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Related Concept Videos

Apoptosis01:30

Apoptosis

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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...
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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
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Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Mitoptosis, Twenty Years After.

K G Lyamzaev1, D A Knorre1,2, B V Chernyak3

  • 1Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, 119991, Russia.

Biochemistry. Biokhimiia
|March 11, 2021
PubMed
Summary
This summary is machine-generated.

Mitoptosis is the programmed elimination of mitochondria, crucial for cell health and various biological processes. This programmed cell death protects against damaged mitochondria and plays roles in development, aging, and disease.

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Area of Science:

  • Cell Biology
  • Mitochondrial Biology
  • Programmed Cell Death

Background:

  • Mitoptosis, the programmed elimination of mitochondria, was initially proposed to protect cells from damaged mitochondria.
  • A novel mechanism involving mitochondrial clustering and formation of mitoptotic bodies under oxidative stress was identified.
  • Mitoptosis is now recognized to be involved in diverse physiological and pathological processes beyond mitochondrial damage.

Purpose of the Study:

  • To review the multifaceted roles of mitoptosis in cellular and organismal biology.
  • To explore the mechanisms and implications of mitoptosis in both normal and pathological conditions.
  • To highlight the potential of mitoptosis research for therapeutic development.

Main Methods:

  • Literature review and synthesis of existing research on mitoptosis.
  • Analysis of experimental models demonstrating mitoptosis mechanisms, including oxidative stress-induced elimination.
  • Examination of mitoptosis in various biological contexts such as cell differentiation, stem cell maintenance, and inheritance patterns.

Main Results:

  • Mitoptosis is essential for eliminating malfunctioning mitochondria and occurs in processes like cell differentiation and stem cell self-maintenance.
  • Specific mechanisms include perinuclear clustering, mitoptotic body formation, and asymmetric inheritance of mitochondria.
  • Release of mitochondrial components during mitoptosis can mediate intercellular signaling and contribute to inflammatory and autoimmune diseases.
  • Selective elimination of mitochondria with deleterious mutations occurs in mammalian oogenesis.

Conclusions:

  • Mitoptosis is a fundamental cellular process with broad implications for health and disease.
  • Understanding mitoptosis mechanisms is critical for insights into development, aging, and diseases like neurodegeneration.
  • Targeting mitoptosis pathways offers potential therapeutic strategies for various human ailments.