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Titolo:
TROPHIC SUPPORT PROMOTES SURVIVAL OF BCL-X-DEFICIENT TELENCEPHALIC CELLS IN-VITRO
Autore:
SHINDLER KS; YUNKER AMR; CAHN R; ZHA JP; KORSMEYER SJ; ROTH KA;
Indirizzi:
WASHINGTON UNIV,SCH MED,DEPT PATHOL,HOWARD HUGHES MED INST,660 S EUCLID AVE,BOX 8118 ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,DEPT PATHOL,HOWARD HUGHES MED INST ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT MED ST LOUIS MO 63110
Titolo Testata:
Cell death and differentiation
fascicolo: 10, volume: 5, anno: 1998,
pagine: 901 - 910
SICI:
1350-9047(1998)5:10<901:TSPSOB>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-I; CEREBELLAR GRANULE NEURONS; NERVOUS-SYSTEM; SYMPATHETIC NEURONS; GENE-EXPRESSION; POSTMITOTIC NEURONS; PROTEIN EXPRESSION; MURINE DEVELOPMENT; STRIATAL NEURONS; CEREBRAL-CORTEX;
Keywords:
BCL-X; BCL-2; BAX; INSULIN; INSULIN-LIKE GROWTH FACTORS; APOPTOSIS; TELENCEPHALON;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
67
Recensione:
Indirizzi per estratti:
Citazione:
K.S. Shindler et al., "TROPHIC SUPPORT PROMOTES SURVIVAL OF BCL-X-DEFICIENT TELENCEPHALIC CELLS IN-VITRO", Cell death and differentiation, 5(10), 1998, pp. 901-910

Abstract

Survival of immature neurons is regulated by Bcl-x(L), as targeted disruption of bcl-x significantly increases cell death in vivo and in vitro. Death of cultured bcl-x-deficient and wildtype telencephalic cells can be prevented by fetal calf serum or chemically-defined medium (ITS), suggesting trophic factors in these media potentiate survival through a pathway independent of Bcl-x(L), Addition of trophic factors tobasal medium revealed that insulin and insulin-like growth factors (IGFs), but not other trophic factors, reduced apoptosis of wild-type and bcl-x-deficient telencephalic cells. Antibodies raised against IGF-Ireceptors and wortmannin both attenuated the effects of IGF-I, indicating survival was mediated by IGF-I receptors and phosphatidylinositol3'-kinase signaling, whereas effects of ITS were only partially reduced by these agents. The survival promoting effects of ITS were reducedin cells lacking both bcl-x and bcl-2, indicating Bcl-2 plays a supportive role to Bcl-x(L) in maintaining telencephalic cell survival. Furthermore, the ratio of expression of the pro-apoptotic bar gene to theanti-apoptotic bcl-2 gene was reduced in bcl-x-deficient cultures grown in ITS, suggesting that the interaction between these bcl-2 family members may, in part, regulate a Bcl-x(L) independent survival pathway. Finally, the pro-apoptotic bad gene does not appear to play a role in these interactions as targeted disruption of bad did not alter apoptosis in telencephalic cultures.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 09:55:46