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Related Concept Videos

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...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
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.
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.
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...

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Related Experiment Video

Updated: Jun 27, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Regulation of apoptosis by type III interferons.

W Li1, A Lewis-Antes1, J Huang1

  • 1Department of Biochemistry and Molecular Biology, New Jersey Medical School-University Hospital Cancer Center, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.

Cell Proliferation
|December 2, 2008
PubMed
Summary

Type III interferons (IFNs) can trigger apoptosis, a form of cell death, through their receptor. This intrinsic function, particularly potent with type III IFNs, suggests significant cytotoxic potential for cancer therapy.

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Last Updated: Jun 27, 2026

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Type I and Type III interferons (IFNs) share signaling pathways but use distinct receptors.
  • Type III IFNs exhibit anti-tumor activity, yet their role in regulating cell population growth is not well understood.

Purpose of the Study:

  • To investigate the ability of Type III IFNs to regulate cell population growth by inducing apoptosis.
  • To characterize the signaling mechanisms and cytotoxic potential of Type III IFNs.

Main Methods:

  • Utilized intact and modified human colorectal adenocarcinoma HT29 cells.
  • Studied apoptosis regulation induced by Type III IFNs and other IFN types.

Main Results:

  • The IFN-lambda receptor 1 (IFN-lambdaR1) chain intrinsically triggers apoptosis, causing cell cycle arrest and DNA fragmentation.
  • Apoptosis extent correlated with receptor expression and prolonged signaling; caspase activation was observed.
  • Type III IFNs induced more robust apoptosis than Type I or II IFNs, with IFN-gamma sensitizing cells to Type III IFN-mediated apoptosis.

Conclusions:

  • Type III IFNs possess an intrinsic ability to induce apoptosis, highlighting their potential as cytotoxic agents.
  • The Type III IFN receptor complex plays a key role in initiating apoptosis signaling.
  • Type III IFNs may be valuable in cancer therapy, alone or in combination treatments.