PMID- 8806768
OWN - NLM
STAT- MEDLINE
DCOM- 19961029
LR  - 20171116
IS  - 0003-9861 (Print)
IS  - 0003-9861 (Linking)
VI  - 333
IP  - 1
DP  - 1996 Sep 1
TI  - Differential regulation of mouse Ah receptor gene expression in cell lines of 
      different tissue origins.
PG  - 170-8
AB  - The dioxin-binding Ah receptor (AHR) is a ligand-activated transcription factor 
      that regulates the expression of several drug-metabolizing enzymes and has been 
      implicated in immunosuppression, teratogenesis, cell-specific hyperplasia, and 
      certain types of malignancies and toxicities. In order to examine tissue-specific 
      regulation of the mouse Ah receptor gene (Ahr), we studied chimeric deletion 
      constructs, containing the Ahr 5' flanking region and the firefly luciferase 
      reporter gene (Luc). Transient transfection assays were performed in five 
      established mouse cell lines: Hepa-1c1c7 (derived from hepatoma), JB6-C1 41-5a 
      (epidermis), MLE-12 (lung epithelium), F9 (embryonal carcinoma), and NIH/3T3 
      (fibroblasts). Treatment of the cell lines included: dioxin 
      (2,3,7,8-tetrachlorodibenzo-p-dioxin), retinoic acid (RA), cyclic adenosine 
      3':5'-monophosphate (cAMP), or 12-O-tetradecanoylphorbol 13-acetate (TPA). 
      Expression levels of Luc varied widely from one untreated cell line to another, 
      this finding was also confirmed by measurements of AHR mRNA steady-state levels. 
      In all cell lines except F9 cells, maximal constitutive expression was observed 
      with constructs containing 78 bp of Ahr promoter sequences, which include several 
      putative binding sites for the transcription factor Sp1. In contrast, in F9 
      cells, inclusion of sequences between -174 and -78 resulted in a fourfold 
      stimulation of constitutive expression, suggesting that other transcription 
      factors are important in Ahr gene expression in these cells. In MLE-12 and 41-5a 
      cells, expression was significantly decreased by treatment with dioxin, RA, cAMP, 
      or TPA. A similar inhibitory effect was observed in cAMP-treated MLE-12 and F9 
      cells; this result was confirmed by RT-PCR measurements of AHR mRNA steady-state 
      levels. These results indicate that both up- and down-regulation of the Ahr gene 
      occur and exhibit tissue-and cell-type specificity.
FAU - FitzGerald, C T
AU  - FitzGerald CT
AD  - Department of Environmental Health, University of Cincinnati Medical Center, Ohio 
      45267-0056, USA.
FAU - Fernandez-Salguero, P
AU  - Fernandez-Salguero P
FAU - Gonzalez, F J
AU  - Gonzalez FJ
FAU - Nebert, D W
AU  - Nebert DW
FAU - Puga, A
AU  - Puga A
LA  - eng
SI  - GENBANK/U50336
GR  - P30 ES06096/ES/NIEHS NIH HHS/United States
GR  - R01 ES06273/ES/NIEHS NIH HHS/United States
GR  - R01 ES06811/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Arch Biochem Biophys
JT  - Archives of biochemistry and biophysics
JID - 0372430
RN  - 0 (DNA Primers)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - EC 1.13.12.- (Luciferases)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - Base Sequence
MH  - Cell Line
MH  - Chimera/genetics
MH  - Coleoptera/enzymology/genetics
MH  - DNA Primers/genetics
MH  - *Gene Expression Regulation
MH  - Genes, Insect/genetics
MH  - Luciferases/genetics
MH  - Mice
MH  - Molecular Sequence Data
MH  - Promoter Regions, Genetic
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptors, Aryl Hydrocarbon/*genetics
MH  - Tissue Distribution
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
AID - S0003-9861(96)90378-1 [pii]
AID - 10.1006/abbi.1996.0378 [doi]
PST - ppublish
SO  - Arch Biochem Biophys. 1996 Sep 1;333(1):170-8. doi: 10.1006/abbi.1996.0378.