9. doi: 10.1074/jbc.274.38.26713.