FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1965482783> ?p ?o ?g. }

• W1965482783 endingPage "42" @default.
• W1965482783 startingPage "31" @default.
• W1965482783 abstract "Modulation of Ca(2+) channels has been shown to alter cellular functions. It can play an important role in the amplification of signals in the endocrine system, including the pleiotropically regulated pituitary lactotropes. Prolactin (PRL) secretion is tonically inhibited by dopamine (DA), the escape from which triggers acute episodes of hormone secretion. The magnitude of these episodes is explained by a potentiation of the PRL-releasing action of secretagogues such as thyrotropin-releasing hormone (TRH). While the mechanisms of this potentiation are not fully understood, it is known to be mimicked by the dihydropyridine, L-type Ca(2+) channel agonist Bay K 8644 and blocked by nifedipine and methoxyverapamil. The potentiation is also blocked by inhibitors of cyclic AMP-dependent protein kinase and protein kinase C. We recently described that the escape from tonic actions of DA results in increased macroscopic Ca(2+) currents in GH(4)C(1) lactotropic clonal cells transfected with a cDNA encoding the long form of the human D(2)-DA receptor. Here we show that the withdrawal from DA potentiates the PRL-releasing action of TRH in GH(4)C(1)/D(2)-DAR cells to the same extent as in enriched lactotropes in primary culture. In both experimental models a low density of dihydropyridine receptors was shown by (+)-[(3)H]PN200-110 binding. Photoaffinity labelling with the dihydropyridine [(3)H]azidopine revealed a protein consistent with the alpha(1) subunit of L-type Ca(2+) channels of 165-170 kDa. In both experimental models, the facilitation of TRH action triggered by the escape from DA was correlated with an enhanced rate of phosphorylation of this putative alpha(1) subunit, the nature of which was further supported by immunoprecipitation with selective antibodies directed against the alpha(1C) and alpha(1D) subunit of voltage-gated calcium channels. We propose that PKA- and PKC-dependent phosphorylation of the alpha(1) subunit of high voltage activated, L-type Ca(2+) channels is responsible for the facilitation of Ca(2+) currents in lactotropes, and hence for the potentiation of secretagogue-mediated PRL secretion. Thus, phosphorylation of Ca(2+) channels in endocrine cells may be a mechanism for the regulation of various functions including amplification of hormone secretion." @default.
• W1965482783 created "2016-06-24" @default.
• W1965482783 creator A5001514418 @default.
• W1965482783 creator A5003722780 @default.
• W1965482783 creator A5009164698 @default.
• W1965482783 creator A5053923166 @default.
• W1965482783 creator A5072360373 @default.
• W1965482783 date "1999-01-01" @default.
• W1965482783 modified "2023-10-18" @default.
• W1965482783 title "Potentiation of Prolactin Secretion following Lactotrope Escape from Dopamine Action" @default.
• W1965482783 cites W1509652229 @default.
• W1965482783 cites W1519616830 @default.
• W1965482783 cites W1554714271 @default.
• W1965482783 cites W1575322130 @default.
• W1965482783 cites W1577600603 @default.
• W1965482783 cites W1578425722 @default.
• W1965482783 cites W1588419581 @default.
• W1965482783 cites W1588914893 @default.
• W1965482783 cites W1608800757 @default.
• W1965482783 cites W1775749144 @default.
• W1965482783 cites W1968124094 @default.
• W1965482783 cites W1974164985 @default.
• W1965482783 cites W1978850926 @default.
• W1965482783 cites W1981061907 @default.
• W1965482783 cites W1981613914 @default.
• W1965482783 cites W1983458197 @default.
• W1965482783 cites W1983649348 @default.
• W1965482783 cites W1995117576 @default.
• W1965482783 cites W1995179761 @default.
• W1965482783 cites W1995245595 @default.
• W1965482783 cites W1997727911 @default.
• W1965482783 cites W1997879352 @default.
• W1965482783 cites W200300496 @default.
• W1965482783 cites W2009667219 @default.
• W1965482783 cites W2009790347 @default.
• W1965482783 cites W2010880470 @default.
• W1965482783 cites W2015996939 @default.
• W1965482783 cites W2019742836 @default.
• W1965482783 cites W2025841456 @default.
• W1965482783 cites W2031246578 @default.
• W1965482783 cites W2042746171 @default.
• W1965482783 cites W2044315058 @default.
• W1965482783 cites W2046638916 @default.
• W1965482783 cites W2047774667 @default.
• W1965482783 cites W2049768827 @default.
• W1965482783 cites W2051789222 @default.
• W1965482783 cites W2053546036 @default.
• W1965482783 cites W2060469754 @default.
• W1965482783 cites W2061056399 @default.
• W1965482783 cites W2062034010 @default.
• W1965482783 cites W2064123037 @default.
• W1965482783 cites W2064918881 @default.
• W1965482783 cites W2068378623 @default.
• W1965482783 cites W2068615144 @default.
• W1965482783 cites W2071013566 @default.
• W1965482783 cites W2071578692 @default.
• W1965482783 cites W2071870771 @default.
• W1965482783 cites W2072422599 @default.
• W1965482783 cites W2073512265 @default.
• W1965482783 cites W2075780481 @default.
• W1965482783 cites W2078440798 @default.
• W1965482783 cites W2078840743 @default.
• W1965482783 cites W2086443820 @default.
• W1965482783 cites W2088342810 @default.
• W1965482783 cites W2088862126 @default.
• W1965482783 cites W2094431803 @default.
• W1965482783 cites W2095523071 @default.
• W1965482783 cites W2117206237 @default.
• W1965482783 cites W2117945992 @default.
• W1965482783 cites W2131649189 @default.
• W1965482783 cites W2135192859 @default.
• W1965482783 cites W2136901642 @default.
• W1965482783 cites W2161841093 @default.
• W1965482783 cites W2161879454 @default.
• W1965482783 cites W2163744984 @default.
• W1965482783 cites W2166217068 @default.
• W1965482783 cites W2166282543 @default.
• W1965482783 cites W2168763159 @default.
• W1965482783 cites W2171851218 @default.
• W1965482783 cites W2341644169 @default.
• W1965482783 cites W2395357588 @default.
• W1965482783 cites W2396010100 @default.
• W1965482783 cites W2396792520 @default.
• W1965482783 cites W2402378341 @default.
• W1965482783 cites W2414433720 @default.
• W1965482783 cites W2468304855 @default.
• W1965482783 cites W2469549338 @default.
• W1965482783 cites W2742499161 @default.
• W1965482783 cites W55686175 @default.
• W1965482783 cites W565916577 @default.
• W1965482783 doi "https://doi.org/10.1159/000054457" @default.
• W1965482783 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10420091" @default.
• W1965482783 hasPublicationYear "1999" @default.
• W1965482783 type Work @default.
• W1965482783 sameAs 1965482783 @default.
• W1965482783 citedByCount "8" @default.
• W1965482783 countsByYear W19654827832017 @default.
• W1965482783 crossrefType "journal-article" @default.

• next