Video Experimental Relacionado
Updated: May 13, 2026
11:58
A Simple, Rapid, and Quantitative Assay to Measure Repair of DNA-protein Crosslinks on Plasmids Transfected into Mammalian Cells
Published on: March 5, 2018
Las oncoproteínas del adenovirus inactivan el complejo de reparación del ADN Mre11-Rad50-NBS1
Travis H Stracker1, Christian T Carson, Matthew D Weitzman
1Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
Nature
|July 19, 2002
Resumen
El complejo Mre11-Rad50-NBS1 es crucial para reparar las rupturas de doble hebra del ADN. Las proteínas del adenovirus E4 inactivan este complejo, impidiendo la formación de concatémero de ADN viral y promoviendo la transformación celular.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Virología Virología.
- Genética La genética.
Sus antecedentes:
- El complejo Mre11-Rad50-NBS1 (MRN) es vital para la reparación del ADN y la estabilidad del genoma en las células de mamíferos.
- La infección por adenovirus puede conducir a la formación de grandes concatémeres de ADN desembalables en ausencia de la región temprana E4 (E4).
Objetivo del estudio:
- Para investigar las proteínas celulares involucradas en la formación de concatémeres de ADN de adenovirus.
- Para entender cómo los productos del adenovirus E4 inactivan estas proteínas celulares durante la infección.
Principales métodos:
- Investigó el papel del complejo Mre11-Rad50-NBS1 en la concatemerización del ADN del adenovirus.
- Analizó la localización y el destino del complejo MRN durante la infección por adenovirus de tipo salvaje.
- Se identificaron oncoproteínas virales responsables de la inactivación del complejo MRN.
Principales resultados:
- Las proteínas funcionales Mre11 y NBS1 son necesarias para la concatemerización del ADN del adenovirus.
- El complejo MRN forma focos adyacentes a los centros de replicación viral.
- La infección por adenovirus de tipo salvaje conduce a la reorganización y degradación del complejo MRN.
- Tres oncoproteínas virales median la inactivación del complejo MRN, evitando la concatemerización.
Conclusiones:
- El adenovirus utiliza oncoproteínas virales para atacar e inactivar el complejo MRN de la célula huésped, un actor clave en la estabilidad genómica.
- Este mecanismo de inactivación previene la formación de concatémero de ADN viral y puede contribuir a la transformación de "golpe y fuga" mediada por el adenovirus.
Videos de Conceptos Relacionados
01:08Nucleotide Excision Repair
Overview
01:08Nucleotide Excision Repair
Overview
02:36DNA 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...
02:31Homologous Recombination
The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
01:38Nucleotide Excision Repair
DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
02:36DNA 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...