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Titolo:
ACTIVATION OF MUSCARINIC RECEPTORS INHIBITS APOPTOSIS IN PC12M1 CELLS
Autore:
LINDENBOIM L; PINKASKRAMARSKI R; SOKOLOVSKY M; STEIN R;
Indirizzi:
TEL AVIV UNIV,GEORGE S WISE FAC LIFE SCI,DEPT BIOCHEM IL-69978 RAMAT AVIV ISRAEL TEL AVIV UNIV,GEORGE S WISE FAC LIFE SCI,DEPT BIOCHEM IL-69978 RAMAT AVIV ISRAEL WEIZMANN INST SCI,DEPT CHEM IMMUNOL IL-76100 REHOVOT ISRAEL
Titolo Testata:
Journal of neurochemistry
fascicolo: 6, volume: 64, anno: 1995,
pagine: 2491 - 2499
SICI:
0022-3042(1995)64:6<2491:AOMRIA>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; PHEOCHROMOCYTOMA CELLS; REGULATE SURVIVAL; NEURONAL DEATH; SYSTEM; RAT; NEUROTRANSMITTERS; GANGLION; PROTEIN; CALCIUM;
Keywords:
PROGRAMMED CELL DEATH; MUSCARINIC RECEPTORS; PC12 CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
49
Recensione:
Indirizzi per estratti:
Citazione:
L. Lindenboim et al., "ACTIVATION OF MUSCARINIC RECEPTORS INHIBITS APOPTOSIS IN PC12M1 CELLS", Journal of neurochemistry, 64(6), 1995, pp. 2491-2499

Abstract

Previous studies have shown that PC12 cells depend on growth factors for their survival. When deprived of growth factors, the cells undergoa dying process termed ''apoptosis'' (programed cell death). We show here that muscarinic agonists inhibited the apoptotic death of growth factor-deprived PC12M1 cells (PC12 cells stably expressing cloned m1 muscarinic acetylcholine receptors). This protective effect of the muscarinic agonists was observed in both proliferating and neuronal PC12M1cells, was blocked by the muscarinic antagonist atropine, and was notobserved in PC12 cells lacking m1 receptors. Muscarinic receptors therefore mediate inhibition of apoptosis in these cells. In addition to its effect on survival, the muscarinic agonist oxotremorine induced inhibition of DNA synthesis as well as growth arrest of exponentially growing PC12M1 cells at the S and G(2)/M phases of the cell cycle. Muscarinic receptors in these cells may therefore mediate inhibition of cell cycle progression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 18:26:19