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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...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
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...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...

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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
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LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Mitochondrial cell death effectors.

Dirk Brenner1, Tak W Mak

  • 1The Campbell Family Cancer Research Institute, Ontario Cancer Institute, University Health Network, Toronto, Ontario, Canada. dbrenner@uhnresearch.ca

Current Opinion in Cell Biology
|October 14, 2009
PubMed
Summary
This summary is machine-generated.

Programmed cell death, or apoptosis, is vital for development and health. This review focuses on the intrinsic apoptosis pathway, its regulation by BCL-2 proteins, and potential cancer therapies.

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Immunodetection of Outer Membrane Proteins by Flow Cytometry of Isolated Mitochondria
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Immunodetection of Outer Membrane Proteins by Flow Cytometry of Isolated Mitochondria

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Immunodetection of Outer Membrane Proteins by Flow Cytometry of Isolated Mitochondria
11:53

Immunodetection of Outer Membrane Proteins by Flow Cytometry of Isolated Mitochondria

Published on: September 18, 2014

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Programmed cell death (apoptosis) is essential for normal development and maintaining tissue health.
  • Dysregulation of apoptosis is linked to diseases such as cancer, immunodeficiency, and autoimmune disorders.
  • Apoptosis occurs via extrinsic and intrinsic pathways, both involving caspase activation.

Purpose of the Study:

  • To review recent advancements in understanding the intrinsic pathway of apoptosis.
  • To highlight the roles of BCL-2 family members and BH3-only proteins in mitochondrial integrity.
  • To discuss the significance of mitochondria-released cytotoxic factors in apoptosis.

Main Methods:

  • Literature review of recent research on the intrinsic apoptosis pathway.
  • Analysis of the mechanisms involving BCL-2 family proteins and BH3-only proteins.
  • Examination of the role of mitochondrial integrity and cytotoxic factors.

Main Results:

  • BCL-2 family members play a critical role in regulating mitochondrial integrity during apoptosis.
  • BH3-only proteins are key regulators that can either promote or inhibit apoptosis by interacting with BCL-2 proteins.
  • Mitochondria release cytotoxic factors that contribute to the execution of apoptosis.

Conclusions:

  • The intrinsic apoptosis pathway is a complex process involving intricate regulation by BCL-2 family proteins.
  • Understanding the interplay between BCL-2 homologues and BH3-only proteins offers potential therapeutic strategies for cancer.
  • Targeting the intrinsic apoptosis pathway presents a promising avenue for future cancer treatments.