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

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...

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.

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...

Phagocytosis of Apoptotic Cells

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.

Autophagic Cell Death

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

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 2026 Richard Perham Prize winner: Angela M. Gronenborn.

The FEBS journal·2026

Same author

The FEBS Journal in 2026: Safeguarding scientific integrity amid the rise of the machines.

The FEBS journal·2026

Same author

A TAK1 cytokine toxicity checkpoint controls anti-cancer immunity.

Cell reports·2025

Same author

Endothelial IL-36 receptor activation promotes vascular stability to limit pathological microvessel permeability in the CNS.

Cell reports·2025

Same author

Fbxo42 promotes the degradation of Ataxin-2 granules to trigger terminal Xbp1 signaling.

Nature communications·2025

Same author

The FEBS Journal in 2025: in all science, error precedes the truth.

The FEBS journal·2025

Search research articles

Related Experiment Video

Updated: Jun 19, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Apoptosis: calling time on apoptosome activity.

Colin Adrain¹, Seamus J Martin

¹Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 0QH, UK.

Science Signaling

|October 8, 2009

Summary

This summary is machine-generated.

Apoptosis involves caspase-9 activation within the apoptosome. This study reveals caspase-9 processing acts as a molecular timer, limiting its activity and preventing uncontrolled cell death.

More Related Videos

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Published on: February 1, 2018

Detection and Isolation of Apoptotic Bodies to High Purity

Detection and Isolation of Apoptotic Bodies to High Purity

Published on: August 12, 2018

Related Experiment Videos

Last Updated: Jun 19, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Published on: February 1, 2018

Detection and Isolation of Apoptotic Bodies to High Purity

Detection and Isolation of Apoptotic Bodies to High Purity

Published on: August 12, 2018

Area of Science:

Cellular biology
Molecular mechanisms of apoptosis

Background:

Apoptosis is programmed cell death, regulated by caspases.
Caspase-9 activation occurs in the apoptosome complex.
The necessity of caspase-9 autocatalytic processing remained unclear.

Purpose of the Study:

To elucidate the functional role of caspase-9 autocatalytic processing within the apoptosome.

Main Methods:

Investigated caspase-9 processing and its effect on apoptosome dynamics.
Focused on the displacement of processed caspase-9 from the apoptosome complex.

Main Results:

Caspase-9 processing within the apoptosome promotes its displacement.
This displacement leads to the inactivation of caspase-9.
Autoprocessing functions as a molecular timer, regulating protease activity.

Conclusions:

Caspase-9 autoprocessing acts as a crucial timer mechanism in apoptosis.
This timer prevents excessive caspase activation by limiting protease activity.
Ensures apoptosis is initiated only when sufficient apoptosomes are assembled.