Fanconi anemia protein FANCD2 inhibits TRF1 polyADP-ribosylation through tankyrase1-dependent manner
Lyakhovich, Alex (Universitat Autònoma de Barcelona. Departament de Genètica i de Microbiologia)
Ramírez de Haro, Ma. José (Duke-NUS Graduate Medical School. Cancer and Stem Cell Research Program)
Castellanos, Andrés (Universitat Autònoma de Barcelona. Departament de Genètica i de Microbiologia)
Castellà, Maria (Universitat Autònoma de Barcelona. Departament de Genètica i de Microbiologia)
Simons, A. M. (Harvard Medical School. Department of Pathology)
Parvin, J. D. (Harvard Medical School. Department of Pathology)
Surrallés i Calonge, Jordi (Universitat Autònoma de Barcelona. Departament de Genètica i de Microbiologia)

Date:	2011
Abstract:	Background: Fanconi anemia (FA) is a rare autosomal recessive syndrome characterized by developmental abnormalities, progressive bone marrow failure, and predisposition to cancer. The key FA protein FANCD2 crosstalks with members of DNA damage and repair pathways that also play a role at telomeres. Therefore, we investigated whether FANCD2 has a similar involvement at telomeres. Results: We reveal that FANCD2 may perform a novel function separate to the FANCD2/BRCA pathway. This function includes FANCD2 interaction with one of the telomere components, the PARP family member tankyrase-1. Moreover, FANCD2 inhibits tankyrase-1 activity in vitro. In turn, FANCD2 deficiency increases the polyADP-ribosylation of telomere binding factor TRF1. Conclusions: FANCD2 binding and inhibiting tankyrase-1PARsylation at telomeres may provide an additional step within the FA pathway for the regulation of genomic integrity.
Rights:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Language:	Anglès
Document:	Article ; Versió publicada
Published in:	Genome integrity, Vol. 2, N. 4 (February 2011) , p. 1-10, ISSN 2041-9414

DOI: 10.1186/2041-9414-2-4
PMID: 21314979

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