Cross Talk Between Cellular Redox State and the Antiapoptotic Protein Bcl-2-Reference-Cited by-同舟云学术

Cross Talk Between Cellular Redox State and the Antiapoptotic Protein Bcl-2

Published:2018-11 Issue:13 Volume:29 Page:1215-1236
ISSN:1523-0864
Container-title:Antioxidants & Redox Signaling
language:en
Short-container-title:Antioxidants & Redox Signaling

Author:

Pohl Sebastian Öther-Gee¹²,Agostino Mark¹²³,Dharmarajan Arun¹²,Pervaiz Shazib²⁴⁵⁶

Affiliation:

1. Stem Cell and Cancer Biology Laboratory, Curtin Health and Innovation Research Institute, Curtin University, Bentley, Western Australia.

2. School of Biomedical Sciences, Curtin University, Perth, Western Australia.

3. Curtin Institute for Computation, Curtin University, Perth, Western Australia.

4. Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.

5. NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, Singapore.

6. National University Cancer Institute, National University Health System, Singapore, Singapore.

Publisher

Mary Ann Liebert Inc

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry,Cell Biology,Clinical Biochemistry,Molecular Biology,Physiology,Biochemistry

Link

https://www.liebertpub.com/doi/pdf/10.1089/ars.2017.7414

Reference195 articles.

1. Apoptosis-associated release of Smac/DIABLO from mitochondria requires active caspases and is blocked by Bcl-2

2. Bcl-2 Regulates Reactive Oxygen Species Signaling and a Redox-Sensitive Mitochondrial Proton Leak in Mouse Pancreatic β-Cells

3. Bcl-2 protects from oxidative damage and apoptotic cell death without interfering with activation of NF-κB by TNF

4. Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer

5. Wnt Proteins Prevent Apoptosis of Both Uncommitted Osteoblast Progenitors and Differentiated Osteoblasts by β-Catenin-dependent and -independent Signaling Cascades Involving Src/ERK and Phosphatidylinositol 3-Kinase/AKT

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