Related Experiment Video

Updated: Aug 8, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

K+ channels in apoptosis

E D Burg1, C V Remillard, J X-J Yuan

  • 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, San Diego, 9500 Gilman Drive, MC 0725, La Jolla, 92093-0725, USA.

The Journal of Membrane Biology
|May 11, 2006
PubMed

Insights

Programmed cell death, or apoptosis, is crucial for tissue balance. This review explores how potassium (K+) channels regulate apoptosis, impacting diseases like cancer and neurodegeneration.

Area of Science:

  • Cell biology
  • Ion channel physiology
  • Disease mechanisms

Background:

  • Apoptosis is essential for tissue homeostasis; dysregulation contributes to diseases like cancer and neurodegeneration.
  • Ion transport across cell and organelle membranes is increasingly linked to disease states.
  • Potassium (K+) channels play a critical role in cellular processes, including programmed cell death.

Purpose of the Study:

  • To review the role of potassium (K+) channels in regulating apoptosis.
  • To investigate the involvement of K+ channels in various phases of apoptosis.
  • To examine the function of mitochondrial K+ channels in cell death pathways.

Main Methods:

  • Literature review of K+ channel types and their functions in apoptosis.
  • Analysis of studies linking K+ transport to apoptotic events.
  • Examination of research on mitochondrial K+ channels in cell death.

Main Results:

  • Different types of K+ channels are identified and characterized.
  • K+ channels are shown to control key apoptotic phases: cell shrinkage, cytochrome c release, caspase activation, and DNA fragmentation.
  • Mitochondrial K+ channels exhibit both anti- and pro-apoptotic roles, particularly in neurons and cardiomyocytes.

Conclusions:

  • Potassium (K+) channels are critical regulators of apoptosis.
  • Targeting K+ channels may offer therapeutic strategies for diseases involving apoptosis dysregulation.
  • Mitochondrial K+ channels are key players in neuronal and cardiomyocyte cell death.

More Related Videos

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila13:21

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

Published on: November 27, 2016

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depolarization10:45

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depolarization

Published on: January 13, 2012

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.