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Titolo:
DEFECTS IN REGULATION OF APOPTOSIS IN CASPASE-2-DEFICIENT MICE
Autore:
BERGERON L; PEREZ GI; MACDONALD G; SHI LF; SUN Y; JURISICOVA A; VARMUZA S; LATHAM KE; FLAWS JA; SALTER JCM; HARA H; MOSKOWITZ MA; LI E; GREENBERG A; TILLY JL; YUAN JY;
Indirizzi:
HARVARD UNIV,SCH MED,DEPT CELL BIOL BOSTON MA 02115 HARVARD UNIV,SCH MED,DEPT CELL BIOL BOSTON MA 02115 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OBSTET & GYNECOL,VINCENT CTR REPROD BIOL BOSTON MA 02114 UNIV MANITOBA,MANITOBA CANC TREATMENT & RES FDN,MANITOBA INST CELL BIOL WINNIPEG MB R3E 0V9 CANADA CHILDRENS HOSP,DEPT NEUROL,DIV NEUROSCI BOSTON MA 02115 UNIV TORONTO,DEPT ZOOL TORONTO ON M5S 3G5 CANADA UNIV TORONTO,DEPT OBSTET & GYNECOL TORONTO ON M5S 3G5 CANADA TEMPLE UNIV,SCH MED,FELS INST CANC RES & MOL BIOL PHILADELPHIA PA 19140 TEMPLE UNIV,SCH MED,DEPT BIOCHEM PHILADELPHIA PA 19140 UNIV MARYLAND,SCH MED,DEPT ANAT BALTIMORE MD 21201 MASSACHUSETTS GEN HOSP,DEPT SURG,NEUROSURG SERV CHARLESTOWN MA 02129 MASSACHUSETTS GEN HOSP,DEPT NEUROL CHARLESTOWN MA 02129 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR CHARLESTOWN MA 02129
Titolo Testata:
Genes & development
fascicolo: 9, volume: 12, anno: 1998,
pagine: 1304 - 1314
SICI:
0890-9369(1998)12:9<1304:DIROAI>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; AMYOTROPHIC-LATERAL-SCLEROSIS; ICE-LIKE PROTEASES; GRANZYME-B; INTERLEUKIN-1-BETA-CONVERTING ENZYME; IL-1-BETA-CONVERTING ENZYME; CONVERTING-ENZYME; INDUCE APOPTOSIS; NEURONAL DEATH; GENE CED-3;
Keywords:
CASPASE-2; ICH1; NEDD2; APOPTOSIS; CASPASES; CELL DEATH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
L. Bergeron et al., "DEFECTS IN REGULATION OF APOPTOSIS IN CASPASE-2-DEFICIENT MICE", Genes & development, 12(9), 1998, pp. 1304-1314

Abstract

During embryonic development, a large number of cells die naturally to shape the new organism. Members of the caspase family of proteases are essential intracellular death effecters. Herein, we generated caspase-2-deficient mice to evaluate the requirement for this enzyme in various paradigms of apoptosis. Excess numbers of germ cells were endowedin ovaries of mutant mice and the oocytes were found to be resistant to cell death following exposure to chemotherapeutic drugs. Apoptosis mediated by granzyme B and perforin was defective in caspase-2-deficient B lymphoblasts. In contrast, cell death of motor neurons during development was accelerated in caspase-2-deficient mice. In addition, caspase-2-deficient sympathetic neurons underwent apoptosis more effectively than wild-type neurons when deprived of NGF. Thus, caspase-2 acts both as a positive and negative cell death effector, depending upon cell lineage and stage of development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:09:50