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Related Concept Videos

Caspases01:24

Caspases

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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...
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The Extrinsic Apoptotic Pathway01:17

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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...
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The Intrinsic Apoptotic Pathway01:31

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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...
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Apoptosis01:30

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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...
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Autophagic Cell Death01:18

Autophagic Cell Death

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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...
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CRISPR01:59

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Genome editing technologies allow scientists to modify an organism’s DNA via the addition, removal, or rearrangement of genetic material at specific genomic locations. These types of techniques could potentially be used to cure genetic disorders such as hemophilia and sickle cell anemia. One popular and widely used DNA-editing research tool that could lead to safe and effective cures for genetic disorders is the CRISPR-Cas9 system. CRISPR-Cas9 stands for Clustered Regularly Interspaced...
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Related Experiment Video

Updated: Mar 7, 2026

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex
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Caspase-8: not so silently deadly.

Rebecca Feltham1, James E Vince1, Kate E Lawlor1

  • 1Inflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.

Clinical & Translational Immunology
|February 16, 2017
PubMed
Summary
This summary is machine-generated.

Programmed cell death, apoptosis, is usually silent. However, lytic cell death forms like necroptosis and pyroptosis are inflammatory. Caspase-8 has novel roles in regulating these processes and inflammasome activation, linking cell death to autoinflammatory diseases.

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Area of Science:

  • Immunology
  • Cell Biology
  • Genetics

Background:

  • Apoptosis is a programmed cell death pathway generally considered immunologically silent.
  • Lytic cell death pathways, including necroptosis and pyroptosis, are inflammatory due to damage-associated molecular pattern (DAMP) release.
  • Caspase-8, traditionally linked to apoptosis, has emerging roles in regulating inflammatory cell death and cytokine production.

Purpose of the Study:

  • To review the crosstalk between cell death mechanisms and innate immune inflammatory signaling.
  • To focus on the non-apoptotic functions of caspase-8.
  • To highlight the association between cell death machinery defects and autoinflammatory diseases.

Main Methods:

  • Literature review of recent advances in cell death research.
  • Analysis of the role of caspase-8 in necroptosis and pyroptosis.
  • Examination of the link between inflammasome activation and autoinflammatory conditions.

Main Results:

  • Caspase-8 negatively regulates necroptosis.
  • Caspase-8 cleaves and activates interleukin-1β (IL-1β), either directly or via the NLRP3 inflammasome.
  • Mutations in cell death regulators are linked to inappropriate inflammasome activation and autoinflammatory diseases.

Conclusions:

  • Emerging evidence reveals significant crosstalk between cell death pathways and innate immune signaling.
  • Non-apoptotic functions of caspase-8 are critical in regulating inflammation and inflammasome activation.
  • Dysregulation of cell death machinery contributes to the pathogenesis of autoinflammatory diseases.