Paclitaxel sensitivity of breast cancer cells requires efficient mitotic arrest and disruption of Bcl-xL/Bak interaction. (Q39444559)

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16 January 2020

title

Paclitaxel sensitivity of breast cancer cells requires efficient mitotic arrest and disruption of Bcl-xL/Bak interaction (English)

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16 January 2020

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5

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16 January 2020

Miguel A Japón

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16 January 2020

author name string

M Luz Flores

1

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16 January 2020

Carolina Castilla

2

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16 January 2020

Rainiero Ávila

3

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16 January 2020

Manuel Ruiz-Borrego

4

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language of work or name

English

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publication date

11 November 2011

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Breast Cancer Research and Treatment

16 January 2020

published in

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volume

133

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issue

3

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page(s)

917-928

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MicroRNA-125b confers the resistance of breast cancer cells to paclitaxel through suppression of pro-apoptotic Bcl-2 antagonist killer 1 (Bak1) expression.

16 January 2020

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Bcl-2 phosphorylation has pathological significance in human breast cancer.

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Posttranslational modifications of Bcl2 family members--a potential therapeutic target for human malignancy

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Small inhibitor of Bcl-2, HA14-1, selectively enhanced the apoptotic effect of cisplatin by modulating Bcl-2 family members in MDA-MB-231 breast cancer cells

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Paclitaxel-induced FasL-independent apoptosis and slow (non-apoptotic) cell death.

21 January 2018

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Decoding the links between mitosis, cancer, and chemotherapy: The mitotic checkpoint, adaptation, and cell death.

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Dependence of paclitaxel sensitivity on a functional spindle assembly checkpoint

21 January 2018

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21 January 2018

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Displacement of Bim by Bmf and Puma rather than increase in Bim level mediates paclitaxel-induced apoptosis in breast cancer cells

21 January 2018

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21 January 2018

Identifiers

DOI

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16 January 2020

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