Apaf1 Is Required for Mitochondrial Pathways of Apoptosis and Brain Development

Hiroki Yoshida, Y. K. Kong, +5 authors Tak W Mak
Published 1998 in Cell

Abstract

Apoptosis is essential for the precise regulation of cellular homeostasis and development. The role in vivo of Apaf1, a mammalian homolog of C. elegans CED-4, was investigated in gene-targeted Apaf1-/- mice. Apaf1-deficient mice exhibited reduced apoptosis in the brain and striking craniofacial abnormalities with hyperproliferation of neuronal cells. Apaf1… (More)

DOI: 10.1016/S0092-8674(00)81733-X

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References

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Showing 1-10 of 33 references

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1998

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Apoptosis by Death Factor

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Science
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1998

Apaf1 Is Required for Mitochondrial Pathways of Apoptosis and Brain Development

Abstract

Topics

7 Figures and Tables

Cited By

Coibamide A Induces mTOR-Independent Autophagy and Cell Death in Human Glioblastoma Cells

Cytochrome c Deficiency Causes Embryonic Lethality and Attenuates Stress-Induced Apoptosis

Apaf1 in embryonic development - shaping life by death, and more.

Apoptotic Caspases Prevent the Induction of Type I Interferons by Mitochondrial DNA

Apoptotic Caspases Suppress mtDNA-Induced STING-Mediated Type I IFN Production

Death pathways activated in the neurotrophic factror-deprived neurons

Developing postmitotic mammalian neurons in vivo lacking Apaf-1 undergo programmed cell death by a caspase-independent, nonapoptotic pathway involving autophagy.

Embryonic stem cells assume a primitive neural stem cell fate in the absence of extrinsic influences

Proapoptotic BAX and BAK control multiple initiator caspases.

Apaf-1 and caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation

References

Apaf-1 form a ternary complex

Interaction between the C. elegans cell-death regulators CED-9 and CED-4.

but not negative selection in thymocytes

Cell death during development of the nervous system.

Control of embryonic motoneuron survival in vivo by ciliary neurotrophic factor.

Apoptosis by Death Factor

Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked.

Caspases: key mediators of apoptosis.

Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes.

gans cell death gene ced-3 and the mammalian IL-1 beta-converting P

Slides referencing similar topics

Apaf1 Is Required for Mitochondrial Pathways of Apoptosis and Brain Development

Abstract

Topics

7 Figures and Tables

Cited By

Coibamide A Induces mTOR-Independent Autophagy and Cell Death in Human Glioblastoma Cells

Cytochrome c Deficiency Causes Embryonic Lethality and Attenuates Stress-Induced Apoptosis

Apaf1 in embryonic development - shaping life by death, and more.

Apoptotic Caspases Prevent the Induction of Type I Interferons by Mitochondrial DNA

Apoptotic Caspases Suppress mtDNA-Induced STING-Mediated Type I IFN Production

Death pathways activated in the neurotrophic factror-deprived neurons

Developing postmitotic mammalian neurons in vivo lacking Apaf-1 undergo programmed cell death by a caspase-independent, nonapoptotic pathway involving autophagy.

Embryonic stem cells assume a primitive neural stem cell fate in the absence of extrinsic influences

Proapoptotic BAX and BAK control multiple initiator caspases.

Apaf-1 and caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation

References

Apaf-1 form a ternary complex

Interaction between the C. elegans cell-death regulators CED-9 and CED-4.

but not negative selection in thymocytes

Cell death during development of the nervous system.

Control of embryonic motoneuron survival in vivo by ciliary neurotrophic factor.

Apoptosis by Death Factor

Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked.

Caspases: key mediators of apoptosis.

Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes.

gans cell death gene ced-3 and the mammalian IL-1 beta-converting P

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Slides referencing similar topics