(Q24300914)

negative regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathway

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Caspase 3

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Caspase 12

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Caspase 9

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author name string

Nobuhiro Morishima

1

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Keiko Nakanishi

2

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Hiromi Takenouchi

3

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Takehiko Shibata

4

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Yukuto Yasuhiko

Journal of Biological Chemistry

5

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language of work or name

English

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publication date

13 September 2002

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published in

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volume

277

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issue

37

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page(s)

34287-94

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cites work

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Crystal structure of the cysteine protease interleukin-1 beta-converting enzyme: a (p20/p10)2 homodimer

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In vitro assays for caspase-3 activation and DNA fragmentation

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Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade

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Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3

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Tripartite management of unfolded proteins in the endoplasmic reticulum

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Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9

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Differential requirement for caspase 9 in apoptotic pathways in vivo.

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Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors

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Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

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Calcium signaling in the ER: its role in neuronal plasticity and neurodegenerative disorders

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Autoactivation of procaspase-9 by Apaf-1-mediated oligomerization

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Integration of endoplasmic reticulum signaling in health and disease

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A conserved XIAP-interaction motif in caspase-9 and Smac/DIABLO regulates caspase activity and apoptosis

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Structure and mechanism of interleukin-1 beta converting enzyme

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Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta

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The three-dimensional structure of apopain/CPP32, a key mediator of apoptosis

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Caspase-9 processing by caspase-3 via a feedback amplification loop in vivo

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Inhibition of tumor growth and metastasis of human melanoma by intracellular anti-ATF-1 single chain Fv fragment.

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Apoptotic crosstalk between the endoplasmic reticulum and mitochondria controlled by Bcl-2

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Changes in nuclear morphology during apoptosis correlate with vimentin cleavage by different caspases located either upstream or downstream of Bcl-2 action

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A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis

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CREB and its associated proteins act as survival factors for human melanoma cells

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An APAF-1.cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9

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Cytochrome c and dATP-mediated oligomerization of Apaf-1 is a prerequisite for procaspase-9 activation

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Apaf-1/cytochrome c-independent and Smac-dependent induction of apoptosis in multiple myeloma (MM) cells

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Identification of a caspase-9 substrate and detection of its cleavage in programmed cell death during mouse development

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Coupling endoplasmic reticulum stress to the cell death program. An Apaf-1-independent intrinsic pathway

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Cross-talk between two cysteine protease families. Activation of caspase-12 by calpain in apoptosis

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Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization.

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Two CD95 (APO-1/Fas) signaling pathways

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The Ca2+ concentration of the endoplasmic reticulum is a key determinant of ceramide-induced apoptosis: significance for the molecular mechanism of Bcl-2 action

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Genes Coding for Tumor Antigens Recognized by Cytolytic T Lymphocytes

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Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

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Caspases: enemies within

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Targeting of the c-Abl tyrosine kinase to mitochondria in endoplasmic reticulum stress-induced apoptosis

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7 January 2021

Identifiers

DOI

10.1074/JBC.M204973200

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Consolidated OpenCitations Corpus – April 2017

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Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

12097332

1 reference

Consolidated OpenCitations Corpus – April 2017