Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Electron Transport Chain: Complex I and II

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

The Supercomplexes in the Crista Membrane

The Supercomplexes in the Crista Membrane

The mitochondrial cristae membrane is the primary site for the oxidative phosphorylation (OXPHOS) process of energy conversion mediated through respiratory complexes I to V. These complexes have been widely studied for decades, and it has been proven that they form supramolecular structures called respiratory supercomplexes (SC). These higher-order complexes may be crucial in maintaining the biochemical structure and improving the physiological activity of the individual complexes while...

The Intrinsic Apoptotic Pathway

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 Pathway

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...

Apoptosis

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.

Caspases

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.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

The IMPACT of the COVID-19 Pandemic on Prescription Drug Use in Patients with Psoriasis Vulgaris in Germany.

Dermatology and therapy·2023

Same author

TMEFF2: A Transmembrane Proteoglycan with Multifaceted Actions in Cancer and Disease.

Cancers·2020

Same author

Glucocorticoid receptor antagonism reverts docetaxel resistance in human prostate cancer.

Endocrine-related cancer·2015

Same author

Optomotor-blind negatively regulates Drosophila eye development by blocking Jak/STAT signaling.

PloS one·2015

Same author

IκΒα inhibits apoptosis at the outer mitochondrial membrane independently of NF-κB retention.

The EMBO journal·2014

Same author

Introduction.

Advances in experimental medicine and biology·2014

Search research articles

Related Experiment Video

Updated: May 18, 2026

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

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

Published on: April 1, 2011

Respiratory chain complex II as general sensor for apoptosis.

¹Department of Experimental Medicine and Toxicology, Imperial College London, London, UK. s.grimm@imperial.ac.uk

Biochimica Et Biophysica Acta

|September 25, 2012

Summary

Mitochondrial complex II acts as a general apoptosis sensor, activated by pH changes during cell death. This leads to excessive reactive oxygen species production, causing cell demise and linking complex II mutations to disease.

More Related Videos

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

Published on: November 27, 2016

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Published on: August 2, 2021

Related Experiment Videos

Last Updated: May 18, 2026

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

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

Published on: April 1, 2011

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

Published on: November 27, 2016

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Published on: August 2, 2021

Area of Science:

Cellular respiration
Mitochondrial physiology
Apoptosis signaling

Background:

Complex II (succinate dehydrogenase) mutations are implicated in neurodegenerative diseases and cancer.
Metabolic alterations in cancer cells affect the respiratory chain, particularly complex II.
Anticancer compounds reveal differential apoptosis sensitivity in complex II-deficient versus wild-type cells.

Purpose of the Study:

To review evidence supporting complex II as a general sensor for apoptosis induction.
To explain the mechanism by which complex II mediates apoptosis signals.
To highlight the role of complex II in disease pathogenesis and therapeutic strategies.

Main Methods:

Review of existing evidence from studies on neurodegenerative diseases and cancer.
Analysis of data from experiments with anticancer compounds.
Mechanistic understanding of complex II function and its regulation during apoptosis.

Main Results:

Complex II acts as a general sensor for apoptosis induction.
Apoptosis is triggered by pH changes, causing dissociation of SDHA/SDHB subunits.
Uncontrolled succinate dehydrogenase (SDH) activity generates excessive reactive oxygen species (ROS).

Conclusions:

Complex II's role in apoptosis is mediated by pH-induced subunit dissociation and subsequent ROS overproduction.
Mutations in complex II subunits contribute to neurodegenerative diseases and tumorigenesis.
Further research may reveal novel therapeutic targets for complex II-related diseases.