Fanconi Anemia Group D2 Protein Participates in Replication Origin FiringPanneerselvam J1, Shen Y1, Che R1,2 and Fei P1,2*
- *Corresponding Author:
- Peiwen Fei
University of Hawaii Cancer Center
701Ilalo Street, USA
E-mail: [email protected]
Received date: April 21, 2016; Accepted date: June 09, 2016; Published date: June 14, 2016
Citation: Panneerselvam J, Shen Y, Che R, Fei P (2016) Fanconi Anemia Group D2 Protein Participates in Replication Origin Firing. Chemo Open Access 5:206. doi:10.4172/2167-7700.1000206
Copyright: © 2016 2016 Panneerselvam J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In the past decade, our laboratory has been greatly interested in studying the Fanconi Anemia (FA) signaling pathway [1-5]. This interest stems from the ability of the FA pathway to maintain genome stability and suppress tumorigenesis. Oncogenic proliferation occurs without sufficient nucleotides to support DNA replication, resulting in replication failure at common fragile sites and leads to the formation of double-strand DNA breaks . The failure in correctly sensing or rescuing stalled replication intermediates is one of underlying causes of several chromosomal instability syndromes such as FA. It is an inherited disorder characterized by congenital abnormalities, bone marrow failure, and cancer proneness . However, much remains unknown regarding how the FA pathway acts under normal conditions and about the manners by which FA proteins contribute a proper progression among individual phases of cell cycle. Moreover, any insight into the FA pathway is important because such insight could lead to understanding of how genomic instability occurs . We expect that the knowledge from understanding this pathway will provide valuable information leading to building up effective tools for cancer prevention as well as therapy.