title: Advances in the understanding of Fanconi Anemia Complementation Group D2 Protein (FANCD2) in human cancer.
abstract: Fanconi anemia (FA) is a rare human genetic disease, resulting from dysfunction in any of 17 known complementation proteins: FANC-A, B, C, D1, D2, E, F, G, I, J, L, M, N, O, P, Q & S, and other unknowns. Besides the severe bone marrow failure, an extremely high incidence of cancer as well as many other clinic symptoms associated with FA patients, FA cells are known of insufficiency in homologous recombination, DNA mismatch repair, nucleotide excision repair, translesion DNA synthesis, and other molecular defects, leading to genome instability. Those similar molecular and cellular/tissue features show that all FA proteins function in one common signaling pathway, namely, the FA pathway. The monoubiquitination of FANCD2 is the central step of the FA pathway activation upon DNA damage or during DNA replication. The molecular functions of FANCD2 emerge as a very attractive filed of investigation in cancer research. Herein, we review the recent progresses in FANCD2 functions at these rapidly progressed aspects.
authors.affiliation: Divisions of Cancer Biology University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA.
authors.forename: Yihang
authors.initials: Y
authors.lastname: Shen
authors.affiliation: Department of Laboratory Medicine and Pathology, Mayo Clinic, MN, USA.
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Divisions of Epidemiology, University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA.
authors.forename: Herbert
authors.initials: H
authors.lastname: Yu
authors.affiliation: Divisions of Cancer Biology University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA.
authors.forename: Peiwen
authors.initials: P
authors.lastname: Fei
keywords: DNA damage; FANCD2; Gain of Function; Replication; Tumor cell sensitivity