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Related Concept Videos

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...
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...
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.
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.
Cellular Injury V: Apoptosis and Autophagy01:22

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 Death01:18

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: Jun 4, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

DNA-Dependent Protein Kinase in Apoptosis.

J J Turchi1

  • 1Department of Biochemistry and Molecular Biology, School of Medicine, Wright State University, Dayton, Ohio.

Methods in Molecular Medicine
|February 23, 2011
PubMed
Summary

Genotoxic stress triggers apoptosis via a caspase cascade, involving cytochrome C release and protease activation. This programmed cell death pathway can be modulated by Bcl-xL and Bcl-xS proteins.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Programmed cell death, or apoptosis, is a crucial cellular process.
  • Apoptosis can be initiated by various stimuli, including genotoxic stress.
  • The process involves a cascade of proteases known as caspases.

Purpose of the Study:

  • To elucidate the molecular mechanisms of apoptosis induction by genotoxic stress.
  • To describe the caspase cascade pathway involved in programmed cell death.
  • To highlight the roles of key regulatory proteins in apoptosis.

Main Methods:

  • The study reviews existing literature and presents a model of the caspase cascade.
  • It discusses the signaling pathway from genotoxic stress to caspase activation.

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In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

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Last Updated: Jun 4, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila
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In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

Published on: November 27, 2016

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

  • Key protein interactions and their roles are described.

    • Main Results:

    • Genotoxic stress leads to cytochrome C release from mitochondria.
    • Cytochrome C facilitates the formation of a complex that activates caspase-9.
    • Active caspase-9 triggers caspase-3, which executes apoptosis by cleaving target proteins like DNA-PKcs.
    • Proteins Bcl-xL and Bcl-xS modulate apoptosis by interacting with cytochrome C and caspase complexes.

    Conclusions:

    • The caspase cascade is a central mechanism for apoptosis execution following genotoxic stress.
    • Mitochondrial integrity and specific protein interactions are critical for regulating this pathway.
    • Understanding these pathways offers insights into cellular regulation and disease.