Arsenic trioxide-induced neuroblastoma cell death is accompanied by proteolytic activation of nuclear Bax. (Q40150435)

17 September 2017

Arsenic trioxide-induced neuroblastoma cell death is accompanied by proteolytic activation of nuclear Bax. (English)

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17 September 2017

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17 September 2017

Karlsson J

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17 September 2017

Beckman S

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17 September 2017

Pettersson HM

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17 September 2017

Larsson C

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17 September 2017

Påhlman S

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17 September 2017

language of work or name

English

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publication date

2 April 2007

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17 September 2017

10

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inferred from page(s)

published in

Oncogene

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17 September 2017

26

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17 September 2017

42

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17 September 2017

6150-6159

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1210439

17 September 2017

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Arsenic trioxide-induced apoptosis and differentiation are associated respectively with mitochondrial transmembrane potential collapse and retinoic acid signaling pathways in acute promyelocytic leukemia

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Cleavage of Bax to p18 Bax accelerates stress-induced apoptosis, and a cathepsin-like protease may rapidly degrade p18 Bax.

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The p18 truncated form of Bax behaves like a Bcl-2 homology domain 3-only protein

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The N-terminal end of Bax contains a mitochondrial-targeting signal.

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Cleavage of Bax is mediated by caspase-dependent or -independent calpain activation in dopaminergic neuronal cells: protective role of Bcl-2.

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Drug approval summaries: arsenic trioxide, tamoxifen citrate, anastrazole, paclitaxel, bexarotene

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Free fatty acids promote hepatic lipotoxicity by stimulating TNF-alpha expression via a lysosomal pathway

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The intriguing Ca2+ requirement of calpain activation

21 January 2018

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N-terminal cleavage of bax by calpain generates a potent proapoptotic 18-kDa fragment that promotes bcl-2-independent cytochrome C release and apoptotic cell death.

21 January 2018

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Characterization of the necrotic cleavage of poly(ADP-ribose) polymerase (PARP-1): implication of lysosomal proteases

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Mitochondria and apoptosis

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Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death

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Multidrug-resistant neuroblastoma cells are responsive to arsenic trioxide at both normoxia and hypoxia

21 January 2018

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Arsenic trioxide-induced death of neuroblastoma cells involves activation of Bax and does not require p53.

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Sorting out the nuclear envelope from the endoplasmic reticulum

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Treatment of high-risk neuroblastoma with intensive chemotherapy, radiotherapy, autologous bone marrow transplantation, and 13-cis-retinoic acid. Children's Cancer Group

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Cadmium induces apoptotic cell death in WI 38 cells via caspase-dependent Bid cleavage and calpain-mediated mitochondrial Bax cleavage by Bcl-2-independent pathway

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Arsenic trioxide inhibits neuroblastoma growth in vivo and promotes apoptotic cell death in vitro.

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Formation of nuclear Bax/p53 complexes is associated with chemotherapy induced apoptosis

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Complete remission after treatment of acute promyelocytic leukemia with arsenic trioxide

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Molecular characterization of mitochondrial apoptosis-inducing factor

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Calpain-induced Bax-cleavage product is a more potent inducer of apoptotic cell death than wild-type Bax.

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Elimination of primer-dimer artifacts and genomic coamplification using a two-step SYBR green I real-time RT-PCR.

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Prohibitin co-localizes with Rb in the nucleus and recruits N-CoR and HDAC1 for transcriptional repression

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Cleavage of Bax enhances its cell death function

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Nuclear targeting of Bax during apoptosis in human colorectal cancer cells

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1070 myeloablative megatherapy procedures followed by stem cell rescue for neuroblastoma: 17 years of European experience and conclusions. European Group for Blood and Marrow Transplant Registry Solid Tumour Working Party

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Detection of apoptosis in live cells by MitoTracker red CMXRos and SYTO dye flow cytometry

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Different cleavage pattern for poly(ADP-ribose) polymerase during necrosis and apoptosis in HL-60 cells

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Bax cleavage is mediated by calpain during drug-induced apoptosis

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7 January 2021

Identifiers

DOI

10.1038/SJ.ONC.1210439

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Dimensions Publication ID

17 September 2017

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