期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 277, 期 5, 页码 3560-3567出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M108410200
关键词
-
资金
- NCI NIH HHS [CA-21765] Funding Source: Medline
Genetic studies in Drosophila and mice have shown that eyes absent (eya) is an important and conserved transcriptional regulator of development. Along with eyeless/Pax6, sine oculis, and dachshund, eya genes function as master regulators in eye development and can induce ectopic eye formation. Furthermore, the loss-of-function mutants of these genes in the fly causes partial or complete loss of the compound eye, and this is associated with inappropriate apoptosis. Conversely, ectopic eyeless expression in the context of eyes absent or sine oculis mutations results in apoptosis, suggesting that the proper ratio of these factors regulates apoptosis. Here we report that enforced expression of fly eya or of one of its mammalian homologs, Eya2, triggers rapid apoptosis in interleukin-3-dependent 32D.3 murine myeloid cells, which express Eya family members but not Pax6. Eya-induced cell death overrides survival factors and has many features typical of apoptosis, including plasma and mitochondrial membrane changes and caspase activation. Eya-induced apoptosis is blocked by Bcl-2 overexpression but not by the broad-spectrum caspase inhibitor z-VAD.fmk, suggesting that mitochondria are a major target in Eya-induced apoptosis. These results support the concept that inappropriate changes in the steady state levels of Eya proteins may trigger programmed cell deaths during development.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据