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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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Overview of Cell Death01:30

Overview of Cell Death

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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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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.
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Related Experiment Video

Updated: Mar 3, 2026

Measuring Caspase Activity Using a Fluorometric Assay or Flow Cytometry
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Caspase-8: regulating life and death.

Bart Tummers1, Douglas R Green1

  • 1Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.

Immunological Reviews
|May 3, 2017
PubMed
Summary
This summary is machine-generated.

Caspase-8 initiates extrinsic apoptosis and prevents necroptosis, crucial for cell death regulation. Dysfunctional caspase-8 contributes to malignancies, highlighting its role in development and homeostasis.

Keywords:
apoptosiscaspase-8developmenthematopoiesisinflammationnecroptosis

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Area of Science:

  • Cellular Biology
  • Molecular Mechanisms of Cell Death

Background:

  • Programmed cell death, including apoptosis and necroptosis, is vital for development, homeostasis, and disease control.
  • Extrinsic apoptosis is triggered by death receptor ligation, while necroptosis is a regulated form of necrosis.
  • Caspase-8 is a key protease regulating both extrinsic apoptosis and necroptosis pathways.

Purpose of the Study:

  • To review the role of caspase-8 in initiating extrinsic apoptosis.
  • To elucidate the mechanism by which caspase-8 inhibits necroptosis.
  • To explore caspase-8's importance in development, homeostasis, and its link to malignancies.

Main Methods:

  • Literature review of programmed cell death pathways.
  • Analysis of molecular mechanisms involving caspase-8, death receptors, and TNF receptor superfamily.
  • Examination of studies on caspase-8 dysfunction in mouse and human cancers.

Main Results:

  • Caspase-8 activation is central to extrinsic apoptosis execution.
  • Caspase-8 actively suppresses necroptosis, maintaining a balance between cell survival and death.
  • Impaired caspase-8 function is implicated in the development of various cancers.

Conclusions:

  • Caspase-8 acts as a critical switch, directing cells towards apoptosis or preventing necroptosis.
  • The balance regulated by caspase-8 is essential for normal development and tissue homeostasis.
  • Targeting caspase-8 pathways may offer therapeutic strategies for cancer treatment.