Effects of growth medium and cyclic AMP analogues on the cAMP-induced differentiation of F9 teratocarcinoma cells

1991 ◽  
Vol 27 (2) ◽  
pp. 158-162 ◽  
Author(s):  
Beth Goldstein ◽  
Helen Kindregan ◽  
Richard M. Niles
Keyword(s):  
Cyclic Amp ◽  
Growth Medium ◽  
Induced Differentiation ◽  
Teratocarcinoma Cells ◽  
F9 Teratocarcinoma

scholarly journals Characterization of motifs which are critical for activity of the cyclic AMP-responsive transcription factor CREB.

1991 ◽  
Vol 11 (3) ◽  
pp. 1306-1312 ◽  
Author(s):  
G A Gonzalez ◽  
P Menzel ◽  
J Leonard ◽  
W H Fischer ◽  
M R Montminy
Keyword(s):  
Transcription Factor ◽  
Cyclic Amp ◽  
Rna Polymerase Ii ◽  
Transcriptional Activation ◽  
Transactivation Domain ◽  
Hormonal Stimulation ◽  
Eukaryotic Genes ◽  
Teratocarcinoma Cells ◽  
A Site ◽  
F9 Teratocarcinoma

Cyclic AMP mediates the hormonal stimulation of a number of eukaryotic genes by directing the protein kinase A (PK-A)-dependent phosphorylation of transcription factor CREB. We have previously determined that although phosphorylation at Ser-133 is critical for induction, this site does not appear to participate directly in transactivation. To test the hypothesis that CREB ultimately activates transcription through domains that are distinct from the PK-A site, we constructed a series of CREB mutants and evaluated them by transient assays in F9 teratocarcinoma cells. Remarkably, a glutamine-rich region near the N terminus appeared to be important for PK-A-mediated induction of CREB since removal of this domain caused a marked reduction in CREB activity. A second region consisting of a short acidic motif (DLSSD) C terminal to the PK-A site also appeared to synergize with the phosphorylation motif to permit transcriptional activation. Biochemical experiments with purified recombinant CREB protein further demonstrate that the transactivation domain is more sensitive to trypsin digestion than are the DNA-binding and dimerization domains, suggesting that the activator region may be structured to permit interactions with other proteins in the RNA polymerase II complex.

Characterization of motifs which are critical for activity of the cyclic AMP-responsive transcription factor CREB

1991 ◽  
Vol 11 (3) ◽  
pp. 1306-1312
Author(s):  
G A Gonzalez ◽  
P Menzel ◽  
J Leonard ◽  
W H Fischer ◽  
M R Montminy
Keyword(s):  
Transcription Factor ◽  
Cyclic Amp ◽  
Rna Polymerase Ii ◽  
Transcriptional Activation ◽  
Transactivation Domain ◽  
Hormonal Stimulation ◽  
Eukaryotic Genes ◽  
Teratocarcinoma Cells ◽  
A Site ◽  
F9 Teratocarcinoma

Cyclic AMP mediates the hormonal stimulation of a number of eukaryotic genes by directing the protein kinase A (PK-A)-dependent phosphorylation of transcription factor CREB. We have previously determined that although phosphorylation at Ser-133 is critical for induction, this site does not appear to participate directly in transactivation. To test the hypothesis that CREB ultimately activates transcription through domains that are distinct from the PK-A site, we constructed a series of CREB mutants and evaluated them by transient assays in F9 teratocarcinoma cells. Remarkably, a glutamine-rich region near the N terminus appeared to be important for PK-A-mediated induction of CREB since removal of this domain caused a marked reduction in CREB activity. A second region consisting of a short acidic motif (DLSSD) C terminal to the PK-A site also appeared to synergize with the phosphorylation motif to permit transcriptional activation. Biochemical experiments with purified recombinant CREB protein further demonstrate that the transactivation domain is more sensitive to trypsin digestion than are the DNA-binding and dimerization domains, suggesting that the activator region may be structured to permit interactions with other proteins in the RNA polymerase II complex.

scholarly journals Analysis of the DNA-binding activities of Myc/Max/Mad network complexes during induced differentiation of U-937 monoblasts and F9 teratocarcinoma cells

Oncogene ◽  
1997 ◽  
Vol 15 (6) ◽  
pp. 737-748 ◽  
Author(s):  
Lars-Gunnar Larsson ◽  
Fuad Bahram ◽  
Hannelore Burkhardt ◽  
Bernhard Lüscher
Keyword(s):  
Dna Binding ◽  
Induced Differentiation ◽  
Teratocarcinoma Cells ◽  
F9 Teratocarcinoma
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