Intersectin-1s Regulates the Mitochondrial Apoptotic Pathway in Endothelial Cells (Q58201468)

2

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Ivana Knezevic

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Irene K. Klein

4

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Asrar B. Malik

Journal of Biological Chemistry

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language of work or name

English

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publication date

3 April 2007

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published in

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volume

282

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issue

23

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page(s)

17166-17178

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cites work

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Intersectin 2, a new multimodular protein involved in clathrin-mediated endocytosis

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Intersectin regulates fission and internalization of caveolae in endothelial cells.

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Two isoforms of a human intersectin (ITSN) protein are produced by brain-specific alternative splicing in a stop codon

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Neuronal distribution of EHSH1/intersectin: molecular linker between clathrin-mediated endocytosis and signaling pathways.

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The human intersectin genes and their spliced variants are differentially expressed

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EHSH1/intersectin, a protein that contains EH and SH3 domains and binds to dynamin and SNAP-25. A protein connection between exocytosis and endocytosis?

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Intersectin can regulate the Ras/MAP kinase pathway independent of its role in endocytosis

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The endocytic protein intersectin is a major binding partner for the Ras exchange factor mSos1 in rat brain

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Intersectin, an adaptor protein involved in clathrin-mediated endocytosis, activates mitogenic signaling pathways

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Dap160/intersectin scaffolds the periactive zone to achieve high-fidelity endocytosis and normal synaptic growth.

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Intersectin activates Ras but stimulates transcription through an independent pathway involving JNK.

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Cdc42 and Ras cooperate to mediate cellular transformation by intersectin-L.

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Endothelial transcytotic machinery involves supramolecular protein-lipid complexes

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Assays for cytochrome c release from mitochondria during apoptosis

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A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis

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Mechanisms of cytochrome c release by proapoptotic BCL-2 family members

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Caspase-mediated loss of mitochondrial function and generation of reactive oxygen species during apoptosis

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Caspase-2 induces apoptosis by releasing proapoptotic proteins from mitochondria

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Requirement for caspase-2 in stress-induced apoptosis before mitochondrial permeabilization

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The permeability transition pore triggers Bax translocation to mitochondria during neuronal apoptosis

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Inhibition of mitochondrial permeability transition prevents mitochondrial dysfunction, cytochrome c release and apoptosis induced by heart ischemia

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Transient and long-lasting openings of the mitochondrial permeability transition pore can be monitored directly in intact cells by changes in mitochondrial calcein fluorescence

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DPP10 is an inactivation modulatory protein of Kv4.3 and Kv1.4.

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JNK suppresses apoptosis via phosphorylation of the proapoptotic Bcl-2 family protein BAD

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Characterization of superoxide-producing sites in isolated brain mitochondria

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Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis

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Movement of Bax from the Cytosol to Mitochondria during Apoptosis

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Mitochondrial membrane permeabilization: the sine qua non for cell death

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Oncogenic tyrosine kinase NPM/ALK induces activation of the MEK/ERK signaling pathway independently of c-Raf.

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BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak

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BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis

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Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c.

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Mechanisms of cytochrome c release from mitochondria

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Multiple pathways of cytochrome c release from mitochondria in apoptosis

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Caspase-2 permeabilizes the outer mitochondrial membrane and disrupts the binding of cytochrome c to anionic phospholipids

21 January 2018

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Mitochondrial cytochrome c release may occur by volume-dependent mechanisms not involving permeability transition

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Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario

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The apoptosome: physiological, developmental, and pathological modes of regulation

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Mitochondrial fission in apoptosis, neurodegeneration and aging

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Mitochondrial fission in apoptosis

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https://api.crossref.org/works/10.1074/JBC.M608996200

Multiple Bcl-2 family members demonstrate selective dimerizations with Bax

21 January 2018

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https://api.crossref.org/works/10.1074/JBC.M608996200

Cytosol-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis

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

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The role of the Bcl-2 family in the regulation of outer mitochondrial membrane permeability

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Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis

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Suppression of survival kinases and activation of JNK mediate ethanol-induced cell death in the developing rat brain

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Granzyme B proteolyzes receptors important to proliferation and survival, tipping the balance toward apoptosis

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Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities

21 January 2018

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