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Titolo:
G(I-ALPHA-2)-MEDIATED AND G(O-ALPHA)-MEDIATED SIGNALING IN THE PIT-1-DEPENDENT INHIBITION OF THE PROLACTIN GENE PROMOTER - CONTROL OF TRANSCRIPTION BY DOPAMINE D2 RECEPTORS
Autore:
LEW AM; YAO H; ELSHOLTZ HP;
Indirizzi:
UNIV TORONTO,DEPT CLIN BIOCHEM,100 COLL ST TORONTO M5G 1L5 ON CANADA UNIV TORONTO,DEPT CLIN BIOCHEM TORONTO M5G 1L5 ON CANADA UNIV TORONTO,BANTING & BEST DIABET CTR TORONTO M5G 1L5 ON CANADA
Titolo Testata:
The Journal of biological chemistry
fascicolo: 16, volume: 269, anno: 1994,
pagine: 12007 - 12013
SICI:
0021-9258(1994)269:16<12007:GAGSIT>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTERIOR-PITUITARY-CELLS; INOSITOL PHOSPHATE PRODUCTION; CYCLIC-AMP ACCUMULATION; RAT LACTOTROPH CELLS; G-PROTEIN; GROWTH-HORMONE; FACTOR PIT-1; EXPRESSION; BINDING; PHOSPHORYLATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
A.M. Lew et al., "G(I-ALPHA-2)-MEDIATED AND G(O-ALPHA)-MEDIATED SIGNALING IN THE PIT-1-DEPENDENT INHIBITION OF THE PROLACTIN GENE PROMOTER - CONTROL OF TRANSCRIPTION BY DOPAMINE D2 RECEPTORS", The Journal of biological chemistry, 269(16), 1994, pp. 12007-12013

Abstract

Dopaminergic signaling in pituitary lactotrophs is dependent on coupling of D2 receptors to several inhibitory G-protein subtypes, resulting in the activation of multiple signaling pathways. In prolactin-secreting GH4 cells that express cloned D2 receptors, dopamine selectively inhibits the activity of the prolactin gene promoter, a response mediated in part by the pituitary transcription factor Pit-1. Transfected gain-of-function mutants of the G(alpha) subtypes, G(i alpha 2) (Q205L)and G(o alpha) (Q205L), mimic the promoter-specific and Pit-1-dependent inhibition by dopamine. Whereas the activated G(i alpha 2) subtype suppresses cAMP levels, the G(o alpha) mutant does not, demonstrating a cAMP-independent pathway in the inhibition of the prolactin gene. This alternate pathway could involve other regulators, possibly calcium. Interestingly, in Ltk(-) cells in which cloned D2 receptors modestly suppress cAMP,but elevate [Ca2+](i), the activity of the prolactin promoter is enhanced rather than inhibited by dopamine. The response is promoter-specific, dependent on Pit-1, and completely blocked by low concentrations of EGTA, consistent with a calcium-regulated pathway. Last, in GH4 cells, the absence of additivity between G(i alpha 2) and G(o alpha) mutants suggests a convergent mechanism in the reduction of prolactin promoter activity, in which either signaling pathway may be sufficient for maximum inhibition. This apparent redundancy in inhibitory control mechanisms may be of physiological importance for maintaining efficient tonic suppression of prolactin synthesis.

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Documento generato il 21/01/20 alle ore 01:47:21