Disruption of the hexokinase-VDAC complex for tumor therapy (Q46602642)

23 December 2017

title

Disruption of the hexokinase-VDAC complex for tumor therapy (English)

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23 December 2017

1

L Galluzzi

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23 December 2017

O Kepp

2

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Guido Kroemer

object named as

G Kroemer

series ordinal

4

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author name string

N Tajeddine

series ordinal

3

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23 December 2017

language of work or name

English

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publication date

12 May 2008

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23 December 2017

published in

Oncogene

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23 December 2017

volume

27

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23 December 2017

issue

34

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23 December 2017

page(s)

4633-4635

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23 December 2017

https://scigraph.springernature.com/pub.10.1038/onc.2008.114

exact match

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cites work

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Protein kinase Cepsilon interacts with and inhibits the permeability transition pore in cardiac mitochondria

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Complexes between porin, hexokinase, mitochondrial creatine kinase and adenylate translocator display properties of the permeability transition pore. Implication for regulation of permeability transition by the kinases

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Suppression of adenine nucleotide translocase-2 by vector-based siRNA in human breast cancer cells induces apoptosis and inhibits tumor growth in vitro and in vivo

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Caspase-independent cell death

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Chemosensitization by knockdown of adenine nucleotide translocase-2.

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Programmed anuclear cell death delimits platelet life span.

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Akt mediates mitochondrial protection in cardiomyocytes through phosphorylation of mitochondrial hexokinase-II.

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An inhibitor of Bcl-2 family proteins induces regression of solid tumours

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Glucose phosphorylation and mitochondrial binding are required for the protective effects of hexokinases I and II.

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The adenine nucleotide translocator: a target of nitric oxide, peroxynitrite, and 4-hydroxynonenal

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Bid acts on the permeability transition pore complex to induce apoptosis

21 January 2018

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Methyl jasmonate binds to and detaches mitochondria-bound hexokinase

21 January 2018

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Activation of glycogen synthase kinase 3beta disrupts the binding of hexokinase II to mitochondria by phosphorylating voltage-dependent anion channel and potentiates chemotherapy-induced cytotoxicity

31 March 2020

1 reference

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31 March 2020

Identifiers

DOI

10.1038/ONC.2008.114

1 reference

23 December 2017

1 reference

23 December 2017