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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

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.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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...
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...
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.

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Related Experiment Video

Updated: May 21, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Early decrease in respiration and uncoupling event independent of cytochrome C release in PC12 cells undergoing

Libera Berghella1, Elisabetta Ferraro

  • 1Pathophysiology and Treatment of Cachexia Unit, IRCCS San Raffaele Pisana Institute, 00166 Rome, Italy.

International Journal of Cell Biology
|June 6, 2012
PubMed
Summary

Mitochondria

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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
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Published on: June 29, 2011

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09:08

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Published on: May 31, 2018

Area of Science:

  • Cell Biology
  • Biochemistry
  • Apoptosis Research

Background:

  • Cytochrome c is crucial for both apoptosis and cell respiration.
  • Its release from mitochondria signifies a switch between these functions, impacting cell fate.
  • Understanding early apoptosis events is key to deciphering cytochrome c release mechanisms.

Purpose of the Study:

  • To investigate changes in respiratory chain activity during early apoptosis.
  • To elucidate the mechanisms preceding cytochrome c release from mitochondria.
  • To determine the role of mitochondrial function in initiating apoptosis.

Main Methods:

  • Induction of apoptosis using staurosporine (STS) in PC12 cells.
  • Measurement of endogenous uncoupled respiration and uncoupling events.
  • Assessment of cytochrome c release and nuclear condensation.
  • Evaluation of Bcl-2 overexpression effects on apoptosis markers.

Main Results:

  • Respiratory activity changes, including decreased uncoupled respiration and uncoupling, occur before cytochrome c release during STS-induced apoptosis.
  • These early respiratory changes are partly independent of cytochrome c release.
  • Bcl-2 overexpression inhibits the uncoupling event but not the decline in uncoupled respiration.
  • Early nuclear condensation is reversible and does not depend on cytosolic cytochrome c.

Conclusions:

  • Mitochondrial dysfunction precedes cytochrome c release in early apoptosis.
  • These early events prime mitochondria for the release of apoptogenic factors.
  • Findings offer insights into the intricate mechanisms governing apoptosis initiation.