PMID- 10799572
OWN - NLM
STAT- MEDLINE
DCOM- 20000627
LR  - 20190508
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 74
IP  - 11
DP  - 2000 Jun
TI  - Synergistic action of GA-binding protein and glucocorticoid receptor in 
      transcription from the mouse mammary tumor virus promoter.
PG  - 4988-98
AB  - B lymphocytes are among the first cells to be infected by mouse mammary tumor 
      virus (MMTV), and they play a crucial role in its life cycle. To study 
      transcriptional regulation of MMTV in B cells, we have analyzed two areas of the 
      long terminal repeat (LTR) next to the glucocorticoid receptor binding site, fp1 
      (at position -139 to -146 from the cap site) and fp2 (at -157 to -164). Both 
      showed B-cell-specific protection in DNase I in vitro footprinting assays and 
      contain binding sites for Ets transcription factors, a large family of proteins 
      involved in cell proliferation and differentiation and oncogenic transformation. 
      In gel retardation assays, fp1 and fp2 bound the heterodimeric Ets factor 
      GA-binding protein (GABP) present in B-cell nuclear extracts, which was 
      identified by various criteria: formation of dimers and tetramers, sensitivity to 
      pro-oxidant conditions, inhibition of binding by specific antisera, and 
      comigration of complexes with those formed by recombinant GABP. Mutations which 
      prevented complex formation in vitro abolished glucocorticoid-stimulated 
      transcription from an MMTV LTR linked to a reporter gene in transiently 
      transfected B-cell lines, whereas they did not affect the basal level. 
      Exogenously expressed GABP resulted in an increased level of hormone response of 
      the LTR reporter plasmid and produced a synergistic effect with the coexpressed 
      glucocorticoid receptor, indicating cooperation between the two. This is the 
      first example of GABP cooperation with a steroid receptor, providing the 
      opportunity for studying the integration of their intracellular signaling 
      pathways.
FAU - Aurrekoetxea-Hernandez, K
AU  - Aurrekoetxea-Hernandez K
AD  - Institute of Microbiology, University of Lausanne, CH-1011 Lausanne, Switzerland.
FAU - Buetti, E
AU  - Buetti E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (GA-Binding Protein Transcription Factor)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - B-Lymphocytes/cytology
MH  - Base Sequence
MH  - Binding Sites
MH  - DNA-Binding Proteins/genetics/*metabolism
MH  - GA-Binding Protein Transcription Factor
MH  - *Gene Expression Regulation, Viral
MH  - Lymphoma, B-Cell
MH  - Mammary Tumor Virus, Mouse/*genetics
MH  - Mice
MH  - Molecular Sequence Data
MH  - Mutagenesis
MH  - Nuclear Proteins/metabolism
MH  - *Promoter Regions, Genetic
MH  - Receptors, Glucocorticoid/*metabolism
MH  - Response Elements
MH  - Terminal Repeat Sequences
MH  - Transcription Factors/genetics/*metabolism
MH  - *Transcription, Genetic
MH  - Tumor Cells, Cultured
PMC - PMC110850
EDAT- 2000/05/09 09:00
MHDA- 2000/07/06 11:00
PMCR- 2000/06/01
CRDT- 2000/05/09 09:00
PHST- 2000/05/09 09:00 [pubmed]
PHST- 2000/07/06 11:00 [medline]
PHST- 2000/05/09 09:00 [entrez]
PHST- 2000/06/01 00:00 [pmc-release]
AID - 1401 [pii]
AID - 10.1128/jvi.74.11.4988-4998.2000 [doi]
PST - ppublish
SO  - J Virol. 2000 Jun;74(11):4988-98. doi: 10.1128/jvi.74.11.4988-4998.2000.