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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...
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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.
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

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Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
06:26

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Published on: April 1, 2011

Mitochondrial Ca(2+) and apoptosis.

Carlotta Giorgi1, Federica Baldassari, Angela Bononi

  • 1Department of Experimental and Diagnostic Medicine, Section of General Pathology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.

Cell Calcium
|April 7, 2012
PubMed
Summary
This summary is machine-generated.

Mitochondria play a crucial role in apoptosis by releasing factors that trigger cell death. Regulating mitochondrial calcium (Ca2+) levels can effectively blunt this apoptotic response.

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Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
06:26

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Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
08:29

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

Published on: April 27, 2018

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Mitochondria are central to apoptosis, releasing pro-apoptotic factors into the cytosol.
  • Mitochondrial calcium (Ca2+) overload is a key mechanism inducing outer membrane rupture and factor release.

Purpose of the Study:

  • To review proteins involved in mitochondrial Ca2+ homeostasis.
  • To understand how these proteins modulate Ca2+-dependent apoptotic stimuli.

Main Methods:

  • Literature review of experimental evidence.
  • Analysis of molecular mechanisms of Ca2+ transport and apoptosis.

Main Results:

  • Mitochondrial Ca2+ overload is a critical trigger for apoptotic cell death.
  • Proteins regulating mitochondrial Ca2+ homeostasis significantly impact apoptosis effectiveness.

Conclusions:

  • Modulating mitochondrial Ca2+ levels offers a strategy to control apoptosis.
  • Reduced mitochondrial Ca2+ overload blunts the apoptotic response, irrespective of the specific molecular pathway.