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The Role of Apaf-1 in Programmed Cell Death: From Worm to Tumor (Physiological and Pathological Roles of Cell Death)

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The Role of Apaf-1 in Programmed Cell Death: From Worm to Tumor(Physiological and Pathological Roles of Cell Death)

国立国会図書館請求記号
Z53-V38
国立国会図書館書誌ID
6487134
資料種別
記事
著者
Hiroshi Yoshida
出版者
Kyoto : Japan Society for Cell Biology
出版年
2003-02
資料形態
掲載誌名
Cell Structure and Function 28(1) 2003.2
掲載ページ
p.3~9
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資料種別
記事
著者・編者
Hiroshi Yoshida
著者標目
タイトル(掲載誌)
Cell Structure and Function
巻号年月日等(掲載誌)
28(1) 2003.2
掲載巻
28
掲載号
1
掲載ページ
3~9
掲載年月日(W3CDTF)
2003-02
ISSN(掲載誌)
0386-7196
ISSN-L(掲載誌)
0386-7196
出版事項(掲載誌)
Kyoto : Japan Society for Cell Biology
出版地(国名コード)
JP
本文の言語コード
eng
NDLC
対象利用者
一般
所蔵機関
国立国会図書館
請求記号
Z53-V38
連携機関・データベース
国立国会図書館 : 国立国会図書館雑誌記事索引
書誌ID(NDLBibID)
6487134
整理区分コード
632

デジタル

要約等
Apoptosis or programmed cell death is an important process to eliminate unnecessary or hazardous cells. Apaf-1, a mammalian homologue of CED-4 of <i>C. elegans</i>, is the essential adaptor molecule in the mitochondrial pathway of apoptosis. Mice lacking Apaf-1 show accumulation of neurons in the developing central nervous system due to reduced apoptosis. Apaf-1-deficient cells are remarkably resistant to various apoptotic stimuli. Apaf-1-mediated apoptosis plays a role in the prevention of tumorigenesis. However, Apaf-1-independent cell death pathways are also indicated. In this review, we will summarize what has been learned about the role of Apaf-1 by biochemical and genetical approaches.<br>
DOI
10.1247/csf.28.3
オンライン閲覧公開範囲
インターネット公開
連携機関・データベース
科学技術振興機構 : J-STAGE

デジタル

要約等
Apoptosis or programmed cell death is an important process to eliminate unnecessary or hazardous cells. Apaf-1, a mammalian homologue of CED-4 of <i>C. elegans</i>, is the essential adaptor molecule in the mitochondrial pathway of apoptosis. Mice lacking Apaf-1 show accumulation of neurons in the developing central nervous system due to reduced apoptosis. Apaf-1-deficient cells are remarkably resistant to various apoptotic stimuli. Apaf-1-mediated apoptosis plays a role in the prevention of tumorigenesis. However, Apaf-1-independent cell death pathways are also indicated. In this review, we will summarize what has been learned about the role of Apaf-1 by biochemical and genetical approaches.<br>
オンライン閲覧公開範囲
インターネット公開
参照
Role of cytochrome c and dATP/ATP hydrolysis in Apaf-1-mediated caspase-9 activation and apoptosis
Programmed cell death is a universal feature of embryonic and postnatal neuroproliferative regions throughout the central nervous system
Developmental defects and tumor predisposition in Rb mutant mice
Cytochrome c Deficiency Causes Embryonic Lethality and Attenuates Stress-Induced Apoptosis
The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1β-converting enzyme
The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease.
Cytochrome c activation of CPP32-like proteolysis plays a critical role in a Xenopus cell-free apoptosis system
Caspase-Independent Cell Death and Mitochondrial Disruptions Observed in the Apaf1-Deficient Cells
The fly caspases
An APAF-1·Cytochrome c Multimeric Complex Is a Functional Apoptosome That Activates Procaspase-9
A model for p53-induced apoptosis
Bcl-xL Regulates the Membrane Potential and Volume Homeostasis of Mitochondria
Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome
Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
WD-40 Repeat Region Regulates Apaf-1 Self-association and Procaspase-9 Activation
Defective Cytochrome c-dependent Caspase Activation in Ovarian Cancer Cell Lines due to Diminished or Absent Apoptotic Protease Activating Factor-1 Activity
Adult Apaf-1-Deficient Mice Exhibit Male Infertility
Apaf-1 protein deficiency confers resistance to cytochromec–dependent apoptosis in human leukemic cells
Genetic control of programmed cell death in the nematode C. elegans
Apaf-1 and Caspase-9 in p53-Dependent Apoptosis and Tumor Inhibition
Debcl, a Proapoptotic Bcl-2 Homologue, Is a Component of the <i>Drosophila melanogaster</i> Cell Death Machinery
p53AIP1, a Potential Mediator of p53-Dependent Apoptosis, and Its Regulation by Ser-46-Phosphorylated p53
Apaf1 (CED-4 Homolog) Regulates Programmed Cell Death in Mammalian Development
Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization
Altered Cytochrome c Display Precedes Apoptotic Cell Death in <i>Drosophila </i>
Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c
Essential Role of Voltage-Dependent Anion Channel in Various Forms of Apoptosis in Mammalian Cells
Molecular characterization of mitochondrial apoptosis-inducing factor
Inactivation of the apoptosis effector Apaf-1 in malignant melanoma
Epistatic and independent functions of Caspase-3 and Bcl-X <sub>L</sub> in developmental programmed cell death
Early ontogeny of the secondary proliferative population of the embryonic murine cerebral wall
Widespread programmed cell death in proliferative and postmitotic regions of the fetal cerebral cortex
<i>Apaf-1</i> deficiency and neural tube closure defects are found in <i>fog</i> mice
Interdigital cell death can occur through a necrotic and caspase-independent pathway
Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
Cytochrome c and dATP-mediated Oligomerization of Apaf-1 Is a Prerequisite for Procaspase-9 Activation
Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes
Apoptotic Molecular Machinery: Vastly Increased Complexity in Vertebrates Revealed by Genome Comparisons
The Apoptotic Protease-Activating Factor 1-Mediated Pathway of Apoptosis Is Dispensable for Negative Selection of Thymocytes
Mitochondrial permeability transition in apoptosis and necrosis
Apaf-1, a Human Protein Homologous to C. elegans CED-4, Participates in Cytochrome c–Dependent Activation of Caspase-3
The Fas Death Factor
Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
Differential requirement for Apaf1 and Bcl-XL in the regulation of programmed cell death during development
The cell cycle of the pseudostratified ventricular epithelium of the embryonic murine cerebral wall
Cytochrome c Promotes Caspase-9 Activation by Inducing Nucleotide Binding to Apaf-1
The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis
Apoptotic Protease Activating Factor 1 (Apaf-1)–Independent Cell Death Suppression by Bcl-2
Programmed Cell Death in Animal Development
Apaf1 Is Required for Mitochondrial Pathways of Apoptosis and Brain Development
Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade
Drosophila Pro-apoptotic Bcl-2/Bax Homologue Reveals Evolutionary Conservation of Cell Death Mechanisms
Caenorhabditis elegans gene ced-9 protects cells from programmed cell death
Endonuclease G is an apoptotic DNase when released from mitochondria
Bcl-2 proteins: regulators of apoptosis or of mitochondrial homeostasis?
Differential Requirement for Caspase 9 in Apoptotic Pathways In Vivo
Frameshift mutations in Fas, Apaf-1, and Bcl-10 in gastro-intestinal cancer of the microsatellite mutator phenotype
Reduced Apoptosis and Cytochrome c–Mediated Caspase Activation in Mice Lacking Caspase 9
Autoactivation of Procaspase-9 by Apaf-1-Mediated Oligomerization
Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
Proteases to die for
Regulation of Apoptotic Protease Activating Factor-1 Oligomerization and Apoptosis by the WD-40 Repeat Region
連携機関・データベース
国立情報学研究所 : CiNii Research
提供元機関・データベース
Japan Link Center
雑誌記事索引データベース
Crossref
PubMed
CiNii Articles
CiNii Articles
書誌ID(NDLBibID)
6487134
NII論文ID
130004053827
50000775056