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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...

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...

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.

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.

Interactions Between Signaling Pathways

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

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.

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Related Experiment Video

Updated: May 13, 2026

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes

Published on: September 27, 2014

Ebola virus does not block apoptotic signaling pathways.

Judith Olejnik¹, Jesus Alonso, Kristina M Schmidt

¹Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, USA.

Journal of Virology

|March 8, 2013

Summary

Ebola virus (EBOV) infection causes necrotic cell death, not apoptosis. EBOV-infected cells remain sensitive to apoptosis, suggesting new antiviral strategies targeting this pathway.

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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Related Experiment Videos

Last Updated: May 13, 2026

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes

Modeling The Lifecycle Of Ebola Virus Under Biosafety Level 2 Conditions With Virus-like Particles Containing Tetracistronic Minigenomes

Published on: September 27, 2014

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Area of Science:

Virology
Cell Biology
Immunology

Background:

Viruses utilize host cell machinery for replication.
Apoptosis is a crucial cellular defense against viral infections.
Understanding Ebola virus (EBOV) cell death mechanisms is vital for therapeutic development.

Purpose of the Study:

To elucidate the mechanism of cell death induced by EBOV infection.
To determine if EBOV actively blocks apoptosis induction pathways.
To explore potential antiviral therapeutic strategies based on apoptosis.

Main Methods:

Assaying for apoptosis and necrosis markers in EBOV-infected cells.
Treating EBOV-infected cells with apoptosis-inducing agents.
Investigating EBOV's effect on receptor- and mitochondrion-mediated apoptosis signaling.
Analyzing double-stranded RNA (dsRNA)-induced apoptosis and protein kinase R (PKR) activation.
Evaluating the efficacy of dsRNA-dependent caspase recruiter (dsCARE) in reducing EBOV titers.

Main Results:

EBOV infection leads to necrotic cell death, not apoptosis.
EBOV-infected cells retain sensitivity to externally induced apoptosis.
Neither receptor- nor mitochondrion-mediated apoptosis signaling is inhibited by EBOV.
While dsRNA-induced PKR activation is blocked, dsRNA-mediated apoptosis is not suppressed.
Treatment with dsCARE significantly reduced EBOV titers in infected cells.

Conclusions:

EBOV induces a non-apoptotic form of cell death characterized by necrosis.
EBOV does not inhibit the host cell's intrinsic apoptotic machinery.
The susceptibility of EBOV-infected cells to apoptosis presents a promising avenue for novel antiviral therapies.