APOPTOSIS;
COMPLEX I DEFICIENCY;
DNA REPAIR;
ENERGY METABOLISM;
FANCONI ANEMIA;
GENE MUTATION;
HUMAN;
MITOCHONDRION;
MOLECULAR INTERACTION;
OXIDATION REDUCTION REACTION;
PROTEIN FUNCTION;
PROTEIN PHOSPHORYLATION;
RESPIRATORY FAILURE;
SHORT SURVEY;
Elevated levels of IL-1β in Fanconi anaemia group A patients due to a constitutively active phosphoinositide 3-kinase-Akt pathway are capable of promoting tumour cell proliferation
Ibanez A., et al. Elevated levels of IL-1β in Fanconi anaemia group A patients due to a constitutively active phosphoinositide 3-kinase-Akt pathway are capable of promoting tumour cell proliferation. Biochem. J. 2009, 422:161-170.
New insights into redox response modulation in Fanconi's anemia cells by hydrogen peroxide and glutathione depletors
Cuccarolo P., et al. New insights into redox response modulation in Fanconi's anemia cells by hydrogen peroxide and glutathione depletors. FEBS J. 2012, 279:2479-2494.
Mitochondrial respiratory chain complex I defects in Fanconi anemia complementation group A
Ravera S., et al. Mitochondrial respiratory chain complex I defects in Fanconi anemia complementation group A. Biochimie 2013, 10.1016/j.biochi.2013.06.006.
Changes in vimentin, lamin A/C and mitofilin induces aberrant cell organization in fibroblasts from Fanconi anemia complementation group A (FA-A) patients
Capanni C., et al. Changes in vimentin, lamin A/C and mitofilin induces aberrant cell organization in fibroblasts from Fanconi anemia complementation group A (FA-A) patients. Biochimie 2013, 10.1016/j.biochi.2013.06.024.