HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yajima, Y. Articles by Saito, T. Search for Related Content PubMed PubMed Citation Articles by Yajima, Y. Articles by Saito, T. Social Bookmarking                      What's this?

J. Biol. Chem., Vol. 261, Issue 6, 2684-2689, Feb, 1986

Pertussis toxin blocks the inhibitory effects of somatostatin on cAMP- dependent vasoactive intestinal peptide and cAMP-independent thyrotropin releasing hormone-stimulated prolactin secretion of GH3 cells

Y Yajima, Y Akita and T Saito

It was shown that somatostatin (SRIF) inhibited cAMP-dependent vasoactive intestinal peptide (VIP)-stimulated prolactin (PRL) release by a GH3 clonal strain of rat pituitary tumor cells and decreased basal PRL secretion and inhibited PRL release in response to thyrotropin releasing hormone (TRH) whose action was independent of prior synthesis of cAMP. Pretreatment of these cells with pertussis toxin prevented SRIF's inhibitory effects on basal and TRH-stimulated hormone secretion as well as its VIP-stimulated responses. The blockade of SRIF's inhibitory effect on the actions of TRH or VIP was dependent on both the duration of preincubation and concentration of the toxin and was correlated with the ability of the toxin to catalyze the ADP- ribosylation of the 39,000-Da membrane protein. It is likely that this pertussis toxin substrate is involved in signal transduction of SRIF on cAMP-dependent actions of VIP and cAMP-independent action of TRH. However, the mechanism of SRIF's action on TRH is not clear, since SRIF did not affect the intracellular responses by TRH, neither intracellular Ca2+ mobilization nor the increase of 1,2-diacylglycerol formation following the breakdown of polyphosphoinositides.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S. K. Hall and D. L. Armstrong Conditional and Unconditional Inhibition of Calcium-activated Potassium Channels by Reversible Protein Phosphorylation J. Biol. Chem., February 11, 2000; 275(6): 3749 - 3754. [Abstract] [Full Text] [PDF]

				P. Sarret, D. Nouel, C. Dal Farra, J.-P. Vincent, A. Beaudet, and J. Mazella Receptor-mediated Internalization Is Critical for the Inhibition of the Expression of Growth Hormone by Somatostatin in the Pituitary Cell Line AtT-20 J. Biol. Chem., July 2, 1999; 274(27): 19294 - 19300. [Abstract] [Full Text] [PDF]

				Y. Yajima, K. Uchino, H. Ito, and S. Kawashima Mastoparan-Stimulated Prolactin Secretion in Rat Pituitary GH3 Cells Involves Activation of Gq/11 Proteins Endocrinology, May 1, 1997; 138(5): 1949 - 1958. [Abstract] [Full Text] [PDF]