Search results for "Fanconi Anemia Complementation Group D2 Protein"

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FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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Compromised repair of radiation-induced DNA double-strand breaks in Fanconi anemia fibroblasts in G2

2020

Fanconi anemia (FA) is a rare chromosomal instability syndrome with various clinical features and high cancer incidence. Despite being a DNA repair disorder syndrome and a frequently observed clinical hypersensitivity of FA patients towards ionizing radiation, the experimental evidence regarding the efficiency of radiation-induced DNA double-strand break (DSB) repair in FA is very controversial. Here, we performed a thorough analysis of the repair of radiation-induced DSBs in G1 and G2 in FA fibroblasts of complementation groups A, C, D1 (BRCA2), D2, E, F, G and P (SLX4) in comparison to normal human lung and skin fibroblasts. γH2AX, 53BP1, or RPA foci quantification after X-irradiation was…

DNA End-Joining RepairBiologyBiochemistryFanconi Anemia Complementation Group F ProteinHistonesRecombinases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaChromosome instabilitymedicineHumansDNA Breaks Double-StrandedFanconi Anemia Complementation Group G ProteinMolecular BiologyCells Cultured030304 developmental biologyBRCA2 ProteinChromosome Aberrations0303 health sciencesFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinX-RaysCell CycleFanconi Anemia Complementation Group C ProteinRecombinational DNA RepairChromosomeDNACell BiologyFibroblastsCell cyclemedicine.diseaseFanconi Anemia Complementation Group E ProteinComplementationKineticsenzymes and coenzymes (carbohydrates)Fanconi Anemiachemistry030220 oncology & carcinogenesisPremature chromosome condensationMutationCancer researchChromatidTumor Suppressor p53-Binding Protein 1DNADNA Repair
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