PMID- 1851294
OWN - NLM
STAT- MEDLINE
DCOM- 19910611
LR  - 20190501
IS  - 0305-1048 (Print)
IS  - 1362-4962 (Electronic)
IS  - 0305-1048 (Linking)
VI  - 19
IP  - 7
DP  - 1991 Apr 11
TI  - Cooperation between structural elements in hormono-regulated transcription from 
      the mouse mammary tumor virus promoter.
PG  - 1563-9
AB  - The mouse mammary tumor virus (MMTV) promoter is under the control of several 
      types of regulatory agents. The proximal promoter within the long terminal repeat 
      (LTR), from -200 to the CAP site and its regulation by steroid hormones have been 
      extensively studied. However the precise role of sequences located upstream of 
      this region remain unclear. We have constructed MMTV LTR deletion mutants coupled 
      to the luciferase reporter gene and assayed their activities after transient 
      transfection into transformed mammary epithelial cells (34i) and immortalized 
      fibroblasts (NIH-3T3). In the absence of hormone, the MMTV promoter is almost 
      silent, and deletions in the LTR have no significant effect on basal activity. In 
      the presence of hormone, deletions spanning from the 5'-end to -455 have only 
      slight effects on luciferase levels. In contrast, deletion of the region spanning 
      from -450 to -201 leads to a dramatic decrease in transcription. A substantial 
      decrease, more marked in 34i cells, is also clear when 90bp between -290 and -201 
      are deleted. At least one element cooperating positively with the glucocorticoid 
      response element (GRE) is present between -223 and -201, as supported by the 
      results of substitution mutation experiments. In 34i cell line, dexamethasone 
      stimulates the MMTV LTR transcriptional activity to a level comparable to that of 
      SV40. In contrast, in NIH-3T3 cells, MMTV promoter inducibility is weak. This 
      results from a glucocorticoid receptor content 10-fold lower in NIH-3T3 cells 
      than in 34i cells. Transfection of a glucocorticoid receptor expression plasmid 
      allows recovery of a high inducibility of the MMTV promoter. This was true with 
      all the MMTV LTR mutants studied here and suggests that NIH-3T3 cells possess all 
      the factors necessary to cooperate with the steroid hormone in order to achieve a 
      high transcriptional activity.
FAU - Gouilleux, F
AU  - Gouilleux F
AD  - Unite de recherches sur les communications hormonales, INSERM U-33, Hopital du 
      Kremlin Bicetre, France.
FAU - Sola, B
AU  - Sola B
FAU - Couette, B
AU  - Couette B
FAU - Richard-Foy, H
AU  - Richard-Foy H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Nucleic Acids Res
JT  - Nucleic acids research
JID - 0411011
RN  - 0 (Receptors, Glucocorticoid)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - EC 1.13.12.- (Luciferases)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Cell Line
MH  - Dexamethasone/*pharmacology
MH  - Luciferases/genetics
MH  - Mammary Tumor Virus, Mouse/*genetics
MH  - Mice
MH  - Molecular Sequence Data
MH  - Mutation
MH  - Plasmids
MH  - *Promoter Regions, Genetic
MH  - Receptors, Glucocorticoid/genetics
MH  - Regulatory Sequences, Nucleic Acid
MH  - *Transcription, Genetic
MH  - Transfection
MH  - Tumor Cells, Cultured
PMC - PMC333916
EDAT- 1991/04/11 00:00
MHDA- 1991/04/11 00:01
CRDT- 1991/04/11 00:00
PHST- 1991/04/11 00:00 [pubmed]
PHST- 1991/04/11 00:01 [medline]
PHST- 1991/04/11 00:00 [entrez]
AID - 10.1093/nar/19.7.1563 [doi]
PST - ppublish
SO  - Nucleic Acids Res. 1991 Apr 11;19(7):1563-9. doi: 10.1093/nar/19.7.1563.