Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injury (Q28509883)

24 January 2017

title

Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injury (English)

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BH3 interacting domain death agonist

24 January 2017

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GOA release 2020-03-11

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BCL2-associated X protein

GOA release 2020-03-11

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GOA release 2020-03-11

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Y. Zhao

1

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24 January 2017

S. Li

2

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24 January 2017

E. E. Childs

3

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24 January 2017

D. K. Kuharsky

4

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24 January 2017

X. M. Yin

5

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24 January 2017

publication date

20 July 2001

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Journal of Biological Chemistry

24 January 2017

language of work or name

English

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published in

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24 January 2017

volume

276

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24 January 2017

issue

29

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24 January 2017

page(s)

27432–27440

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Tumor necrosis factor (TNF).

24 January 2017

cites work

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Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection

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Mice lacking the tumour necrosis factor receptor 1 are resistant to TNF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes

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Detection of circulating tumor necrosis factor after endotoxin administration

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Recombinant human tumor necrosis factor produces hemodynamic changes characteristic of sepsis and endotoxemia

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An endotoxin-induced serum factor that causes necrosis of tumors

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Tumor necrosis factor's cytotoxic activity is signaled by the p55 TNF receptor

21 January 2018

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Molecular mechanisms of tumor necrosis factor-induced cytotoxicity. What we do understand and what we do not.

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RAIDD is a new 'death' adaptor molecule

21 January 2018

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Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways

21 January 2018

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Death Receptors: Signaling and Modulation

21 January 2018

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Caspase activation: the induced-proximity model

21 January 2018

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21 January 2018

Caspases: Enemies Within

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Mitochondria and apoptosis

21 January 2018

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Biochemical pathways of caspase activation during apoptosis

21 January 2018

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21 January 2018

Bcl-2 family proteins

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The Bcl-2 protein family: arbiters of cell survival

21 January 2018

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BCL-2 family members and the mitochondria in apoptosis

21 January 2018

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The mitochondrial permeability transition is required for tumor necrosis factor alpha-mediated apoptosis and cytochrome c release

21 January 2018

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Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death

21 January 2018

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Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis

21 January 2018

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Nitric oxide prevents tumor necrosis factor alpha-induced rat hepatocyte apoptosis by the interruption of mitochondrial apoptotic signaling through S-nitrosylation of caspase-8.

21 January 2018

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Cytochrome c-dependent activation of caspase-3 by tumor necrosis factor requires induction of the mitochondrial permeability transition

21 January 2018

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

21 January 2018

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Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors

21 January 2018

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Bax-deficient mice with lymphoid hyperplasia and male germ cell death

21 January 2018

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BID: a novel BH3 domain-only death agonist

21 January 2018

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Regulated targeting of BAX to mitochondria.

21 January 2018

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

21 January 2018

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Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis

21 January 2018

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Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane

21 January 2018

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Granzyme B-mediated cytochrome c release is regulated by the Bcl-2 family members bid and Bax.

21 January 2018

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Redox regulation of TNF signaling

21 January 2018

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The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol

21 January 2018

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Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity

21 January 2018

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Ion channel activity of the BH3 only Bcl-2 family member, BID.

21 January 2018

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Conformation of the Bax C-terminus regulates subcellular location and cell death

21 January 2018

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Withdrawal of IL-7 induces Bax translocation from cytosol to mitochondria through a rise in intracellular pH.

21 January 2018

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Bax in Murine Thymus Is a Soluble Monomeric Protein That Displays Differential Detergent-induced Conformations

21 January 2018

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

21 January 2018

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p38 MAP kinase mediates bax translocation in nitric oxide-induced apoptosis in neurons

21 January 2018

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Bax directly induces release of cytochrome c from isolated mitochondria

21 January 2018

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Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria

21 January 2018

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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

21 January 2018

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21 January 2018

Identifiers

DOI

10.1074/JBC.M102465200

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