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The Intrinsic Apoptotic Pathway

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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...

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Related Experiment Video

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

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

Published on: March 23, 2015

Apoptogenic factors released from mitochondria.

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

Summary

This summary is machine-generated.

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

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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.