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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.

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...

Cellular Injury V: Apoptosis and Autophagy

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...

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.

Anaphase Promoting Complex

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...

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Related Experiment Video

Updated: May 16, 2026

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Detecting Anastasis In Vivo by CaspaseTracker Biosensor

Published on: February 1, 2018

A caspase cascade regulating developmental axon degeneration.

David J Simon¹, Robby M Weimer, Todd McLaughlin

¹Laboratory of Brain Development and Repair, Rockefeller University, New York, New York 10065, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|December 11, 2012

Summary

Caspase-3 activation is critical for sensory axon degeneration, a process previously overlooked. This study reveals a pathway involving Caspase-9, Caspase-3, and Caspase-6, impacting both developmental and withdrawal-induced axon loss.

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Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

Axon degeneration shares similarities with programmed cell death.
Previous studies questioned the role of Caspase-3 in axon degeneration.
Caspase-6 was recently suggested to play a role.

Purpose of the Study:

To investigate the role of Caspase-3 and Caspase-6 in axon degeneration.
To elucidate the biochemical cascade leading to axon degeneration.
To understand the involvement of caspases in developmental axon pruning.

Main Methods:

Genetic deletion of Caspase-3 and Caspase-6 in vitro and in vivo.
Biochemical assays to determine caspase activation pathways.
Analysis of developmental axon pruning in knockout mice.

Main Results:

Genetic deletion of Caspase-6 offered partial protection against degeneration.
Caspase-6 activation was dependent on Caspase-3.
Genetic deletion of Caspase-3 fully protected against trophic factor withdrawal-induced degeneration.
A cascade from Bcl2 family regulators to Caspase-9, Caspase-3, and Caspase-6 was identified.
Caspase-3 and Caspase-6 knockout mice exhibited delayed developmental axon pruning.

Conclusions:

Caspase-3 plays a critical, previously underestimated role in sensory axon degeneration.
A specific caspase cascade (Caspase-9 -> Caspase-3 -> Caspase-6) drives degeneration.
Both Caspase-3 and Caspase-6 are implicated in normal developmental axon pruning.