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Related Concept Videos

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.
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.
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...
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...
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...

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Related Experiment Video

Updated: Jun 9, 2026

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

Apoptosis: embedded in membranes.

Christian Bogner1, Brian Leber, David W Andrews

  • 1Department of Biochemistry and Biomedical Sciences, McMaster University, 1200 Main Street West, Room 4H-41, Hamilton, Ontario, Canada L8N 3Z5.

Current Opinion in Cell Biology
|August 31, 2010
PubMed
Summary
This summary is machine-generated.

Cell death signals converge on mitochondrial outer membrane permeabilization, regulated by Bcl-2 proteins. Membrane interactions induce crucial conformational changes, controlling cell fate.

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

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Related Experiment Videos

Last Updated: Jun 9, 2026

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

Quantification of Efferocytosis by Single-cell Fluorescence Microscopy
06:15

Quantification of Efferocytosis by Single-cell Fluorescence Microscopy

Published on: August 18, 2018

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

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Cell death pathways often converge on the mitochondria.
  • The Bcl-2 protein family regulates mitochondrial outer membrane permeabilization (MOMP).
  • Understanding Bcl-2 interactions is key to controlling cell death.

Purpose of the Study:

  • To elucidate the role of intracellular membranes in Bcl-2 protein regulation.
  • To investigate how membrane insertion affects Bcl-2 protein conformation and function.

Main Methods:

  • Structural analyses of Bcl-2 family proteins.
  • Biochemical assays to study protein-membrane interactions.
  • Conformational change studies upon membrane insertion.

Main Results:

  • Key regulatory interactions of Bcl-2 proteins occur at intracellular membranes.
  • Membrane insertion induces functionally significant conformational changes in Bcl-2 proteins.
  • These conformational changes are critical for regulating MOMP.

Conclusions:

  • Bcl-2 protein function is intimately linked to their interaction with and insertion into intracellular membranes.
  • Membrane-associated conformational changes are central to the regulation of MOMP and cell death.
  • Targeting these membrane interactions offers potential therapeutic strategies for controlling cell death.