A connection in life and death: The BCL-2 family coordinates mitochondrial network dynamics and stem cell fate

被引：16

作者：

Rasmussen, Megan L. ^{[1
]}

Gama, Vivian ^{[1
,2
,3
,4
]}

机构：

[1] Vanderbilt Univ, Dept Cell & Dev Biol, 221 Kirkland Hall, Nashville, TN 37235 USA

[2] Vanderbilt Univ, Med Ctr, Neurosci Program, Nashville, TN 37235 USA

[3] Vanderbilt Univ, Med Ctr, Vanderbilt Brain Inst, Nashville, TN 37235 USA

[4] Vanderbilt Univ, Vanderbilt Ctr Stem Cell Biol, 221 Kirkland Hall, Nashville, TN 37235 USA

来源：

CELL DEATH REGULATION IN HEALTH AND DISEASE - PT C | 2020年 / 353卷

关键词：

CYTOCHROME-C RELEASE; PROTEIN DRP1; PROTEOLYTIC CLEAVAGE; SYNAPSE FORMATION; QUALITY-CONTROL; OPA1; ISOFORMS; LIVING CELLS; X-L; FISSION; FUSION;

D O I：

10.1016/bs.ircmb.2019.12.005

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The B cell CLL/lymphoma-2 (BCL-2) family of proteins control the mitochondrial pathway of apoptosis, also known as intrinsic apoptosis. Direct binding between members of the BCL-2 family regulates mitochondrial outer membrane permeabilization (MOMP) after an apoptotic insult. The ability of the cell to sense stress and translate it into a death signal has been a major theme of research for nearly three decades; however, other mechanisms by which the BCL-2 family coordinates cellular homeostasis beyond its role in initiating apoptosis are emerging. One developing area of research is understanding how the BCL-2 family of proteins regulate development using pluripotent stem cells as a model system. Understanding BCL-2 family-mediated regulation of mitochondrial homeostasis in cell death and beyond would uncover new facets of stem cell maintenance and differentiation potential.

引用

页码：255 / 284

页数：30

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