(Q40437209)

20 September 2017

title

Role of poly(ADP-ribose) polymerase activity in imatinib mesylate-induced cell death (English)

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20 September 2017

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Moehring A

1

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20 September 2017

Wohlbold L

series ordinal

2

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20 September 2017

Aulitzky WE

series ordinal

3

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20 September 2017

van der Kuip H

series ordinal

4

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20 September 2017

publication date

1 June 2005

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Cell Death & Differentiation

20 September 2017

published in

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20 September 2017

volume

12

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20 September 2017

issue

6

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20 September 2017

page(s)

627-636

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https://scigraph.springernature.com/pub.10.1038/sj.cdd.4401608

20 September 2017

exact match

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Imatinib mesylate (STI571) prevents the mutator phenotype of Bcr-Abl in hematopoietic cell lines

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Selective induction of apoptosis in Philadelphia chromosome-positive chronic myelogenous leukemia cells by an inhibitor of BCR–ABL tyrosine kinase, CGP 57148

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A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL-positive human leukemic cells: caspase-independent, necrosis-like programmed cell death mediated by serine protease activity

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Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heart.

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Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.

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The phosphatidylinositol 3-Kinase AKT pathway in human cancer

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7 January 2021

The phosphoinositide 3-kinase pathway

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7 January 2021

Identifiers

DOI

10.1038/SJ.CDD.4401608

1 reference

Dimensions Publication ID

20 September 2017

1028815640

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1 reference