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ProteomicsCrosslinking/mass spectrometry analysis of Fanconi anemia (FA) pathway FANCD2-FANCI complexes
DNA interstrand crosslinks (ICLs) are repaired by the Fanconi anemia (FA) pathway. The FA pathway is activated by phosphorylation of FANCI in FANCD2-FANCI complex. To investigate how phosphorylation regulates FA pathway activation and function, recombinant FANCD2-FANCI complexes prepared using eithe...
ORGANISM(S): Cellular Organisms 
2022-11-18 | PXD031632 | JPOST Repository
TranscriptomicsFanconi anemia proteins interact with CtBP1 and modulate the expression of the Wnt antagonist Dickkopf-1
Fanconi anemia (FA) is a genetic disorder characterized by congenital abnormalities, bone marrow failure and increased susceptibility to cancer. Of the fifteen FA proteins, Fanconi anemia group C (FANCC) is one of eight FA core complex components of the FA pathway. Unlike other FA core complex prote...
ORGANISM(S): Homo sapiens 
2013-04-05 | E-GEOD-43330 | biostudies-arrayexpress
GenomicsWhole-exome sequencing of Fanconi anemia
We performed whole-exome sequencing of two Fanconi anemia patients without mutation of known FA genes, and identified a novel FA gene FANCT.
EGAS00001001103 | EGA
TranscriptomicsOxymetholone therapy of Fanconi anemia suppresses osteopontin transcription and induces hematopoietic stem cell cycling
We used Fancd2-/- mice to understand its mechanism of action. Transcriptome analysis of cKit+ Sca1+ Lin- (KSL) cells discovered that only four genes changed their expression levels significantly after chronic OXM administration in both Fancd2−/− and wild-type mice: mKi67 and Cenpf were up-regualted ...
ORGANISM(S): Mus musculus 
2015-01-06 | E-GEOD-58724 | biostudies-arrayexpress
ModelsFanconi anemia and checkpoint recovery
The FA/BRCA pathway repairs DNA interstrand crosslinks. Mutations in this pathway cause Fanconi anemia (FA), a chromosome instability syndrome with bone marrow failure and cancer predisposition. Upon DNA damage, normal and FA cells inhibit the cell cycle progression, until the G2/M checkpoint is tur...
4790 | Cell Collective
ProteomicsPLK1 inhibition induces synthetic lethality in Fanconi anemia pathway-deficient acute myeloid leukemia
Overall survival of acute myeloid leukemia (AML) remains limited. Inhibitors of the master mitotic kinase PLK1 have emerged as promising therapeutics, demonstrating efficacy in an undefined subset of AML patients. However, the clinical success of PLK1 inhibitors remains hindered by a lack of predict...
ORGANISM(S): Homo Sapiens (ncbitaxon:9606) 
2024-12-09 | MSV000096625 | MassIVE
TranscriptomicsGene expression based identification of potential genes involved in Fanconi anemia
Fanconi anemia is a rare inherited hematological disorder which commonly presents with bone marrow failure, developmental abnormalities and susceptibility to cancer with high rates of prevalence in ethnic populations. The objective of this study was to identify potential genes that aid in the progr...
ORGANISM(S): Homo sapiens 
2010-06-24 | E-GEOD-17233 | biostudies-arrayexpress
ProteomicsDual role of PCNA-monoubiquitination in facilitating Fanconi Anemia-mediated interstrand crosslink repair
The Fanconi Anemia (FA) repair pathway governs the repair of highly genotoxic DNA interstrand crosslinks (ICLs) with the assistance of translesion synthesis (TLS), that is facilitated by site-specific monoubiquitination of PCNA (PCNA-Ub) at lysine 164 (K164). Mutation at this residue (K164R) renders...
ORGANISM(S): Mus musculus (Mouse) 
2024-08-09 | PXD035337 | Pride
Lc-msms Rime Interstrand crosslink repair Mouse Dna damage tolerance Mismatch repair Fanconi anemia Pcna ubiquitination 
GenomicsFANCD2 Activates Transcription of TAp63 and Suppresses Tumorigenesis
Fanconi Anemia (FA) is a rare genetic disorder characterized by an increased susceptibility to squamous cell cancers. Fifteen FA genes are known, and the encoded proteins cooperate in a common DNA repair pathway. A critical step is the monoubiquitination of the FANCD2 protein, and cells from most...
ORGANISM(S): Homo sapiens 
2013-06-27 | E-GEOD-46902 | biostudies-arrayexpress
ProteomicsCooperation of the NEIL3 and Fanconi Anemia/BRCA Pathways in Interstrand Crosslink Repair
The NEIL3 DNA glycosylase is a base excision repair enzyme that excises bulky base lesions from DNA. Although NEIL3 has been shown to unhook interstrand crosslinks (ICL) in Xenopus extracts, how NEIL3 participants in ICL repair in human cells and its corporation with the canonical Fanconi anemia (FA...
ORGANISM(S): Homo sapiens (Human) 
2020-01-20 | PXD016256 | Pride
Neil3 Psoralen interstrand crosslink Fanconi anemia 
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