Neurotransmitter Receptors: Mechanisms of Action and by Michio Ui, Toshiaki Katada, Toshihiko Murayama, Hitoshi

By Michio Ui, Toshiaki Katada, Toshihiko Murayama, Hitoshi Kurose (auth.), Shozo Kito M.D., Ph.D., Tomio Segawa Ph.D., Kinya Kuriyama M.D., Henry I. Yamamura Ph.D., Richard W. Olsen Ph.D. (eds.)

This assembly was once held commemorating Dr. Kito's tenth Anniversary as Professor of the 3rd division of inner drugs, Hiroshima collage tuition of drugs. Dr. Kito used to be born in 1927 in Nagoya, graduated from Tokyo college university of medication and got his M. D. in 1951. He spent his first educational years as a learn affiliate (1952 - 1968) on the 3rd division of inner Medi­ cine, Tokyo collage institution of medication. in this interval he studied for twelve months (1952 - 1953) at Illinois college tuition of drugs, and bought his Ph. D. in 1959. In 1968 he turned teacher and in 1971 he was once appointed as Assistant Professor of Tokyo Women's clinical university. In 1973, he grew to become Professor of the 3rd division of inner medication, Hiroshima college college of drugs. Dr. Kito is a clinician yet he's continually keen about simple medication. His significant learn box matters neurotrans­ mitters and their receptors within the valuable worried procedure. He prefers a mixture of neurotransmitter immunohistochemistry and receptor autoradiography as study strategies. he's additionally engaged in biochemical experiences on amyloid proteins. whilst the 8th Inter­ nationwide Congress of Pharmacology was once held in Tokyo in 1981, Dr. Segawa, Dr. Yamamura, and Dr. Kuriyama prepared a satellite tv for pc Symposium on Neurotransmitter Receptors in Hiroshima. Dr. Kito attended this assembly and used to be deeply inspired by way of the lively displays and discussions. for you to make a few contribution to the growth of neuro­ sciences, Dr.

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GTPase IN BIDIRECTIONAL REGULATION OF ADENYLATE CYCLASE 45 45. K. Aktories, G. H. Jakobs, Islet-activating protein prevents nicotinic acid-induced GTPase stimulation and GTP but not GTpyS-induced adenylate cyclase inhibition in rat adipocytes, FEBS Lett. 156:88 (1983). 46. L. L. Hewle~J. Moss, and M. Vaughan, Pertussis toxin inhibits enkephalin stimulation of GTPase of NG108-15 cells, J. BioI. Chem. 258:1435 (1983). 47. K. Aktories, G. H. Jakobs, Adenylate cyclase inhibition and GTPase stimulation by somatostatin in S49 lymphoma cyc- variants are prevented by islet-activating protein, FEBS Lett.

Codina, R. R. Manclark, and L. Birnbaumer, Stimulation and inhibition of adenylyl cyclases mediated by distinct regulatory proteins, Nature 302:706 (1983). 49. H. Jakobs, K. Aktories, and G. Schultz, Mechanism of pertussis toxin action on the adenylate cyclase: Inhibition of the turnon reaction of the inhibitory regulatory site, submitted for publication. SO. M. Ross, T. R. E. Pedersen, Interaction of S-adrenergic receptors and the stimulatory GTP-binding protein of adenylate cyclase in reconstituted vesicles, 15th FEBS Meeting, Brussels, Abstr.

5). The NEM treatment appears to selectively inactivate the magnesium-dependent GTP effect, although the effect of GTP alone is retained. 5 mM) NEM treatment (Fig. 6). 5 mM NEM treatment, an effect of GTP is retained, but this is to decrease the affinity for adenosine, even though this experiment is performed in the presence of magnesium. Thus, it appears that the effect of NEM treatment is to eliminate the effect of magnesium ion. The functional consequence of the loss of the magnesium effect is examined in Table 1.

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