1: FEBS Lett. 2005 Aug 29;579(21):4610-4. 

Defective binding of transcriptional repressor ZEB via DNA methylation
contributes to increased constitutive levels of p73 in Fanconi anemia cells.

Pipaon C, Real PJ, Fernandez-Luna JL.

Unidad de Genetica Molecular, Hospital Universitario Marques de Valdecilla,
Edificio Escuela Universitaria de Enfermeria, Servicio Cantabro de Salud, Av.
Valdecilla s/n, 39008 Santander, Spain.

Little is known about the molecular mediators of the Fanconi anemia (FA) pathway
involved in the machinery that maintains genomic integrity. Here, we report that
the levels of p73 and its target genes, are increased in cells derived from FA
patients belonging to complementation group A (FA-A). Moreover, functional
correction of FA-A cells by gene transfer reduces the expression of p73. We also
demonstrate that DNA methylation contributes to increased levels of p73 in FA-A
cells by hampering the binding of the transcriptional repressor ZEB to an
intronic regulatory region of the p73 gene. Together, our data may help explain
the susceptibility of these cells to DNA damaging agents.

PMID: 16087177 [PubMed - indexed for MEDLINE]


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