Se requiere AID para las rupturas cromosómicas en c-myc que conducen a translocaciones c-myc/IgH
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Recombinant Retroviral Production and Infection of B Cells
Published on: February 19, 2011
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Davide F Robbiani1, Anne Bothmer, Elsa Callen
1Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.
Cell
|December 17, 2008
Resumen
La desaminasa citidina inducida por activación (AID) causa roturas de ADN en el oncogén c-myc, lo que lleva a translocaciones. Esta enzima es crucial para el daño oncogénico, no solo las mutaciones genéticas de anticuerpos.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Genética La genética.
- Investigación del cáncer Investigación del cáncer.
Sus antecedentes:
- Las translocaciones cromosómicas, como la translocación c-myc / IgH en el linfoma de Burkitt, son impulsadas por roturas de doble cadena de ADN (DSB) en diferentes cromosomas.
- Se sabe que la desaminasa citidina inducida por activación (AID) causa DSB en los genes de cadena pesada de inmunoglobulina (IgH) durante la diversificación de anticuerpos.
Objetivo del estudio:
- Para investigar la fuente de las rupturas de ADN en el locus oncogénico del c-myc.
- Para determinar si AID es responsable de generar DSBs en c-myc que contribuyen a las translocaciones c-myc/IgH.
Principales métodos:
- Los experimentos se llevaron a cabo utilizando linfocitos B primarios.
- Se evaluó el papel de la región promotora c-myc en la orientación del daño del ADN.
- Se analizaron los daños en el ADN mediados por AID y la posterior formación de DSB.
Principales resultados:
- La evidencia indica que la región promotora c-myc es esencial para dirigir el daño al ADN mediado por AID.
- Las DSB se producen en el gen c-myc, facilitando las translocaciones c-myc/IgH.
- El papel de la AID se extiende más allá de los genes de anticuerpos para incluir lesiones oncogénicas.
Conclusiones:
- La región promotora de c-myc apunta a AID para inducir DSBs en c-myc.
- La AID es responsable de las lesiones del ADN en los oncogenes, iniciando translocaciones.
- Este hallazgo amplía la comprensión de la función de AID en la oncogénesis y el daño al ADN.
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