Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on curation of immunofluorescence data
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Oligomeric ring structure of the Bloom's syndrome helicase.
Association of the Bloom syndrome protein with topoisomerase IIIalpha in somatic and meiotic cells.
Nuclear structure in normal and Bloom syndrome cells.
Replication protein A physically interacts with the Bloom's syndrome protein and stimulates its helicase activity.
Potent inhibition of werner and bloom helicases by DNA minor groove binding drugs.
Regulation and localization of the Bloom syndrome protein in response to DNA damage.
The Bloom's and Werner's syndrome proteins are DNA structure-specific helicases.
The N-terminal internal region of BLM is required for the formation of dots/rod-like structures which are associated with SUMO-1.
Inhibition of the Bloom's and Werner's syndrome helicases by G-quadruplex interacting ligands.
The Bloom syndrome protein interacts and cooperates with p53 in regulation of transcription and cell growth control.
Colocalization, physical, and functional interaction between Werner and Bloom syndrome proteins.
Telomere-binding protein TRF2 binds to and stimulates the Werner and Bloom syndrome helicases.
Characterization and mutational analysis of the RecQ core of the bloom syndrome protein.
Functional interaction between the Bloom's syndrome helicase and the RAD51 paralog, RAD51L3 (RAD51D).
Stimulation of flap endonuclease-1 by the Bloom's syndrome protein.
Association and regulation of the BLM helicase by the telomere proteins TRF1 and TRF2.
A major role for mitotic CDC2 kinase inactivation in the establishment of the mitotic DNA damage checkpoint.
BLAP75, an essential component of Bloom's syndrome protein complexes that maintain genome integrity.
Physical and functional mapping of the replication protein a interaction domain of the werner and bloom syndrome helicases.
POT1 stimulates RecQ helicases WRN and BLM to unwind telomeric DNA substrates.
MPS1-dependent mitotic BLM phosphorylation is important for chromosome stability.
The Werner and Bloom syndrome proteins catalyze regression of a model replication fork.
Structural and functional analyses of disease-causing missense mutations in Bloom syndrome protein.
Interaction of human SUV3 RNA/DNA helicase with BLM helicase; loss of the SUV3 gene results in mouse embryonic lethality.
Telomeric D-loops containing 8-oxo-2'-deoxyguanosine are preferred substrates for Werner and Bloom syndrome helicases and are bound by POT1.
Systematic analysis of human protein complexes identifies chromosome segregation proteins.
Structure and function of the regulatory HRDC domain from human Bloom syndrome protein.
Rif1 provides a new DNA-binding interface for the Bloom syndrome complex to maintain normal replication.
Crystal structures of RMI1 and RMI2, two OB-fold regulatory subunits of the BLM complex.
Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome.
BLM-DNA2-RPA-MRN and EXO1-BLM-RPA-MRN constitute two DNA end resection machineries for human DNA break repair.
Scaffolding protein SPIDR/KIAA0146 connects the Bloom syndrome helicase with homologous recombination repair.
Role of replication protein A in double holliday junction dissolution mediated by the BLM-Topo IIIα-RMI1-RMI2 protein complex.
Ubiquitin-dependent recruitment of the Bloom syndrome helicase upon replication stress is required to suppress homologous recombination.
hPrimpol1/CCDC111 is a human DNA primase-polymerase required for the maintenance of genome integrity.
Structure of human Bloom's syndrome helicase in complex with ADP and duplex DNA.
The dissolution of double Holliday junctions.
Crystal structure of the Bloom's syndrome helicase indicates a role for the HRDC domain in conformational changes.
A human interactome in three quantitative dimensions organized by stoichiometries and abundances.
A balance between elongation and trimming regulates telomere stability in stem cells.
A helical bundle in the N-terminal domain of the BLM helicase mediates dimer and potentially hexamer formation.
hSSB1 associates with and promotes stability of the BLM helicase.
Functional conservation of RecQ helicase BLM between humans and Drosophila melanogaster.
OpenCell: Endogenous tagging for the cartography of human cellular organization.
The Bloom's syndrome gene product is homologous to RecQ helicases.
The Bloom's syndrome gene product is a 3'-5' DNA helicase.
BLM (the causative gene of Bloom syndrome) protein translocation into the nucleus by a nuclear localization signal.
Bloom's and Werner's syndrome genes suppress hyperrecombination in yeast sgs1 mutant: implication for genomic instability in human diseases.
The Bloom's syndrome helicase unwinds G4 DNA.
Formation of the Flap Intermediate on the C-strand
SUMOylation of BLM with SUMO2,3
Binding of ATR:ATRIP to RPA at resected DNA DSBs
CHEK1 is recruited to resected DNA DSBs
Activation of CHEK1 at resected DNA DSBs
ATR activation at DNA DSBs
BCDX2 complex stabilizes RAD51 filament
CX3 complex binds D-loop structures
EXO1 or DNA2 in complex with BLM or WRN binds initially resected DNA DSBs along with BRIP1 recruitment
Long-range resection of DNA DSBs by EXO1 or DNA2
SPIDR binds BLM:TOP3A:RMI1:RMI2
BLM mediates dissolution of double Holliday junction
MUS81:EME1,EME2 cleaves D-loop
Resolution of D-loops cleaved by MUS81:EME1 or MUS81:EME2
Resolution of Holliday junctions cleaved by GEN1 or SLX1A:SLX4:MUS81:EME1,(MUS81:EME2)
RAD52 promotes single strand annealing at resected DNA DSBs
ERCC1:XPF cleaves flaps generated by SSA
Ligation of DNA and formation of Holliday structures following repair synthesis
Association of RPA complexes with ssDNA at resected DNA DSBs
RAD51 binds BRCA2 at resected DNA DSBs
Association of RAD51 with RAD52:DNA double-strand break ends
Association of RAD52 with the RPA complex at resected DNA DSBs
Cleavage of Holliday junctions by GEN1 or SLX1A:SLX4:MUS81:EME1,(MUS81:EME2)
D-loop dissociation and strand annealing
D-loop extension by DNA polymerases
D-loop formation mediated by PALB2, BRCA2 and RAD51
Defective D-loop formation mediated by PALB2, BRCA2 and RAD51 due to loss-of-function of BRCA1 in PALB2 binding
Defective D-loop formation mediated by PALB2, BRCA2 and RAD51 due to loss-of-function of PALB2 in BRCA1 binding
Defective D-loop formation mediated by PALB2, BRCA2 and RAD51 due to loss-of-function of PALB2 in binding to BRCA2/RAD51/RAD51C
BRCA2 mutants with BRC defects or a defect in the C-terminal RAD51 binding site do not bind RAD51
Defective recruitment of BRCA2 and RAD51 due to loss of BRCA2 function in PALB2 binding
ERCC1:XPF binds DNA DSBs with annealed 3' ssDNA overhangs and displaced flaps generated by SSA