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Titolo:
BAX DEFICIENCY PREVENTS THE INCREASED CELL-DEATH OF IMMATURE NEURONS IN BCL-X-DEFICIENT MICE
Autore:
SHINDLER KS; LATHAM CB; ROTH KA;
Indirizzi:
WASHINGTON UNIV,SCH MED,DEPT PATHOL,660 S EUCLID AVE,BOX 8118 ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,DEPT PATHOL ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,DEPT MOL BIOL & PHARMACOL ST LOUIS MO 63110
Titolo Testata:
The Journal of neuroscience
fascicolo: 9, volume: 17, anno: 1997,
pagine: 3112 - 3119
SICI:
0270-6474(1997)17:9<3112:BDPTIC>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYMPATHETIC NEURONS; IN-VIVO; HOMOLOG BAK; SPINAL-CORD; APOPTOSIS; PROTEIN; GENE; SYSTEM; PROTOONCOGENE; EXPRESSION;
Keywords:
APOPTOSIS; PROGRAMMED CELL DEATH; BCL-X; BAX; BCL-2; DEVELOPMENT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
54
Recensione:
Indirizzi per estratti:
Citazione:
K.S. Shindler et al., "BAX DEFICIENCY PREVENTS THE INCREASED CELL-DEATH OF IMMATURE NEURONS IN BCL-X-DEFICIENT MICE", The Journal of neuroscience, 17(9), 1997, pp. 3112-3119

Abstract

The intracellular balance between pro- and antiapoptotic members of the Bcl-2 gene family is thought to regulate cell death. Targeted disruption of bcl-x, a death repressing member, causes massive cell death of immature neurons in the developing mouse CNS, whereas targeted disruption of bax, a pro-apoptotic member, blocks the death of specific populations of sympathetic and motor neurons. In the present study, mice deficient in both Bcl-x(L) and Bar (bcl-x(-/-)/bau(-/-)) are used to examine the relative significance and potential interactions of Bcl-x(L) and Bar during early CNS development. bcl-x(-/-)/ bax(-/-) mice demonstrate greatly reduced levels of apoptosis both in vivo and in vitro compared with the CNS of Bcl-x(L)-deficient mice, as assessed by histology and terminal deoxytransferase-mediated deoxyuridine triphosphate nick end-labeling. Bax-deficient mice, however, contain occasional apoptotic cells in the developing CNS, and cultures of bax-deficient telencephalic cells demonstrate similar levels of apoptosis as wild-type cultures. These results suggest that Bar critically interacts with Bcl-x(L) to regulate survival of immature neurons, but indicate that othercell death regulating proteins, in addition to Bcl-x(L) and Bax, alsofunction during CNS development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 21:04:32