Results 131 to 140 of about 7,414 (159)
Medulloblastoma in children with Fanconi anemia: Association with FA-D1/FA-N, SHH type and poor survival independent of treatment strategies. [PDF]
Sönksen M +17 more
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Mutagenesis of the PALB2 WD40 domain identifies variants defective in interaction with BRCA2 and DNA repair. [PDF]
Gomes TT +12 more
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Deubiquitomic and bioinformatic analyses in cisplatin-treated lung cancer cells. [PDF]
Jin SK +4 more
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Comprehensive genetic and epigenetic characterization of Lynch-like syndrome patients. [PDF]
Pirini F +18 more
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The Fanconi Anemia Complementation Group A Protein Contains a Peroxidase Domain
Molecular Genetics and Metabolism, 1998Computational analysis of the Fanconi anemia (FA) complementation group A protein suggests that it contains a peroxidase domain. FA proteins may be part of a general mechanism that protects cells from oxidative damage.
I S, Mian, M J, Moser
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Biochemical and Biophysical Research Communications, 1999
The function of the Fanconi anemia complementation group A (FANCA) protein remains unclear. To investigate possible protein-protein interactions, we performed yeast two-hybrid screening using a FANCA fragment as bait. Sorting nexin 5 (SNX5), a new member of the human SNX family, was identified as a putative FANCA-binding protein.
T, Otsuki +3 more
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The function of the Fanconi anemia complementation group A (FANCA) protein remains unclear. To investigate possible protein-protein interactions, we performed yeast two-hybrid screening using a FANCA fragment as bait. Sorting nexin 5 (SNX5), a new member of the human SNX family, was identified as a putative FANCA-binding protein.
T, Otsuki +3 more
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Intracellular Localization of the Fanconi Anemia Complementation Group A Protein
Biochemical and Biophysical Research Communications, 1999Mutations in the Fanconi anemia (FA) complementation group A (FANCA) gene leads to bone marrow failure, developmental abnormalities and cancer predisposition. To map the intracellular site of FANCA, we constructed a plasmid vector which linked in-frame the enhanced green fluorescent protein (EGFP cDNA) to the 5' end of the FANCA cDNA (pDAS-3).
C E, Walsh, M R, Yountz, D A, Simpson
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Molecular Genetics and Metabolism, 2001
Fanconi anemia (FA) is an autosomal recessive disorder manifested by chromosomal breakage, birth defects, and susceptibility to bone marrow failure and cancer. At least seven complementation groups have been identified, and the genes defective in four groups have been cloned. The most common subtype is complementation group A.
J, Ren, H, Youssoufian
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Fanconi anemia (FA) is an autosomal recessive disorder manifested by chromosomal breakage, birth defects, and susceptibility to bone marrow failure and cancer. At least seven complementation groups have been identified, and the genes defective in four groups have been cloned. The most common subtype is complementation group A.
J, Ren, H, Youssoufian
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Experimental Hematology, 2015
Bone marrow failure in Fanconi anemia (FA) has been linked in part to overproduction of inflammatory cytokines, to which FA stem and progenitor cells are hypersensitive. In cell lines and murine models p38 mitogen-activated protein kinase (MAPK)-dependent tumor necrosis factor α (TNF-α) overexpression can be induced by the Toll-like receptors (TLRs) 4 ...
Johanna, Svahn +10 more
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Bone marrow failure in Fanconi anemia (FA) has been linked in part to overproduction of inflammatory cytokines, to which FA stem and progenitor cells are hypersensitive. In cell lines and murine models p38 mitogen-activated protein kinase (MAPK)-dependent tumor necrosis factor α (TNF-α) overexpression can be induced by the Toll-like receptors (TLRs) 4 ...
Johanna, Svahn +10 more
openaire +2 more sources

