Related Experiment Video

Updated: Jun 10, 2026

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
09:27

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

Published on: March 23, 2015

Apoptogenic factors released from mitochondria

David L Vaux1

  • 1La Trobe Institute for Molecular Science, La Trobe University, Kingsbury Drive, Victoria 3086, Australia. d.vaux@latrobe.edu.au

Biochimica Et Biophysica Acta
|August 18, 2010
PubMed

Insights

Cells initiate self-destruction via caspase activation and mitochondrial disruption. This review highlights pro-apoptotic molecules released from mitochondria, crucial for programmed cell death.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Genetics

Background:

  • Programmed cell death (apoptosis) is essential for metazoan development and tissue homeostasis.
  • Apoptosis involves conserved molecular mechanisms, including caspase activation and mitochondrial pathways.
  • Mitochondria play a critical role in regulating cell death.
  • Inhibitor of apoptosis (IAP) proteins regulate caspase activity.

Purpose of the Study:

  • To review the role of mitochondria in releasing pro-apoptotic molecules.
  • To elucidate the interplay between mitochondrial function and caspase activation in apoptosis.
  • To discuss the regulation of apoptosis by IAP proteins.

Main Methods:

  • Literature review focusing on apoptosis and mitochondrial pathways.
  • Analysis of molecular mechanisms linking mitochondria and caspases.
  • Discussion of Bcl-2 family proteins and IAP interactions.

Main Results:

  • Mitochondria release specific proteins that trigger caspase activation.
  • Active caspases can influence mitochondrial outer membrane permeability and Bcl-2 family proteins.
  • Mitochondria-released proteins can antagonize IAP proteins, promoting cell death.

Conclusions:

  • Mitochondrial outer membrane permeabilization is a key event in apoptosis.
  • Mitochondria actively participate in and regulate the apoptotic cascade.
  • Understanding these pathways offers insights into therapeutic strategies for diseases involving aberrant cell death.

More Related Videos

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

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.
Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial precursors...
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...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...