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Videos de Conceptos Relacionados

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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Video Experimental Relacionado

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 regula la función mitocondrial y la vía de respuesta al daño del ADN.

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
Resumen

Los ratones que carecen de Bmi1 muestran una función mitocondrial deteriorada y un aumento del estrés oxidativo, lo que lleva a daños en el ADN. El tratamiento con antioxidantes o el bloqueo de las vías de reparación del ADN mejoraron estos ratones con deficiencia de Bmi1.

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Last Updated: May 7, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
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Published on: September 28, 2012

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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

Área de la Ciencia:

  • Biología de las células madre Biología de las células madre
  • Biología molecular La biología molecular.
  • La función mitocondrial tiene su función mitocondrial.

Sus antecedentes:

  • El represor de policombos Bmi1 es crucial para la auto-renovación y el desarrollo de las células madre.
  • La deficiencia de Bmi1 conduce a la desrepresión del locus Ink4a/Arf, causando anormalidades del desarrollo.
  • Los mecanismos precisos que subyacen al papel de Bmi1 en estos procesos no se comprenden completamente.

Objetivo del estudio:

  • Para investigar el papel de Bmi1 en el metabolismo celular y el daño del ADN.
  • Explorar el impacto de la deficiencia de Bmi1 en la función mitocondrial y las especies reactivas de oxígeno (ROS).
  • Para determinar si la orientación hacia las vías de disfunción mitocondrial o daño en el ADN puede rescatar fenotipos deficientes en Bmi1.

Principales métodos:

  • Análisis de células derivadas de ratones con deficiencia de Bmi1 (Bmi1(-/-).
  • Evaluación de la función mitocondrial y los niveles intracelulares de ROS.
  • Tratamiento farmacológico con N-acetilcisteína (antioxidante) y eliminación genética de Chk2 (vía de respuesta al daño del ADN).

Principales resultados:

  • Las células Bmi1(-/-) muestran deterioro de la función mitocondrial y niveles elevados de ROS.
  • El aumento de ROS desencadena las vías de respuesta al daño del ADN en las células deficientes en Bmi1.
  • El tratamiento con N-acetilcisteína o la deleción de Chk2 mejoró muchas de las deficiencias asociadas con Bmi1 ((-/-)).

Conclusiones:

  • Bmi1 juega un papel inesperado en el mantenimiento de la función mitocondrial y la homeostasis redox.
  • El metabolismo celular está regulado coordinadamente por las proteínas Polycomb junto con las funciones de las células madre y progenitoras.
  • Dirigirse a las vías de disfunción mitocondrial y daño del ADN ofrece estrategias terapéuticas potenciales para los trastornos relacionados con Bmi1.