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Related Concept Videos

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.
Yeast Signaling01:28

Yeast Signaling

Yeasts are single-celled organisms, but unlike bacteria, they are eukaryotes (cells with a nucleus). Cell signaling in yeast is similar to signaling in other eukaryotic cells. A ligand, such as a protein or a small molecule released from a yeast cell, attaches to a receptor on the cell surface. The binding stimulates second-messenger kinases to activate or inactivate transcription factors that further regulate gene expression. Many of the yeast intracellular signaling cascades have similar...
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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...
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
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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.
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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Published on: August 4, 2019

NO-mediated apoptosis in yeast.

Bruno Almeida1, Sabrina Buttner, Steffen Ohlmeier

  • 1Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal.

Journal of Cell Science
|August 30, 2007
PubMed
Summary
This summary is machine-generated.

Nitric oxide (NO) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) are key players in yeast apoptosis. NO signaling and GAPDH S-nitrosation are linked to hydrogen peroxide-induced cell death and aging.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Nitric oxide (NO) is a signaling molecule involved in various physiological processes, including apoptosis.
  • Yeast apoptosis is a complex process with multiple regulatory pathways.

Purpose of the Study:

  • To investigate the role of NO and GAPDH in yeast apoptosis.
  • To elucidate the mechanism linking NO, GAPDH S-nitrosation, and cell death.

Main Methods:

  • Proteomic, genetic, and biochemical approaches.
  • NO-selective electrode and NOS activity assays.
  • Analysis of GAPDH proteolysis and S-nitrosation.

Main Results:

  • H2O2-induced yeast apoptosis involves NO synthesis with NOS-like activity.
  • GAPDH is proteolyzed and S-nitrosated during apoptosis.
  • Inhibiting NO synthesis reduces GAPDH S-nitrosation, ROS accumulation, and increases survival.
  • NO and GAPDH S-nitrosation also mediate cell death during chronological aging.

Conclusions:

  • NO signaling and GAPDH S-nitrosation are crucial mediators of yeast apoptosis.
  • These pathways play a physiological role in yeast cell death and aging.