Ubiquitylation and the Fanconi anemia pathway
نویسندگان
چکیده
منابع مشابه
Mutated Fanconi anemia pathway in non-Fanconi anemia cancers
An extremely high cancer incidence and the hypersensitivity to DNA crosslinking agents associated with Fanconi Anemia (FA) have marked it to be a unique genetic model system to study human cancer etiology and treatment, which has emerged an intense area of investigation in cancer research. However, there is limited information about the relationship between the mutated FA pathway and the cancer...
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Fanconi anemia (FA), a recessive syndrome with both autosomal and X-linked inheritance, features diverse clinical symptoms, such as progressive bone marrow failure, hypersensitivity to DNA cross-linking agents, chromosomal instability and susceptibility to cancer. At least 12 genetic subtypes have been described (FA-A, B, C, D1, D2, E, F, G, I, J, L, M) and all except FA-I have been linked to a...
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After quite some scientific debate over the last decade, it has become evident that chromosomal instability is a major driving force in the pathogenesis of the vast majority of human cancers [1–3]. In addition, different patterns of chromosomal instability appear to have different clinical implications [4,5]. Yet, unlike for the less common form of genomic instability caused by failing DNA mism...
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Fanconi anemia (FA) represents a paradigm of rare genetic diseases, where the quest for cause and cure has led to seminal discoveries in cancer biology. Although a total of 16 FA genes have been identified thus far, the biochemical function of many of the FA proteins remains to be elucidated. FA is rare, yet the fact that 5 FA genes are in fact familial breast cancer genes and FA gene mutations...
متن کاملRNF4-mediated polyubiquitination regulates the Fanconi anemia/BRCA pathway.
The Fanconi anemia/BRCA (FA/BRCA) pathway is a DNA repair pathway that is required for excision of DNA interstrand cross-links. The 17 known FA proteins, along with several FA-associated proteins (FAAPs), cooperate in this pathway to detect, unhook, and excise DNA cross-links and to subsequently repair the double-strand breaks generated in the process. In the current study, we identified a pati...
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ژورنال
عنوان ژورنال: FEBS Letters
سال: 2011
ISSN: 0014-5793
DOI: 10.1016/j.febslet.2011.04.078