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Titolo:
CALCIUM CALMODULIN-DEPENDENT PROTEIN-KINASE-II ACTIVATION IN RAT PITUITARY-CELLS IN THE PRESENCE OF THYROTROPIN-RELEASING-HORMONE AND DOPAMINE/
Autore:
CUI ZJ; GORELICK FS; DANNIES PS;
Indirizzi:
YALE UNIV,SCH MED,DEPT PHARMACOL,333 CEDAR ST NEW HAVEN CT 06510 YALE UNIV,SCH MED,DEPT PHARMACOL NEW HAVEN CT 06510 YALE UNIV,SCH MED,DEPT CELL BIOL NEW HAVEN CT 06510
Titolo Testata:
Endocrinology
fascicolo: 5, volume: 134, anno: 1994,
pagine: 2245 - 2250
SICI:
0013-7227(1994)134:5<2245:CCPAIR>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
INOSITOL PHOSPHATE PRODUCTION; RECEPTOR ACTIVATION; PROLACTIN-RELEASE; LACTOTROPH CELLS; AUTOPHOSPHORYLATION; CALCIUM; INHIBITION; ARACHIDONATE; FRAGMENT; CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
31
Recensione:
Indirizzi per estratti:
Citazione:
Z.J. Cui et al., "CALCIUM CALMODULIN-DEPENDENT PROTEIN-KINASE-II ACTIVATION IN RAT PITUITARY-CELLS IN THE PRESENCE OF THYROTROPIN-RELEASING-HORMONE AND DOPAMINE/", Endocrinology, 134(5), 1994, pp. 2245-2250

Abstract

PRL release from rat lactotrophs in response to TRH is Ca2+ dependent. TRH-induced PRL release is inhibited either after repeated pulses ofTRH or in the presence of dopamine. TRH, however, generates increasesin intracellular Ca2+ concentrations (Ca2+(i)) in both conditions. Calcium/calmodulin-dependent protein kinase-II (CaM kinase-II) is a ubiquitous enzyme implicated in secretion. To determine whether down-regulation of CaM kinase-II activity caused the lack of responsiveness toincreases in Ca2+(i), we measured the generation of calcium/calmodulin-independent kinase activity. Anterior pituitary cells contain a 50-kilodalton form of CaM kinase-II, determined by immunoblot, and the enzyme is in lactotrophs, determined by immunocytochemistry. TRH rapidly and transiently increased calcium/calmodulin-independent kinase activity; the increase was maximal by 15 sec and returned to basal by 2 min. When TRH pulses (1 mu M 15 sec) were applied every 10 min, each pulse caused an increase in calcium/ calmodulin-independent kinase activity of similar magnitude, and the activity returned to basal values between pulses. Pretreatment of cells with dopamine (1 mu M; 30 min) inhibited PRL release, but did not prevent the increase in calcium/calmodulin-independent kinase activity. These results indicate that TRH stillactivates CaM kinase-II when PRL release is inhibited. Dopamine and repeated pulses of TRH must inhibit PRL release at a site after the TRH-induced increase in Ca2+(i) and at a site other than CaM kinase-II.

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Documento generato il 17/01/20 alle ore 20:35:53