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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.
Phagocytosis of Apoptotic Cells01:17

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.
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...
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.

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Related Experiment Video

Updated: Jun 1, 2026

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

Alpha particles induce apoptosis through the sphingomyelin pathway.

Jonathan H Seideman1, Branka Stancevic, Jimmy A Rotolo

  • 1a  Memorial Sloan-Kettering Cancer Center, Department of Chemistry and Molecular Pharmacology, New York, New York 10065.

Radiation Research
|June 3, 2011
PubMed
Summary
This summary is machine-generated.

High-LET alpha particles induce apoptosis by activating the sphingomyelin pathway. This mechanism, independent of DNA damage, involves ceramide signaling and is inhibited by nystatin, confirming alpha particles

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Detection and Isolation of Apoptotic Bodies to High Purity

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

Published on: December 27, 2016

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Last Updated: Jun 1, 2026

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

Detection and Isolation of Apoptotic Bodies to High Purity
12:17

Detection and Isolation of Apoptotic Bodies to High Purity

Published on: August 12, 2018

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

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:

  • Cellular biology
  • Radiation biology
  • Biochemistry

Background:

  • The sphingomyelin pathway generates ceramide, a key mediator of apoptosis in response to cell stressors.
  • Low-linear energy transfer (LET) gamma radiation triggers this pathway via the cell membrane, independent of DNA damage.
  • The role of high-LET alpha particles in initiating this pathway remains unknown.

Purpose of the Study:

  • To investigate whether high-LET alpha particles can activate the sphingomyelin pathway to induce apoptosis.
  • To determine the mechanism by which alpha particles induce apoptosis in Jurkat cells.

Main Methods:

  • Irradiation of Jurkat cells with alpha particles using a ²²⁵Ac-DOTA-anti-CD3 IgG antibody construct.
  • Treatment of cells with cholesterol-depleting nystatin to assess its effect on alpha-particle-induced apoptosis.
  • External irradiation of cells with collimated alpha particles from a ²⁴¹Am source to control for microdosimetry.

Main Results:

  • Alpha particle irradiation resulted in dose-dependent apoptosis in Jurkat cells.
  • Nystatin significantly reduced alpha-particle-induced apoptosis, indicating involvement of the ceramide pathway.
  • External alpha particle irradiation confirmed the disruption of the ceramide pathway, independent of antibody binding.
  • Increased membrane ceramide concentrations were observed after alpha particle exposure.

Conclusions:

  • Alpha particles can activate the sphingomyelin pathway, leading to apoptosis.
  • This mechanism is independent of DNA damage and involves ceramide signaling.
  • The findings have implications for understanding the biological effects of alpha particle exposure.