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Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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Related Experiment Video

Updated: May 7, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Bmi1 regulates mitochondrial function and the DNA damage response pathway.

Jie Liu1, Liu Cao1, Jichun Chen2

  • 1Translational Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Nature
|May 1, 2009
PubMed
Summary
This summary is machine-generated.

Mice lacking Bmi1 show impaired mitochondrial function and increased oxidative stress, leading to DNA damage. Antioxidant treatment or blocking DNA repair pathways improved these Bmi1-deficient mice.

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High-Throughput Image-Based Quantification of Mitochondrial DNA Synthesis and Distribution

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Related Experiment Videos

Last Updated: May 7, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

High-Throughput Image-Based Quantification of Mitochondrial DNA Synthesis and Distribution
10:47

High-Throughput Image-Based Quantification of Mitochondrial DNA Synthesis and Distribution

Published on: May 5, 2023

Area of Science:

  • Stem cell biology
  • Molecular biology
  • Mitochondrial function

Background:

  • Polycomb repressor Bmi1 is crucial for stem cell self-renewal and development.
  • Bmi1 deficiency leads to Ink4a/Arf locus de-repression, causing developmental abnormalities.
  • The precise mechanisms underlying Bmi1's role in these processes are not fully understood.

Purpose of the Study:

  • To investigate the role of Bmi1 in cellular metabolism and DNA damage.
  • To explore the impact of Bmi1 deficiency on mitochondrial function and reactive oxygen species (ROS).
  • To determine if targeting mitochondrial dysfunction or DNA damage pathways can rescue Bmi1-deficient phenotypes.

Main Methods:

  • Analysis of cells derived from Bmi1-deficient (Bmi1(-/-)) mice.
  • Assessment of mitochondrial function and intracellular ROS levels.
  • Pharmacological treatment with N-acetylcysteine (antioxidant) and genetic deletion of Chk2 (DNA damage response pathway).

Main Results:

  • Bmi1(-/-) cells exhibit impaired mitochondrial function and elevated ROS levels.
  • Increased ROS triggers DNA damage response pathways in Bmi1-deficient cells.
  • N-acetylcysteine treatment or Chk2 deletion ameliorated many Bmi1(-/-) associated deficiencies.

Conclusions:

  • Bmi1 plays an unexpected role in maintaining mitochondrial function and redox homeostasis.
  • Cellular metabolism is coordinately regulated by Polycomb proteins alongside stem and progenitor cell functions.
  • Targeting mitochondrial dysfunction and DNA damage pathways offers potential therapeutic strategies for Bmi1-related disorders.