Related Experiment Video

Updated: Aug 15, 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

The role of the mitochondrial apoptosis induced channel MAC in cytochrome c release

Sonia Martinez-Caballero1, Laurent M Dejean, Elizabeth A Jonas

  • 1Department of Basic Sciences, New York University College of Dentistry, 345 East 24th Street, New York, NY 10010, USA.

Journal of Bioenergetics and Biomembranes
|September 17, 2005
PubMed

Insights

Mitochondrial outer membrane permeabilization during apoptosis involves a channel called MAC, which releases cytochrome c without compromising mitochondrial integrity. This study characterizes MAC

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Mitochondrial outer membrane permeabilization is key in apoptosis, enabling cytochrome c release.
  • The mitochondrial apoptosis-induced channel (MAC) is implicated as the channel for cytochrome c release.
  • MAC formation differs from the permeability transition pore, preserving outer membrane integrity.

Purpose of the Study:

  • To characterize the single-channel behavior and pharmacology of the reconstituted MAC.
  • To compare MAC activity in reconstituted channels with that in intact apoptotic mitochondria.
  • To explore MAC regulation by Bcl-2 family proteins and its molecular composition.

Main Methods:

  • Patch-clamp techniques were used to study reconstituted MAC.
  • Single-channel recordings and pharmacological profiling were performed.
  • MAC activity was compared between isolated channels and mitochondria within cells.

Main Results:

  • The study characterized the single-channel properties and pharmacology of reconstituted MAC.
  • MAC activity in vitro correlated with cytochrome c release in intact cells.
  • Regulation by Bcl-2 proteins and insights into MAC's molecular identity were discussed.

Conclusions:

  • MAC is a high-conductance channel crucial for cytochrome c release during apoptosis.
  • MAC formation is a distinct event from permeability transition pore opening.
  • Further research into MAC's regulation and composition may reveal therapeutic targets.

More Related Videos

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor06:26

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Published on: April 1, 2011

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...
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.
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...
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.