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Addition of choleragen to rat pineal organ cultures caused a long-lasting stimulation of adenylate cyclase activity, and this was followed by increases in seroton N-acetyltransferase and cyclic adenosine monophosphate phosphodiesterase activities. These effects of choleragen were not blocked by the beta-adrenoceptor antagonist propranolol, but the increases in cyclic adenosine monophosphate phosphodiesterase and serotonin N-acetyltransferase activities could be prevented by the protein synthesis inhibitor cycloheximide. The results indicate that cholera toxin can mimic the induction of pineal enzymes that normally follows beta-adrenoceptor activation and suggest that increased cyclic adenosine monophosphate is a necessary and sufficient signal for such changes in enzyme activity.
K P Minneman, and
L L Iversen
January 1963,
Bulletin of the World Health Organization,
K P Minneman, and
L L Iversen
April 1989,
The Journal of biological chemistry,
K P Minneman, and
L L Iversen
June 1982,
Brain research,
K P Minneman, and
L L Iversen
June 1996,
Infection and immunity,
K P Minneman, and
L L Iversen
October 1981,
Biochemical and biophysical research communications,
K P Minneman, and
L L Iversen
June 1982,
In vitro,
K P Minneman, and
L L Iversen
October 1978,
Gastroenterology,
K P Minneman, and
L L Iversen
August 1999,
Molecular cell biology research communications : MCBRC,
K P Minneman, and
L L Iversen
November 2017,
FEBS open bio,
K P Minneman, and
L L Iversen
October 1983,
Biology of reproduction,
