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Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatallyстатья
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 16 декабря 2014 г.
- Авторы: Varfolomeev E.E., Schuchmann M., Luria V., Chiannilkulchai N., Beckmann J.S., Mett I.L., Rebrikov D., Brodianski V.M., Kemper O.C., Kollet O., Lapidot T., Soffer D., Sobe T., Avraham K.B., Goncharov T., Holtmann H., Lonai P., Wallach D.
- Журнал: Immunity
- Том: 9
- Номер: 2
- Год издания: 1998
- Издательство: Cell Press
- Местоположение издательства: United States
- Первая страница: 267
- Последняя страница: 276
- Аннотация: Homozygous targeted disruption of the mouse Caspase 8 (Casp8) gene was found to be lethal in utero. The Caspase 8 null embryos exhibited impaired heart muscle development and congested accumulation of erythrocytes. Recovery of hematopoietic colony-forming cells from the embryos was very low. In fibroblast strains derived from these embryos, the TNF receptors, Fas/Apo1, and DR3 were able to activate the Jun N-terminal kinase and to trigger IkappaB alpha phosphorylation and degradation. They failed, however, to induce cell death, while doing so effectively in wild-type fibroblasts. These findings indicate that Caspase 8 plays a necessary and nonredundant role in death induction by several receptors of the TNF/NGF family and serves a vital role in embryonal development.
- Добавил в систему: Ребриков Денис Владимирович