TY - JOUR
T1 - Inhibitory action of adenosine 3′,5′-monophosphate on phosphatidylinositol turnover
T2 - Difference in tissue response
AU - Kaibuchi, Kozo
AU - Takai, Yoshimi
AU - Ogawa, Yasuhiro
AU - Kimura, Shuji
AU - Nishizuka, Yasutomi
AU - Nakamura, Toshikazu
AU - Tomomura, Akito
AU - Ichihara, Akira
N1 - Funding Information:
*/ This investigation was supported in part by research grants from the Scientific Research Fund of the Ministry of Education, Science and Culture, Japan (1979-1981), the Intractable Diseases Division, Public Health Bureau, the Ministry of Health and Welfare, Japan (1979-1981), a Grant-in-Aid of New Drug Development from the Ministry of Health and Welfare, Japan (1979-1981), and the Yamanouchi Foundation for Research on Metabolic Disorders (1977-1981). §/ To whomc orrespondence should be addressed at the Department of Biochemistry, Kobe University School of Medicine, Kobe 650, Japan. L/ The abbreviations used are: cyclic AMP, adenosine 3',5'-monophosphate; PI, phosphatidylinositol; PHA, phytohemagglutinin; PGEl, prostaglandin El; DBcAMP, dibutyryl cyclic AMP.
PY - 1982/1/15
Y1 - 1982/1/15
N2 - There appear to be considerable differences among tissues in the inhibitory action of adenosine 3′,5′-monophosphate (cyclic AMP) on phosphatidylinositol (PI) turnover induced by various extracellular signals. The present studies were on human peripheral lymphocytes and rat hepatocytes. In the lymphocyte system, cells are activated by phytohemagglutinin that induces PI turnover, and this PI turnover and cellular activation are profoundly blocked by dibutyryl cyclic AMP as well as by prostaglandin E1 which markedly increases cyclic AMP. In contrast, in the hepatocyte system, glycogenolysis is enhanced by α-agonists that induce PI turnover as well as by β-agonists and glucagon that increase cyclic AMP. In these cells the two classes of receptors appear to function independently, and PI turnover is not inhibited by cyclic AMP.
AB - There appear to be considerable differences among tissues in the inhibitory action of adenosine 3′,5′-monophosphate (cyclic AMP) on phosphatidylinositol (PI) turnover induced by various extracellular signals. The present studies were on human peripheral lymphocytes and rat hepatocytes. In the lymphocyte system, cells are activated by phytohemagglutinin that induces PI turnover, and this PI turnover and cellular activation are profoundly blocked by dibutyryl cyclic AMP as well as by prostaglandin E1 which markedly increases cyclic AMP. In contrast, in the hepatocyte system, glycogenolysis is enhanced by α-agonists that induce PI turnover as well as by β-agonists and glucagon that increase cyclic AMP. In these cells the two classes of receptors appear to function independently, and PI turnover is not inhibited by cyclic AMP.
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U2 - 10.1016/0006-291X(82)91946-5
DO - 10.1016/0006-291X(82)91946-5
M3 - Article
C2 - 6280686
AN - SCOPUS:0020074916
VL - 104
SP - 105
EP - 112
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 1
ER -