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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...

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...

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...

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...

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Related Experiment Video

Updated: May 23, 2026

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

Mousing around with caspases and IAPs.

Robert C Rickert¹, Guy S Salvesen, Carl F Ware

¹Programs in Cell Death and Inflammation Research, Sanford-Burnham Medical Research Institute, La Jolla, CA 92037, USA. robert@sanfordburnham.org

The Biochemical Journal

|March 29, 2012

Summary

This summary is machine-generated.

Cellular inhibitor of apoptosis 1 (c-IAP1) is linked to caspase 11, complicating studies on inflammation. Immune functions attributed to c-IAP1 may stem from a linked caspase 11 mutation.

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Last Updated: May 23, 2026

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

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Published on: March 5, 2018

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages

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Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches

Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches

Published on: October 13, 2022

Area of Science:

Immunology
Molecular Biology
Biochemistry

Background:

The role of cellular inhibitor of apoptosis 1 (c-IAP1) in inflammatory processes is under investigation.
Accurate genetic models are crucial for understanding protein function in biological pathways.

Purpose of the Study:

To re-evaluate the function of c-IAP1 in inflammation by assessing its genetic linkage to other key proteins.
To determine if observed immune functions are intrinsic to c-IAP1 or due to co-inherited genetic factors.

Main Methods:

Genetic analysis to assess the co-inheritance of c-IAP1 and caspase 11 loci.
Recombination studies to attempt segregation of the two genes.

Main Results:

Cellular inhibitor of apoptosis 1 (c-IAP1) is genetically linked to caspase 11 and cannot be separated through recombination.
This linkage suggests that immune functions previously attributed to c-IAP1 may be influenced by a co-inherited caspase 11 mutation.

Conclusions:

The genetic linkage between c-IAP1 and caspase 11 complicates the interpretation of previous studies on c-IAP1's role in inflammation.
Researchers must account for this linkage when designing experiments and interpreting results involving c-IAP1 and caspase 11.