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Regulating the BCL2 Family to Improve Sensitivity to Microtubule Targeting Agents

Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA
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Author to whom correspondence should be addressed.
Cells 2019, 8(4), 346; https://doi.org/10.3390/cells8040346
Received: 28 February 2019 / Revised: 28 March 2019 / Accepted: 9 April 2019 / Published: 12 April 2019
(This article belongs to the Special Issue Tubulin: Structure, Functions and Roles in Disease)
Chemotherapeutic targeting of microtubules has been the standard of care in treating a variety of malignancies for decades. During mitosis, increased microtubule dynamics are necessary for mitotic spindle formation and successful chromosomal segregation. Microtubule targeting agents (MTAs) disrupt the dynamics necessary for successful spindle assembly and trigger programmed cell death (apoptosis). As the critical regulators of apoptosis, anti-apoptotic BCL2 family members are often amplified during carcinogenesis that can result in MTA resistance. This review outlines how BCL2 family regulation is positioned within the context of MTA treatment and explores the potential of combination therapy of MTAs with emerging BCL2 family inhibitors. View Full-Text
Keywords: apoptosis; cell cycle; chemotherapy; microtubule; bcl2 family; mitosis; microtubule targeting agents; tubulin; cellular stress apoptosis; cell cycle; chemotherapy; microtubule; bcl2 family; mitosis; microtubule targeting agents; tubulin; cellular stress
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MDPI and ACS Style

Whitaker, R.H.; Placzek, W.J. Regulating the BCL2 Family to Improve Sensitivity to Microtubule Targeting Agents. Cells 2019, 8, 346. https://doi.org/10.3390/cells8040346

AMA Style

Whitaker RH, Placzek WJ. Regulating the BCL2 Family to Improve Sensitivity to Microtubule Targeting Agents. Cells. 2019; 8(4):346. https://doi.org/10.3390/cells8040346

Chicago/Turabian Style

Whitaker, Robert H.; Placzek, William J. 2019. "Regulating the BCL2 Family to Improve Sensitivity to Microtubule Targeting Agents" Cells 8, no. 4: 346. https://doi.org/10.3390/cells8040346

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