Related Experiment Video

Updated: Aug 30, 2026

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Expression of dengue ApoptoM sequence results in disruption of mitochondrial potential and caspase activation

Adeline Catteau1, Gaël Roué, Victor J Yuste

  • 1Unité des Interactions Moléculaires Flavivirus-Hôtes, Institut Pasteur, 25, rue du Dr-Roux, 75015 Paris, France.

Biochimie
|October 31, 2003
PubMed

Insights

A dengue virus M protein sequence, ApoptoM, triggers apoptosis by disrupting mitochondrial potential without reactive oxygen species. This cell death involves caspase-3 activation but not caspase-9, suggesting a specific mitochondrion-dependent pathway.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Apoptotic cell death is a known response to dengue (DEN) virus infection.
  • Mechanisms by which DEN virus replication induces apoptosis remain unclear.
  • A nine-residue sequence of the DEN M protein, termed ApoptoM, exhibits proapoptotic properties.

Purpose of the Study:

  • To investigate if ApoptoM-induced apoptosis is linked to mitochondrial dysfunction.
  • To determine if caspase activation is required for ApoptoM-mediated apoptosis.

Main Methods:

  • Intracellular expression of ApoptoM in various cell types.
  • Assessment of mitochondrial transmembrane potential.
  • Measurement of reactive oxygen species (ROS) generation.
  • Analysis of caspase-like protease activity, including caspase-3 and caspase-9.

Main Results:

  • Intracellular ApoptoM expression disrupted mitochondrial transmembrane potential.
  • No significant generation of reactive oxygen species was observed.
  • ApoptoM-induced apoptosis involved activation of a caspase-like protease pathway.
  • Caspase-3-like activity was detected in ApoptoM-expressing cells.
  • Caspase-9 did not play a role in ApoptoM-mediated cell death.

Conclusions:

  • ApoptoM induces apoptosis through mitochondrial dysfunction.
  • The apoptotic pathway activated by ApoptoM involves caspase-3 but not caspase-9.
  • A specific mitochondrion-dependent apoptotic pathway may mediate ApoptoM's proapoptotic effects.

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

In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening08:16

In Vitro Cleavage Assays using Purified Recombinant Drosophila Caspases for Substrate Screening

Published on: October 6, 2022

Related Concept Videos

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.
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...
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.
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...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...