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Titolo:
PHOSPHATIDYLINOSITOL 3-KINASE IS A NEGATIVE REGULATOR OF CELLULAR-DIFFERENTIATION
Autore:
PTASZNIK A; BEATTIE GM; MALLY MI; CIRULLI V; LOPEZ A; HAYEK A;
Indirizzi:
UNIV CALIF SAN DIEGO,DEPT PEDIAT,WHITTIER INST DIABET & ENDOCRINOL,SCH MED,9894 GENESEE AVE LA JOLLA CA 92037
Titolo Testata:
The Journal of cell biology
fascicolo: 5, volume: 137, anno: 1997,
pagine: 1127 - 1136
SICI:
0021-9525(1997)137:5<1127:P3IANR>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-FETAL PANCREAS; INSULIN GENE-EXPRESSION; SHC ADAPTER PROTEIN; SIGNALING COMPLEXES; TISSUE-CULTURE; BINDING-SITE; MAP KINASES; CELLS; RECEPTOR; PHOSPHORYLATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
A. Ptasznik et al., "PHOSPHATIDYLINOSITOL 3-KINASE IS A NEGATIVE REGULATOR OF CELLULAR-DIFFERENTIATION", The Journal of cell biology, 137(5), 1997, pp. 1127-1136

Abstract

Phosphatidylinositol 3-kinase (PI3K) has been shown to be an important mediator of intracellular signal transduction in mammalian cells. Weshow here, for the first time, that the blockade of PI3K activity in human fetal undifferentiated cells induced morphological and functional endocrine differentiation. This was associated with an increase in mRNA levels of insulin, glucagon, and somatostatin, as well as an increase-in the insulin protein content and secretion in response to secretagogues. Blockade of PI3K also increased the proportion of pluripotentprecursor cells coexpressing multiple hormones and the total number of terminally differentiated cells originating from these precursor cells. We examined whether any of the recently described modulators of endocrine differentiation could participate in regulating PI3K activity in fetal islet cells. The activity of PI3K was inversely correlated with the hepatocyte growth factor/scatter factor-induced downregulation or nicotinamide-induced upregulation of islet specific gene expression, giving support to the role of PI3K, as a negative regulator of endocrine differentiation. In conclusion, our results provide a mechanism for the regulation of hormone-specific gene expression during human fetal neogenesis. They also suggest a novel function for PI3K, as a negative regulator of cellular differentiation.

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Documento generato il 15/07/20 alle ore 06:49:02