Related Experiment Video

Updated: Aug 14, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Apoptin-induced cell death is modulated by Bcl-2 family members and is Apaf-1 dependent

M Burek1, S Maddika, C J Burek

  • 1Department of Immunology and Cell Biology, University of Münster, Münster, Germany.

Oncogene
|November 17, 2005
PubMed

Insights

Apoptin protein triggers cancer cell death through a mitochondrial pathway involving Apaf-1 and caspases, but is inhibited by Bcl-2 and Bcl-xL proteins.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Apoptin, derived from chicken anemia virus, selectively induces apoptosis in transformed cells, showing potential as an anticancer therapeutic.
  • The precise molecular mechanisms underlying apoptin-induced apoptosis remain largely unelucidated.

Purpose of the Study:

  • To investigate the molecular pathway of apoptin-induced apoptosis.
  • To determine the role of Bcl-2 family proteins, caspases, and Apaf-1 in apoptin-mediated cell death.

Main Methods:

  • Utilized various tumor cell lines, including Apaf-1-deficient fibroblasts.
  • Assessed the impact of Bcl-2, Bcl-xL, and Bax expression on cell death.
  • Measured cytochrome c release, caspase activation, and the effect of caspase inhibitors.
  • Evaluated the necessity of Apaf-1 for apoptin-induced apoptosis.

Main Results:

  • Bcl-2 and Bcl-xL were found to inhibit apoptin-induced cell death, contrary to prior assumptions.
  • Bax deficiency conferred resistance, while Bax expression sensitized cells to apoptin.
  • Apoptin induced cytochrome c release, caspase-3 and -7 activation, and required Apaf-1 for its apoptotic effect.
  • A broad-spectrum caspase inhibitor provided significant protection against apoptin-induced cell death.

Conclusions:

  • Apoptin-induced apoptosis is dependent on Bcl-2 family proteins, caspases, and the Apaf-1 apoptosome.
  • The study reveals a mitochondrial death pathway mediated by Apaf-1 in apoptin-induced apoptosis.
  • These findings clarify the mechanism of action for apoptin, supporting its therapeutic potential in cancer treatment.

More Related Videos

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis12:55

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

Published on: February 16, 2015

Evaluation of Caspase Activation to Assess Innate Immune Cell Death10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

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...
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.
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...
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...