A Boolean network model of the FA/BRCA pathway | Zendy

Alfredo Rodríguez | Zendy; David Sosa | Zendy; Leda Torres | Zendy; Bertha Molina | Zendy; Sara Frı́as | Zendy; Luis Mendoza | Zendy

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A Boolean network model of the FA/BRCA pathway

Author(s) -

Alfredo Rodríguez,

David Sosa,

Leda Torres,

Bertha Molina,

Sara Frı́as,

Luis Mendoza

Publication year - 2012

Publication title -

bioinformatics

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.599

H-Index - 390

eISSN - 1367-4811

pISSN - 1367-4803

DOI - 10.1093/bioinformatics/bts036

Subject(s) - fanconi anemia , dna repair , dna damage , dna , biology , genome instability , cell cycle checkpoint , genetics , cancer research , mutation , microbiology and biotechnology , cancer , computational biology , cell cycle , gene

Fanconi anemia (FA) is a chromosomal instability syndrome originated by inherited mutations that impair the Fanconi Anemia/Breast Cancer (FA/BRCA) pathway, which is committed to the repair of DNA interstrand cross-links (ICLs). The disease displays increased spontaneous chromosomal aberrations and hypersensitivity to agents that create DNA interstrand cross-links. In spite of DNA damage, FA/BRCA-deficient cells are able to progress throughout the cell cycle, probably due to the activity of alternative DNA repair pathways, or due to defects in the checkpoints that monitor DNA integrity.

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