Affinage

BLM

RecQ-like DNA helicase BLM · UniProt P54132

Length
1417 aa
Mass
159.0 kDa
Annotated
2026-06-09
100 papers in source corpus 59 papers cited in narrative 59 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 10/10 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BLM is an ATP-dependent 3'→5' DNA helicase that safeguards genome stability by processing and dissolving recombination and replication intermediates (PMID:9840919, PMID:22885301). As the catalytic core of the BLM-TOP3A-RMI (BTR) dissolvasome, it enables TOP3A-mediated single-stranded DNA decatenation to dissolve double Holliday junctions and topologically linked intermediates into noncrossover products, thereby suppressing crossover (sister-chromatid exchange) formation (PMID:20445207, PMID:35119917). BLM operates in two end-resection machineries that generate 3'-ssDNA for homologous recombination: it partners with DNA2-RPA-MRN, where its helicase activity unwinds DNA for DNA2-mediated resection under RPA-enforced polarity, and it stimulates EXO1 nuclease activity through a direct, helicase-independent interaction (PMID:21325134, PMID:18971343). Single-molecule analyses establish that BLM functions as a monomer, unwinding long duplex tracts and repetitively "measuring" and re-initiating, with RPA required for reinitiation (PMID:19165145, PMID:22885301, PMID:31544923). BLM has dual recombination roles—its anti-recombinase activity counteracts RAD51 loading, and RAD51-coated DNA in turn blocks BLM translocation, defining a reciprocal regulatory boundary (PMID:28912125, PMID:31544923). Beyond duplex DNA, BLM resolves G-quadruplexes via cooperativity between its RQC and HRDC domains, unwinds R-loops to suppress transcription-associated instability, and unwinds RNA G-quadruplexes to regulate cytoplasmic stress granules (PMID:25418155, PMID:29042409, PMID:37503837). BLM is recruited to ultrafine anaphase bridges and centromeric DNA threads—via PICH—to complete sister-chromatid decatenation, and its centromeric unwinding is restrained by PLK1 to preserve centromere integrity (PMID:17599064, PMID:21743438, PMID:31253795). BLM activity, stability, and localization are governed by an extensive network of post-translational modifications, including ATM/CDK1/MPS1/PLK1 phosphorylation, MIB1-mediated ubiquitination antagonized by USP37 and TopBP1, SUMOylation that switches its pro- versus anti-recombinogenic roles, and AARS1-mediated lactylation (PMID:19956565, PMID:12034743, PMID:16864798, PMID:24239288, PMID:34606619, PMID:35119917, PMID:40634292). BLM is cleaved by caspase 3 during apoptosis, abolishing its nuclear foci without eliminating helicase activity (PMID:11154689). Catalytically inactivating point mutations found in Bloom syndrome cells abolish ATPase and helicase activities and fail to correct the cellular phenotype, establishing these enzymatic activities as essential to its genome-maintenance function (PMID:9840919).

Mechanistic history

Synthesis pass · year-by-year structured walk · 26 steps
  1. 1998 High

    Established the core enzymatic identity of BLM as an ATP-dependent 3'→5' helicase and tied this activity directly to disease, answering whether catalytic activity underlies its genome-protective role.

    Evidence In vitro ATPase/helicase assays with murine BLM and site-directed mutagenesis of Bloom syndrome point mutations

    PMID:9840919

    Open questions at the time
    • Did not define physiological substrates
    • Oligomeric state and translocation mechanism unresolved
  2. 2001 High

    Mapped the BLM-TopoIIIα interaction to the N-terminus and linked it to recombination suppression and PML nuclear body targeting, beginning definition of the dissolvasome.

    Evidence GFP-BLM deletion constructs, co-IP, and SCE measurement in Bloom syndrome cells

    PMID:11406610

    Open questions at the time
    • Did not establish biochemical mechanism of HR-intermediate dissolution
    • RMI1/2 contribution not yet defined
  3. 2010 High

    Defined the BTR dissolvasome mechanism by showing BLM-RMI1 specifically stimulates TopoIIIα single-stranded DNA decatenase activity to process HR intermediates without crossover.

    Evidence In vitro decatenation assays with purified human BLM, TOP3A, RMI1 on ssDNA catenanes

    PMID:20445207

    Open questions at the time
    • Did not address regulation of dissolvasome activity in vivo
    • Coupling to replication/anaphase timing unresolved
  4. 2008 High

    Placed BLM in two parallel end-resection pathways for HR, resolving how it generates 3'-ssDNA: by stimulating EXO1 nuclease via direct helicase-independent interaction and through evolutionarily conserved DSB processing parallel to EXO1.

    Evidence In vitro nuclease stimulation and strand-exchange assays plus yeast/human genetic epistasis

    PMID:18923075 PMID:18971343

    Open questions at the time
    • Did not define the BLM-DNA2 branch in detail
    • Helicase-dependent versus -independent contributions not fully separated
  5. 2011 High

    Reconstituted the BLM-DNA2-RPA-MRN resection machinery, showing RPA enforces resection polarity and MRN recruits BLM to ends, mechanistically dissecting the helicase and nuclease division of labor.

    Evidence Biochemical reconstitution with purified human proteins and in vitro resection assays

    PMID:21325134

    Open questions at the time
    • Did not address regulation of pathway choice in cells
    • CtIP contribution defined later
  6. 2007 High

    Linked BLM to mitotic fidelity by showing it localizes to anaphase ultrafine bridges and centromeric threads with TopoIIIα to complete sister-chromatid decatenation.

    Evidence Live imaging and immunofluorescence in BLM-deficient vs. corrected cells with PICH/TopoIIIα co-localization

    PMID:17599064

    Open questions at the time
    • Recruitment mechanism to UFBs not yet defined
    • Did not establish how threads are kept nucleosome-free
  7. 2011 High

    Identified PICH as the direct factor recruiting BLM to anaphase centromeric threads and keeping them nucleosome-free, explaining how BLM accesses anaphase substrates.

    Evidence Co-IP, RNAi phenotyping of anaphase threads, and in vitro nucleosome-remodeling assay with purified PICH

    PMID:21743438

    Open questions at the time
    • Did not define the helicase substrate at threads
    • Coordination with decatenation timing unresolved
  8. 2002 High

    Revealed substrate preferences of BLM, showing it preferentially unwinds G4 DNA over Holliday junctions, mapping this preference to the central helicase domain.

    Evidence In vitro helicase assays with G4 and HJ substrates, inhibitor (NMM) studies, and domain mapping

    PMID:12235379

    Open questions at the time
    • Did not resolve domain-level G4 recognition
    • In vivo relevance of G4 unwinding not addressed
  9. 2014 High

    Defined the molecular basis of G4 recognition through RQC-HRDC domain cooperativity and ATP-dependent unfolding, and showed mechanism depends on structural context.

    Evidence Single-molecule FRET with RQC/HRDC domain mutants on defined G4 substrates

    PMID:25418155 PMID:25897130

    Open questions at the time
    • Did not link domain mechanism to specific genomic loci
    • Regulation of G4 unwinding by partners not addressed
  10. 2012 High

    Resolved the catalytic oligomeric state, demonstrating BLM functions as a monomer that dissociates from multimers upon ATP hydrolysis to unwind diverse substrates.

    Evidence Dynamic light scattering, stopped-flow kinetics, and helicase assays on multiple substrates

    PMID:22885301

    Open questions at the time
    • Did not address whether oligomeric forms have regulatory roles
    • Behavior on chromatin substrates not tested
  11. 2009 High

    Visualized the unwinding mechanism directly, showing BLM performs repetitive 'measuring' unwinding with strand switching and requires RPA interaction for reinitiation.

    Evidence Single-molecule FRET on forked substrates comparing wild-type and interaction-deficient BLM

    PMID:19165145

    Open questions at the time
    • Biological purpose of repetitive unwinding unresolved
    • Did not test complex recombination substrates at single-molecule level
  12. 2019 High

    Established BLM as a long-range processive helicase and defined the reciprocal anti-recombinase boundary: BLM cannot translocate on RPA-coated ssDNA or RAD51-coated dsDNA.

    Evidence Single-molecule DNA curtain imaging on RPA- and RAD51-coated substrates

    PMID:31544923

    Open questions at the time
    • Did not address how filament displacement is regulated in cells
    • Cooperation versus antagonism with RPA context-dependent
  13. 2020 High

    Clarified RPA's activating role, showing RPA enables bidirectional BLM unwinding of nicked DNA via targeting independent of direct BLM-RPA contacts.

    Evidence Single-molecule force spectroscopy and fluorescence on nicked dsDNA with/without RPA

    PMID:32101168

    Open questions at the time
    • Reconciliation with RPA-blocking observations not fully resolved
    • Physiological nicked-substrate contexts not defined
  14. 2017 Medium

    Demonstrated BLM's anti-recombinase activity is a tumor-relevant liability, showing its loss restores RAD51 stability and HR in BRCA-deficient cells.

    Evidence CRISPR BLM ablation in BRCA1/2/XRCC2-mutant cells with RAD51 foci, SCE, HR, and survival readouts

    PMID:28912125

    Open questions at the time
    • Single-lab genetic epistasis
    • Direct biochemical demonstration of RAD51 displacement in this context not shown
  15. 2017 High

    Extended BLM-DNA2 resection by identifying CtIP as a stimulator of BLM helicase activity, broadening CtIP's role beyond MRE11 in long-range resection.

    Evidence Reconstitution with purified proteins, helicase and DNA2 cleavage stimulation assays

    PMID:29020620

    Open questions at the time
    • Single lab
    • In vivo regulation of CtIP-BLM coupling not addressed
  16. 2017 Medium

    Mechanistically connected BLM to R-loop suppression by showing BLM resides near DNA:RNA hybrids and unwinds R-loops to prevent transcription-associated instability.

    Evidence BLM depletion, S9.6 immunofluorescence, proximity ligation, in vitro R-loop unwinding, and yeast genetics

    PMID:29042409

    Open questions at the time
    • Single lab
    • Direct in vivo demonstration of R-loop resolution at endogenous loci limited
  17. 2002 High

    Resolved how DNA damage signaling controls BLM, showing ATM directly binds and phosphorylates it (Thr-99) selectively for the DNA damage response but not SCE suppression.

    Evidence Co-IP, phosphospecific antibody, and phosphomutant rescue of radiosensitivity vs. SCE in BS cells

    PMID:11146546 PMID:12034743

    Open questions at the time
    • Did not define downstream effectors of phospho-BLM
    • Structural basis of ATM recognition not addressed
  18. 2006 High

    Established mitotic phospho-regulation by MPS1 at Ser144, creating a PLK1 docking site required for accurate chromosome segregation.

    Evidence Phospho-peptide MS, co-IP with PLK1 polo-box, and phosphomutant chromosome-count analysis

    PMID:16864798

    Open questions at the time
    • Did not define how phospho-BLM acts in segregation mechanistically
    • Interplay with other mitotic kinases unresolved
  19. 2013 High

    Defined cell-cycle-controlled BLM proteostasis, showing MIB1 ubiquitinates BLM for G1 degradation while TopBP1 stabilizes it in S-phase to prevent untimely resection.

    Evidence Co-IP, ubiquitination assays, TopBP1/MIB1 depletion, and undegradable-mutant radiosensitivity readouts

    PMID:24239288

    Open questions at the time
    • Did not define the phospho-degron recognized
    • Resolved structurally in later work
  20. 2017 High

    Provided the structural basis of TopBP1-BLM recognition, showing BRCT5 reads BLM phospho-Ser304 via a conserved pocket and FVPP motif.

    Evidence Crystal structure of TopBP1 BRCT4/5-BLM peptide complex with mutational validation

    PMID:28919440

    Open questions at the time
    • Did not capture full-length complex
    • Upstream kinase generating pSer304 not defined here
  21. 2009 High

    Defined SUMOylation as a molecular switch controlling BLM's pro- versus anti-recombinogenic activity by promoting RAD51 interaction at damaged forks.

    Evidence In vitro SUMO interaction assays and SUMO-mutant cell lines with RAD51 foci, SCE, and HR readouts

    PMID:19956565

    Open questions at the time
    • SUMO ligase and acceptor sites not fully defined
    • Mechanism of RAD51-interaction switch unresolved
  22. 2022 High

    Integrated mitotic kinase signaling, showing a CDK1-TOPBP1-PLK1 feedback loop phosphorylates BLM to stimulate BTR dissolution and enforce crossover avoidance.

    Evidence In vitro phosphorylation/dissolution assays and cellular epistasis of CDK1/PLK1/TOPBP1

    PMID:35119917

    Open questions at the time
    • Phospho-site mapping on dissolution incomplete
    • Spatial coordination with anaphase resolution not addressed
  23. 2021 Medium

    Identified USP37 as the deubiquitinase that opposes MIB1, stabilizing BLM in an ATM-stimulated manner to sustain DSB repair.

    Evidence Co-IP, in vivo/in vitro deubiquitination assays, ATM phosphorylation analysis, USP37 knockdown

    PMID:34606619

    Open questions at the time
    • Single lab
    • Ubiquitin chain types removed not fully characterized
  24. 2025 Medium

    Added lactylation as a metabolic input controlling BLM, showing AARS1-mediated Lys24 lactylation blocks MIB1 ubiquitination, stabilizing BLM and promoting HR and chemoresistance.

    Evidence Global lactylome, co-IP, ubiquitination and HR assays with Lys24 mutants

    PMID:40634292

    Open questions at the time
    • Single lab
    • How Lys24 lactylation enhances repair-factor interactions mechanistically unresolved
  25. 2001 High

    Defined a death-pathway regulation, showing caspase 3 cleaves BLM at Asp415 to disrupt its nuclear foci and matrix association without abolishing helicase activity.

    Evidence In vitro caspase cleavage, cleavage-site mutagenesis, and immunofluorescence

    PMID:11154689

    Open questions at the time
    • Physiological significance of cleavage fragments unresolved
    • Did not address apoptotic timing in vivo
  26. 2025 Medium

    Distinguished gap resection from DSB resection, showing DNA2-WRN/BLM resects 5' ends of ssDNA gaps independent of MRN-CtIP, with consequences for PARPi-treated BRCA1-deficient cells.

    Evidence Single-molecule DNA fiber, electron microscopy, biochemical resection assays, BRCA1-deficient epistasis

    PMID:40127955

    Open questions at the time
    • Single lab
    • Regulation distinguishing gap versus DSB resection not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the dense network of BLM post-translational modifications, partner interactions, and substrate preferences is integrated in real time to choose between resection, dissolution, and anti-recombinase outcomes at specific genomic loci remains unresolved.
  • No unified model linking modification state to substrate/pathway choice
  • Spatiotemporal coordination across S-phase, mitosis, and meiosis incompletely defined
  • Structural basis of full-length BTR engaging substrates unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 3 GO:0140097 catalytic activity, acting on DNA 3 GO:0140657 ATP-dependent activity 3 GO:0016787 hydrolase activity 2 GO:0003723 RNA binding 1
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 2 GO:0005730 nucleolus 2 GO:0005829 cytosol 1
Pathway
R-HSA-1640170 Cell Cycle 3 R-HSA-73894 DNA Repair 3 R-HSA-69306 DNA Replication 2 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-1474165 Reproduction 1
Partners
DNA2EXO1PICHPLK1RAD51RPATOP3ATOPBP1
Complex memberships
BLM-DNA2-RPA-MRN resection complexBTR (BLM-TOP3A-RMI1/2) dissolvasome

Evidence

Reading pass · 59 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 BLM and DNA2 physically interact and together with RPA and MRN constitute one of two core DNA end resection machineries. In this pathway, BLM helicase activity unwinds DNA while DNA2 nuclease activity performs resection; RPA is essential for BLM-mediated unwinding and enforces 5'→3' resection polarity by DNA2; MRN accelerates processing by recruiting BLM to the DNA end. Biochemical reconstitution with purified human proteins (BLM, DNA2, EXO1, MRN, RPA); in vitro resection assays; physical interaction studies Genes & development High 21325134
2008 BLM helicase specifically stimulates the nucleolytic activity of human EXO1 to resect DNA ends via a direct protein-protein interaction that is independent of BLM helicase activity. DNA ends resected by hExo1 and BLM are then used by human RAD51 to promote homologous DNA pairing. In vitro nuclease stimulation assays with purified proteins; protein-protein interaction studies; strand-exchange assays with human RAD51 Proceedings of the National Academy of Sciences of the United States of America High 18971343
2008 BLM (ortholog of yeast Sgs1) promotes DSB resection, DNA damage checkpoint signaling, and homologous recombination-mediated repair in parallel with EXO1, establishing an evolutionarily conserved role for BLM in DSB processing. Genetic epistasis (sgs1/EXO1 double mutants in yeast); BLM depletion in human cells; resection and DSB signaling assays Genes & development High 18923075
2007 BLM is required for faithful chromosome segregation; it localizes to anaphase bridges where it co-localizes with Topoisomerase IIIα and hRMI1 (BLAP75). BLM-positive ultrafine DNA bridges (UFBs) frequently link centromeric loci and are elevated in BLM-deficient cells, implicating BLM in completing sister-chromatid decatenation during anaphase. Live-cell imaging and immunofluorescence in BLM-deficient vs. corrected human cells; co-localization of BLM with TopoIIIα and PICH; quantification of anaphase bridges and lagging chromatin The EMBO journal High 17599064
2001 The first 133 amino acids of BLM are necessary and sufficient for interaction with Topoisomerase IIIα; Topo IIIα is recruited to PML nuclear bodies via its interaction with BLM. Expression of a BLM fragment lacking the Topo IIIα interaction domain (aa 133-1417) results in intermediate (not fully corrected) SCE levels, implicating the BLM-Topo IIIα complex in suppression of recombination. GFP-tagged BLM deletion constructs in BS cells; co-immunoprecipitation; SCE frequency measurement Human molecular genetics High 11406610
2010 Human Topoisomerase IIIα functions as a single-stranded DNA decatenase that is specifically stimulated by the BLM-RMI1 pair. RMI1 interacts directly with Topo IIIα and this interaction is required for the stimulatory effect on decatenase activity. Together, BLM and RMI1 enable Topo IIIα to process homologous recombination intermediates without crossing over. In vitro decatenation assays with purified human proteins; single-stranded catenane substrates; pulldown/interaction assays The Journal of biological chemistry High 20445207
1998 BLM protein has ATP-dependent 3'→5' DNA helicase activity. Single amino acid substitutions found in Bloom syndrome cells abolish both ATPase and helicase activities, demonstrating that these enzymatic activities are essential for BLM's role in maintaining genomic integrity. In vitro ATPase and helicase assays with murine BLM protein; site-directed mutagenesis of BS-associated point mutations Oncogene High 9840919
2002 BLM and Sgs1p preferentially unwind G4 DNA relative to Holliday junction substrates; this substrate preference maps to the conserved central helicase domain. The porphyrin NMM specifically inhibits G4 DNA unwinding by trapping BLM on NMM-G4 complexes. In vitro helicase assays with G4 DNA and Holliday junction substrates; inhibitor studies; domain mapping Nucleic acids research High 12235379
2004 TRF1 and TRF2 directly interact with BLM in vitro and regulate its unwinding activity: TRF2 stimulates BLM unwinding of both telomeric and non-telomeric substrates, while TRF1 specifically inhibits BLM unwinding of telomeric substrates. BLM co-localizes and co-immunoprecipitates with TRF2 in ALT cells during late S and G2/M phases. In vitro helicase assays with purified proteins; co-immunoprecipitation; co-localization by immunofluorescence in ALT cells Human molecular genetics High 15229185
2005 POT1 strongly stimulates BLM to unwind long telomeric forked duplexes and D-loop structures that are otherwise poor substrates. This stimulation is dependent on telomeric sequence in the duplex region. POT1 binds directly to BLM in vitro and co-precipitates endogenous BLM from nuclear extract. In vitro helicase assays with telomeric substrates; pulldown assays with purified POT1 and BLM; co-immunoprecipitation from HeLa nuclear extract The Journal of biological chemistry High 16030011
2009 SUMO modification of BLM regulates its interaction with RAD51 at damaged replication forks. SUMO-modified BLM interacts more efficiently with RAD51 than unmodified BLM. In cells expressing SUMO-mutant BLM, RAD51 localization to hydroxyurea-induced repair foci is impaired, sister-chromatid exchanges are reduced after HU treatment, and HR repair is defective. This SUMOylation acts as a switch between pro- and anti-recombinogenic roles of BLM. In vitro SUMO interaction assays; stable cell lines expressing BLM or SUMO-mutant BLM; RAD51 foci quantification; SCE assays; DNA break measurement PLoS biology High 19956565
2002 BLM directly interacts with ATM; BLM is phosphorylated by ATM during mitosis and in response to ionizing radiation. A phosphospecific antibody against Thr-99 detected radiation-induced phosphorylation that is defective in AT cells. BLM phosphorylation-site mutants fail to correct radiosensitivity in BS cells but do correct SCE, indicating that ATM-dependent phosphorylation of BLM is specifically required for the DNA damage response but not for SCE suppression. Co-immunoprecipitation; phosphospecific antibody; stable cell lines expressing phosphorylation-site mutants; SCE and radiosensitivity assays The Journal of biological chemistry High 12034743
2000 BLM protein accumulates in response to ionizing radiation in an ATM-dependent manner and is phosphorylated through this pathway. BLM-deficient cells display partial escape from the gamma-irradiation-induced G2/M checkpoint, indicating BLM acts as an ATM downstream effector in the DNA damage response. Western blot quantification of BLM after IR; cell cycle checkpoint analysis in BS and AT cells; phosphorylation assays Oncogene Medium 11146546
2001 BLM binds p53 in vivo and in vitro via the C-terminal domain of p53. p53-mediated apoptosis is defective in Bloom syndrome fibroblasts and can be rescued by expression of normal BLM. BLM localizes to PML nuclear bodies (NBs), and p53 mediates nuclear trafficking of BLM to NBs; certain BLM mutants impair localization of wild-type BLM to NBs in a dominant-negative manner. Co-immunoprecipitation in vivo and in vitro; apoptosis rescue assays in BS fibroblasts; immunofluorescence for PML NB localization; dominant-negative BLM mutant analysis The Journal of biological chemistry High 11399766
1997 BLM protein is translocated to the nucleus via a bipartite nuclear localization signal (NLS) in the C-terminus (residues 1334-1349); the distal arm of basic residues is essential for nuclear targeting. Previously reported BLM mutant proteins are retained in the cytoplasm. EGFP-BLM truncation constructs transfected into HeLa cells; immunofluorescence to assess subcellular localization Biochemical and biophysical research communications Medium 9388480
2004 BLM physically interacts with 53BP1 and co-localizes with 53BP1 and H2AX at stalled replication forks. 53BP1 is required for efficient accumulation of BLM and p53 at stalled replication sites. Active Chk1 kinase is essential for accurate focal co-localization of 53BP1 with BLM and stabilization of BLM. Co-immunoprecipitation; immunofluorescence co-localization at replication forks; Chk1 inhibition experiments; 53BP1 knockdown The Journal of cell biology Medium 15364958
2004 The hMSH2/6 mismatch repair complex directly stimulates BLM Holliday junction processing activity in vitro, an effect regulatable by p53. hMSH2 and hMSH6 co-immunoprecipitate with BLM, p53, and RAD51, forming a complex at stalled replication forks. In vitro Holliday junction resolution assay with purified proteins; co-immunoprecipitation; immunofluorescence co-localization at HU-induced foci Oncogene Medium 15064730
2006 BLM is phosphorylated at Ser144 in an MPS1-dependent manner during mitosis. Phospho-Ser144 BLM interacts with PLK1 via PLK1's polo-box domain. BS cells expressing BLM-S144A fail to maintain mitotic arrest when the spindle assembly checkpoint is activated and exhibit increased chromosome number variation, indicating MPS1-dependent BLM phosphorylation is required for accurate chromosome segregation. Co-immunoprecipitation; phospho-peptide mass spectrometry; stable cell lines expressing BLM-S144A; chromosome count analysis; mitotic arrest assay Proceedings of the National Academy of Sciences of the United States of America High 16864798
2011 PICH binds directly to BLM and enables BLM localization to anaphase centromeric DNA threads. PICH or BLM depletion causes failure to resolve centromeric threads in anaphase, resulting in chromatin-containing micronuclei. Purified PICH has nucleosome-remodeling activity in vitro; together PICH and BLM act to keep anaphase DNA threads free of nucleosomes. Co-immunoprecipitation of PICH and BLM; RNAi knockdown of PICH and BLM; immunofluorescence of anaphase threads; in vitro nucleosome-remodeling assay with purified PICH The EMBO journal High 21743438
2013 TopBP1 specifically interacts with BLM in a phosphorylation- and cell-cycle-dependent manner. TopBP1 depletion leads to decreased BLM protein levels and increased SCE. BLM is ubiquitinated by the E3 ligase MIB1 and degraded in G1 cells; TopBP1 stabilizes BLM in S-phase cells. Cells expressing an undegradable BLM mutant show radiation sensitivity due to inappropriate end resection in G1 that inhibits NHEJ. Co-immunoprecipitation; TopBP1 and MIB1 depletion; ubiquitination assays; SCE quantification; cell-cycle-specific protein stability analysis Molecular cell High 24239288
2009 BLM interacts with RAD54 through an internal ten-residue peptide in the N-terminal region of BLM. The N-terminal region of BLM prevents formation of the RAD51-RAD54 complex in vitro and in vivo. BLM stimulates the ATPase and chromatin-remodeling activities of RAD54; an ATPase-dead BLM mutant also stimulates RAD54, indicating this is independent of BLM helicase activity. Co-immunoprecipitation; FRAP; in vitro ATPase and chromatin-remodeling assays; N-terminal BLM peptide competition experiments Journal of cell science Medium 19671661
2011 BLM facilitates RNA polymerase I-mediated ribosomal RNA transcription in the nucleolus. BLM localizes to the nucleolus in an RNA Pol I activity-dependent manner and interacts with RPA194, a subunit of RNA Pol I. BLM unwinds GC-rich rDNA-like substrates that would otherwise inhibit RNA Pol I progression. BLM expression is required for efficient rRNA transcription as shown by 3H-uridine pulse-chase assays. Co-immunoprecipitation of BLM with RPA194; immunofluorescence; 3H-uridine pulse-chase rRNA synthesis assay; in vitro helicase assay on rDNA-like substrates Human molecular genetics Medium 22106380
2012 DNA topoisomerase I directly interacts with the C-terminus of BLM in the nucleolus. DNA topoisomerase I stimulates BLM helicase activity on RNA:DNA hybrid substrates but not DNA:DNA substrates, while BLM enhances the DNA relaxation activity of Topoisomerase I on supercoiled DNA, indicating a coordinated function in nucleolar transcription. Co-immunoprecipitation; in vitro translation; in vitro helicase assays; in vitro DNA relaxation assay Mutation research Medium 23261817
2001 BLM is cleaved by caspase 3 (not caspase 6) during apoptosis at the sequence TEVD (Asp415). Mutation of Asp415 renders BLM resistant to caspase 3 cleavage. Cleavage generates 47- and 110-kDa fragments, abolishes BLM nuclear foci and association with condensed DNA and insoluble matrix, but does not abolish helicase activity. In vitro caspase cleavage of recombinant BLM; site-directed mutagenesis of caspase recognition site; caspase 3 inhibitor experiments; immunofluorescence The Journal of biological chemistry High 11154689
2009 BLM exhibits repetitive 'measuring' unwinding on forked DNA substrates at the single-molecule level: it unwinds a defined length of duplex DNA, then reverses via strand switching and re-initiates unwinding. Interaction between wild-type BLM and hRPA is necessary for unwinding reinitiation on hRPA-coated DNA. Single-molecule FRET microscopy; forked DNA substrates with labeled strands; comparison of wild-type vs. interaction-deficient BLM mutant The EMBO journal High 19165145
2014 BLM interacts with G4 structures via cooperativity between its RQC and HRDC domains: the RQC domain binds the G4 motif and is stabilized by HRDC domain binding to flanking ssDNA. BLM unfolds G4 in an ATP-dependent manner and the mechanism depends on the structural context (3'-ssDNA tail vs. connection to dsDNA via ssDNA). Single-molecule FRET; structure-function analysis with RQC and HRDC domain mutants; defined G4 substrates Nature communications High 25418155
2015 BLM unfolds G4 structures through different mechanisms depending on molecular environment: G4 with a 3'-ssDNA tail is unfolded in three discrete steps via unidirectional translocation, while G4 connected to dsDNA by ssDNA is unfolded repetitively with BLM anchored at the ss/dsDNA junction. ATP is required for G4 unfolding in both contexts. Single-molecule FRET assays; defined G4 substrates in different structural environments Nucleic acids research High 25897130
2012 BLM multimers dissociate upon ATP hydrolysis and function as monomers in DNA unwinding. Steady-state and single-turnover kinetic studies using dynamic light scattering and stopped-flow assays showed monomeric BLM unwinds duplex DNA regardless of enzyme/ATP concentration, 3'-ssDNA tail length, or substrate complexity (including Holliday junctions and D-loops). Dynamic light scattering; stopped-flow kinetics; steady-state and single-turnover ATPase assays; helicase assays with multiple substrates Nucleic acids research High 22885301
2011 BLM interacts with Topoisomerase IIα directly via amino acids 489-587 of BLM, co-localizing predominantly in late G2 and M phases. Deletion of this interaction domain abolishes topoisomerase IIα-dependent enhancement of BLM activity on recombination intermediate substrates but not intrinsic helicase activity. BLM lacking the Topo IIα interaction domain fails to correct elevated chromosome breakage in BLM-deficient cells. Co-immunoprecipitation; domain deletion constructs; in vitro helicase assays; rescue of chromosome breakage in BS cells Cancer research Medium 21224348
2017 CtIP interacts with BLM and enhances its helicase activity, in addition to stimulating DNA2 cleavage, thereby promoting long-range DNA end resection through the BLM-DNA2 pathway. This represents a broader role for CtIP beyond MRE11 regulation in the initial resection step. Biochemical reconstitution with purified proteins; helicase stimulation assays; DNA2 cleavage assays; protein-protein interaction assays Cell reports High 29020620
2017 BLM's anti-recombinase activity counteracts RAD51 loading at DSB sites. Ablation of BLM rescues genomic integrity and cell survival in BRCA1-, BRCA2-, or XRCC2-mutant cells by substantially increasing RAD51 stability at DSB sites and improving HR efficiency. BLM ablation by CRISPR/knockout in BRCA-mutant cells; RAD51 foci quantification; SCE and HR assays; cell survival assays The Journal of cell biology Medium 28912125
2017 The BLM-TOP3A-RMI (BTR) dissolvase complex is required for ALT-mediated telomere synthesis. Recombination intermediates formed during strand invasion at ALT telomeres are processed by the BTR complex, initiating POLD3-dependent telomere synthesis followed by dissolution without overall telomeric DNA exchange. This is counteracted by the SLX4-SLX1-ERCC4 complex, which promotes resolution and telomere exchange. BLM/TOP3A/RMI depletion in ALT cells; telomere synthesis assays; C-circle and telomere exchange readouts; genetic epistasis The EMBO journal Medium 28877996
2019 FANCM-mediated attenuation of ALT requires its DNA translocase activity and its interaction with the BTR (BLM-TOP3A-RMI) complex but not the FA core complex. Depletion of FANCM induces increased break-induced telomere synthesis and ALT biomarkers, implicating the FANCM-BTR interaction in restraining excessive ALT activity. FANCM depletion; translocase-dead mutants; BTR interaction mutants; ALT biomarker quantification; synthetic lethality assays Nature communications Medium 31138797
2019 SLX4IP accumulates at ALT telomeres, interacts with SLX4, XPF, and BLM, and antagonizes BLM activity during ALT recombination. Loss of SLX4IP increases ALT phenotypes, and inactivation of BLM is sufficient to rescue telomere aggregation caused by SLX4IP loss, indicating SLX4IP favors SMX-dependent resolution over BTR-dependent dissolution. Co-immunoprecipitation; SLX4IP depletion; BLM inactivation rescue experiments; ALT telomere phenotype quantification Molecular cell Medium 31447390
2013 BLM physically interacts with RECQL4; RECQL4 specifically stimulates BLM helicase activity on DNA fork substrates in vitro. The BLM-interacting region maps to N-terminus of RECQL4 (aa 361-478) and aa 1-902 of BLM. This interaction is enhanced during S-phase and after ionizing radiation. BLM deficiency shortens RECQL4 retention at DSBs. Co-immunoprecipitation in vivo and in vitro; domain mapping; in vitro helicase stimulation assays; RECQL4 localization at DSBs in BLM-deficient cells Nucleic acids research Medium 22544709
2017 BLM (and its yeast ortholog Sgs1) suppresses R-loop-associated genome instability. BLM depletion leads to R-loop accumulation and γ-H2AX at replication pausing regions and long genes. BLM is physically proximal to DNA:RNA hybrids in human cells and can efficiently unwind R-loops in vitro. BLM depletion in human cells; R-loop immunofluorescence (S9.6 antibody); proximity ligation assay; in vitro R-loop unwinding assay; yeast genetics The Journal of cell biology Medium 29042409
2020 Human RPA (hRPA) activates BLM to unwind nicked double-stranded DNA bidirectionally by permitting translocation on both intact and nicked single-stranded DNA. This activation requires BLM targeting to the nick but is independent of direct BLM-hRPA interactions. Single-molecule combined force spectroscopy and fluorescence imaging; nicked dsDNA substrates; comparison of conditions with and without hRPA eLife High 32101168
2021 The deubiquitinating enzyme USP37 interacts with BLM and deubiquitinates it, stabilizing BLM protein and sustaining the DNA damage response. DNA DSBs promote ATM phosphorylation of USP37, enhancing its binding to BLM. USP37 knockdown increases BLM polyubiquitination and accelerates its proteolysis, impairing DSB repair. Co-immunoprecipitation; ubiquitination assays; ATM phosphorylation analysis; USP37 knockdown; in vivo and in vitro deubiquitination assays Nucleic acids research Medium 34606619
2017 Crystal structure of TopBP1 BRCT4/5 bound to BLM reveals that TopBP1 BRCT5 specifically recognizes BLM phospho-Ser304 (not pSer338) through a conserved pSer-binding pocket, with additional contacts from an FVPP motif N-terminal to pSer304 engaging a hydrophobic groove on BRCT5. Crystal structure determination of TopBP1 BRCT4/5 – BLM peptide complex; mutational validation of binding Structure (London, England : 1993) High 28919440
2022 CDK1 phosphorylates BLM and TOPBP1, promoting their interaction with PLK1. TOPBP1 facilitates phosphorylation of BLM at sites that stimulate BLM-PLK1 and BLM-TOPBP1 binding (positive feedback loop) at the G2-M transition. In vitro, BLM phosphorylation by CDK/PLK1/TOPBP1 stimulates dissolution of topologically linked DNA intermediates by the BTR complex (BLM-TOP3A). This CDK1-TOPBP1-PLK1 axis is required for crossover avoidance in somatic cells. In vitro phosphorylation and dissolution assays with purified proteins; co-immunoprecipitation; genetic epistasis of CDK1, PLK1, and TOPBP1 in crossover suppression Science advances High 35119917
2020 CDK and Cdc5 (PLK1 ortholog) kinases stimulate Sgs1 (BLM ortholog) helicase velocity and processivity during S phase/prophase I. CDK-mediated phosphorylation enhances DNA unwinding and joint molecule processing in vivo. Subsequent hyper-phosphorylation by Cdc5 reduces Sgs1 activity while activating crossover-resolving nucleases, suggesting concerted temporal regulation of recombination outcome. In vitro helicase assays with phosphorylated Sgs1; single-molecule DNA curtain assays; yeast genetics; in vivo joint molecule analysis Developmental cell High 32504558
2018 HERC2 interacts with BLM, WRN, and RPA complexes during S-phase and is required for RPA to associate with BLM. HERC2's E3 ubiquitin ligase activity ubiquitinates RPA2, enabling its release onto ssDNA from BLM complexes. HERC2 deficiency dissociates RPA from BLM, increases G4 formation, and epistasis analysis shows HERC2 acts in the same pathway as BLM to suppress G4. Co-immunoprecipitation; HERC2/BLM/WRN depletion; G4 foci quantification; in vitro RPA release assay; CRISPR deletion of HERC2 E3 domain; epistasis analysis Cancer research Medium 30279242
2009 BLM and FANCD2 co-localize and co-immunoprecipitate following DNA crosslinker treatment or replication arrest. The FA core complex is necessary for BLM phosphorylation and assembly into nuclear foci in response to crosslinked DNA, placing BLM downstream of the FA pathway in the response to crosslinked DNA. Co-immunoprecipitation; immunofluorescence co-localization; BLM phosphorylation analysis; FA core complex knockdown Nature cell biology Medium 19465921
2004 BLM and FANCD2 co-localize and co-immunoprecipitate following DNA crosslinker treatment or replication fork stall. The FA core complex is necessary for BLM phosphorylation and assembly into nuclear foci in response to crosslinked DNA. BLM and MRE11 complex act in two separated branches of a pathway for S-phase checkpoint activation and chromosome integrity. Co-immunoprecipitation; immunofluorescence; MRE11 knockdown in BS cells; checkpoint and survival assays The EMBO journal Medium 15257300
2006 BLM accumulates rapidly (within 10 seconds) at laser-induced DSB sites, co-localizing with γ-H2AX and ATM. The HRDC domain of BLM (specifically C-terminal region aa 1250-1292) is sufficient for early recruitment to DSB sites, independent of ATM, RAD17, DNA-PKcs, NBS1, XRCC3, RAD52, RAD54, or WRN. Live-cell imaging of laser-induced DSBs; GFP-BLM domain deletion constructs; analysis in multiple DT40 gene-knockout backgrounds Biochemical and biophysical research communications Medium 16876111
2019 BLM is a robust helicase that unwinds extensive tracts (~8-10 kb) of dsDNA at ~70-80 bp/second. BLM cannot associate with or translocate on ssDNA bound by RPA, and cannot translocate on dsDNA bound by RAD51, indicating RAD51 blocks BLM's anti-recombinase activity on chromatin-associated substrates. Single-molecule DNA curtain imaging; direct visualization of BLM on individual DNA molecules; RPA- and RAD51-coated substrates Nucleic acids research High 31544923
2021 ATR phosphorylation of EXO5 at T88Q89 regulates EXO5 nuclease activity and its binding to BLM (identified by mass spectrometry). EXO5 and BLM form a functional partnership for replication fork restart; EXO5 depletion decreases fork progression, DNA repair, and cell survival, and EXO5 functions epistatically with SMARCAL1 and BLM. Crystal structure of EXO5-DNA complexes; mass spectrometry identification of BLM binding; phospho-mimetic mutant rescue; epistasis analysis with SMARCAL1 and BLM Molecular cell High 34197737
2018 BLM in G1 phase acts as an adaptor protein enhancing binding of transcription factor c-Jun to its E3 ligase Fbw7α, thereby enhancing K48/K63-linked ubiquitylation and degradation of c-Jun. MIB1-ubiquitylated BLM mediates this function. BS-patient-derived BLM mutants cannot potentiate Fbw7α-dependent c-Jun degradation. Co-immunoprecipitation; ubiquitination assays; transcriptome analysis; promoter-binding ChIP with c-Jun; functional assays in BS cells with patient-derived mutants Cell reports Medium 30044990
2007 Epistasis analysis in DT40 cells demonstrates that XRCC3 activity generates substrates causing elevated SCE in BLM-deficient cells, and that BLM with Topoisomerase IIIα acts downstream of XRCC3 to suppress SCE formation. Disruption of XRCC3 suppresses UV- and MMS-sensitivity and chromosomal aberrations of blm cells, positioning BLM downstream of XRCC3 in the recombination repair pathway. Double and triple DT40 gene-knockout analysis; SCE assays; sensitivity to DNA damage agents; epistasis mapping The Journal of cell biology Medium 17923529
2004 Genetic interaction between BLM and DNA ligase IV (NHEJ factor): deletion of LIG4 suppresses retarded growth, increased mutation rates, and hypersensitivity to replication-blocking agents in BLM-deficient human cells. This indicates that NHEJ is unfavorable for cells lacking BLM, and that BLM deficiency leads to one-ended DSBs that are deleterious when repaired by NHEJ. BLM also affects a DNA ligase IV-independent alternative end-joining pathway. BLM-/- and BLM-/-/LIG4-/- Nalm-6 cells; growth, mutation rate, drug sensitivity, x-ray sensitivity, and I-SceI-based DSB repair assays The Journal of biological chemistry Medium 15509577
2023 BLM is recruited to stress granules (SGs) in the cytoplasm upon stress in an RNA G-quadruplex (rG4)-dependent manner. BLM unwinds RNA G-quadruplexes (rG4s) and negatively regulates SG formation, expanding its known function to regulation of cytoplasmic biomolecular condensates. Immunofluorescence; stress granule marker co-localization; rG4-dependent recruitment assay; in vitro rG4 unwinding assay; SG formation quantification in BLM-depleted cells Nucleic acids research Medium 37503837
2024 BLM helicase acts on lagging strand telomere intermediates specifically in ALT-positive cells to assemble a replication-associated DNA damage response. Loss of ATRX permits BLM localization to ALT telomeres in S and G2 phases. DNA2 nuclease deficiency increases 5'-flap formation in a BLM-dependent manner; telomere C-strand (not G-strand) nicks promote ALT, linking aberrant lagging strand replication with BLM-directed HDR for telomere maintenance. BLM localization studies; ATRX loss-of-function; DNA2 depletion with BLM dependency; C-strand vs. G-strand nick induction assays; telomere damage response quantification Molecular cell Medium 38593805
2019 PLK1 inhibition leads to unlawful unwinding of DNA by BLM helicase at centromere domains underneath kinetochores. Under bipolar spindle tension, BLM-driven centromere disintegration decompacts centromeres into DNA threads leading to centromere rupture and chromosome arm splitting. PLK1 normally suppresses this BLM-mediated centromere unwinding to maintain centromere integrity for chromosome biorientation. PLK1 inhibitor experiments; BLM depletion rescue; live-cell imaging; centromere chromatin analysis Nature communications Medium 31253795
2022 BLM is recruited in a transcription-dependent manner to DSBs in active chromatin where it fosters DNA end resection, RAD51 binding, and accurate homologous recombination repair. In an R-loop dissolution-deficient background, BLM promotes POLD3-dependent DNA synthesis at DSBs, linking BLM activity to toxic outcomes from excessive RNA:DNA hybrid accumulation. BLM depletion; chromatin immunoprecipitation at DSBs; resection assays; RAD51 foci; POLD3 depletion epistasis; R-loop accumulation models Nature communications Medium 35440629
2025 DNA2-WRN/BLM specifically resects the 5' end of ssDNA gaps independent of MRN-CtIP, through a mechanism different from their action at DSB ends. This bidirectional gap resection process alters ssDNA gap repair kinetics, and excessive resection in BRCA1-deficient PARPi-treated cells leads to larger gaps, impaired repair, and DNA breaks in subsequent cell cycle stages. Single-molecule DNA fiber analysis; electron microscopy; biochemical resection assays; BRCA1-deficient cell epistasis Genes & development Medium 40127955
2025 BLM is lactylated at Lys24 by AARS1 in response to chemotherapy. Hyperlactylation of BLM improves its stability by inhibiting MIB1-mediated ubiquitination and increasing its interaction with DNA repair factors, thereby promoting DNA end resection and HR repair. Lys24 mutation impairs HR and increases anthracycline chemosensitivity. Global lactylome; co-immunoprecipitation; ubiquitination assays; Lys24 mutation rescue experiments; HR assays Signal transduction and targeted therapy Medium 40634292
2016 BLM domain VI promotes early activation of FANCD2 monoubiquitination. FANCD2 activation is substantially delayed and attenuated in crosslinking agent-treated BLM-deficient cells. Domain VI-deleted BLM phenocopies inactivated FANCD2, establishing a functional requirement of BLM domain VI for FANCD2 activation. BLM domain deletion analysis; FANCD2 activation (monoubiquitination) assays; BLM-deficient cell complementation with domain VI mutants Oncotarget Medium 27083049
1999 BLM protein localizes to foci along synaptonemal complexes of synapsed autosomal bivalents in late zygonema of meiotic prophase in mouse spermatocytes, co-localizing with RPA. BLM foci dissociate from synapsed axes during early pachynema and are enriched at the pseudoautosomal region (a recombination hotspot), suggesting a role in meiotic recombination. Immunocytology (immunofluorescence and immunoelectron microscopy) on mouse spermatocyte spreads; co-localization with RPA, RAD51, DMC1 Proceedings of the National Academy of Sciences of the United States of America Medium 10318934
2018 RUNX3 interaction with BLM is increased after DNA damage and facilitates efficient FANCD2 chromatin localization. RUNX3 undergoes PARP-dependent poly(ADP-ribosyl)ation which enables its binding to DNA repair structures; BLM is identified as a RUNX3 interaction partner by SILAC mass spectrometry. SILAC mass spectrometry; co-immunoprecipitation; FANCD2 chromatin localization assay; PARP inhibition experiments Cell reports Medium 30110632

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 BLM-DNA2-RPA-MRN and EXO1-BLM-RPA-MRN constitute two DNA end resection machineries for human DNA break repair. Genes & development 590 21325134
2008 DNA helicases Sgs1 and BLM promote DNA double-strand break resection. Genes & development 489 18923075
2007 BLM is required for faithful chromosome segregation and its localization defines a class of ultrafine anaphase bridges. The EMBO journal 354 17599064
2001 SGS1, the Saccharomyces cerevisiae homologue of BLM and WRN, suppresses genome instability and homeologous recombination. Nature genetics 284 11138010
2009 The FANC pathway and BLM collaborate during mitosis to prevent micro-nucleation and chromosome abnormalities. Nature cell biology 272 19465921
2008 Human exonuclease 1 and BLM helicase interact to resect DNA and initiate DNA repair. Proceedings of the National Academy of Sciences of the United States of America 244 18971343
2021 BioSeq-BLM: a platform for analyzing DNA, RNA and protein sequences based on biological language models. Nucleic acids research 204 34581805
2002 G4 DNA unwinding by BLM and Sgs1p: substrate specificity and substrate-specific inhibition. Nucleic acids research 188 12235379
2019 The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT). Nature communications 164 31138797
2005 POT1 stimulates RecQ helicases WRN and BLM to unwind telomeric DNA substrates. The Journal of biological chemistry 157 16030011
2017 BLM and SLX4 play opposing roles in recombination-dependent replication at human telomeres. The EMBO journal 140 28877996
2004 Association and regulation of the BLM helicase by the telomere proteins TRF1 and TRF2. Human molecular genetics 134 15229185
2008 The Human RecQ helicases, BLM and RECQ1, display distinct DNA substrate specificities. The Journal of biological chemistry 132 18448429
2017 FANCM, BRCA1, and BLM cooperatively resolve the replication stress at the ALT telomeres. Proceedings of the National Academy of Sciences of the United States of America 125 28673972
2000 Possible association of BLM in decreasing DNA double strand breaks during DNA replication. The EMBO journal 124 10880455
2001 Functional interaction of p53 and BLM DNA helicase in apoptosis. The Journal of biological chemistry 118 11399766
2002 Coexpression of ephrin-Bs and their receptors in colon carcinoma. Cancer 114 11920461
2001 Evidence for BLM and Topoisomerase IIIalpha interaction in genomic stability. Human molecular genetics 113 11406610
2004 Functional interaction between BLM helicase and 53BP1 in a Chk1-mediated pathway during S-phase arrest. The Journal of cell biology 112 15364958
2002 Functional link between BLM defective in Bloom's syndrome and the ataxia-telangiectasia-mutated protein, ATM. The Journal of biological chemistry 109 12034743
2009 SUMO modification regulates BLM and RAD51 interaction at damaged replication forks. PLoS biology 106 19956565
2017 RECQ-like helicases Sgs1 and BLM regulate R-loop-associated genome instability. The Journal of cell biology 101 29042409
2004 BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forks. The EMBO journal 98 15257300
2013 The BLM dissolvasome in DNA replication and repair. Cellular and molecular life sciences : CMLS 92 23543275
2014 Mechanistic insight into the interaction of BLM helicase with intra-strand G-quadruplex structures. Nature communications 89 25418155
1999 Bloom's syndrome protein, BLM, colocalizes with replication protein A in meiotic prophase nuclei of mammalian spermatocytes. Proceedings of the National Academy of Sciences of the United States of America 83 10318934
2017 BLM helicase regulates DNA repair by counteracting RAD51 loading at DNA double-strand break sites. The Journal of cell biology 79 28912125
2011 PICH and BLM limit histone association with anaphase centromeric DNA threads and promote their resolution. The EMBO journal 79 21743438
2009 Aging-associated dysfunction of Akt/protein kinase B: S-nitrosylation and acetaminophen intervention. PloS one 79 19641606
2015 BLM unfolds G-quadruplexes in different structural environments through different mechanisms. Nucleic acids research 77 25897130
2019 SLX4IP Antagonizes Promiscuous BLM Activity during ALT Maintenance. Molecular cell 76 31447390
2000 Expression and nuclear localization of BLM, a chromosome stability protein mutated in Bloom's syndrome, suggest a role in recombination during meiotic prophase. Journal of cell science 76 10652259
2000 ATM-dependent phosphorylation and accumulation of endogenous BLM protein in response to ionizing radiation. Oncogene 75 11146546
2015 Deleterious Germline BLM Mutations and the Risk for Early-onset Colorectal Cancer. Scientific reports 71 26358404
2009 BLM helicase measures DNA unwound before switching strands and hRPA promotes unwinding reinitiation. The EMBO journal 66 19165145
2010 Human topoisomerase IIIalpha is a single-stranded DNA decatenase that is stimulated by BLM and RMI1. The Journal of biological chemistry 64 20445207
2004 The mismatch DNA repair heterodimer, hMSH2/6, regulates BLM helicase. Oncogene 64 15064730
2018 EphBs and ephrin-Bs: Trans-synaptic organizers of synapse development and function. Molecular and cellular neurosciences 62 30031105
2017 Enhancement of BLM-DNA2-Mediated Long-Range DNA End Resection by CtIP. Cell reports 62 29020620
2014 Structural mechanisms of human RecQ helicases WRN and BLM. Frontiers in genetics 61 25400656
2007 B-S transition in short oligonucleotides. Biophysical journal 59 17557787
1998 Point mutations causing Bloom's syndrome abolish ATPase and DNA helicase activities of the BLM protein. Oncogene 57 9840919
2021 Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword? Frontiers in genetics 56 33777104
2016 Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases. Ageing research reviews 56 27238185
2006 MPS1-dependent mitotic BLM phosphorylation is important for chromosome stability. Proceedings of the National Academy of Sciences of the United States of America 56 16864798
2004 Genetic interactions between BLM and DNA ligase IV in human cells. The Journal of biological chemistry 56 15509577
2007 Role of the BLM helicase in replication fork management. DNA repair 54 17363339
1997 BLM (the causative gene of Bloom syndrome) protein translocation into the nucleus by a nuclear localization signal. Biochemical and biophysical research communications 54 9388480
2018 HERC2 Facilitates BLM and WRN Helicase Complex Interaction with RPA to Suppress G-Quadruplex DNA. Cancer research 51 30279242
2012 The human RecQ helicases BLM and RECQL4 cooperate to preserve genome stability. Nucleic acids research 50 22544709
2011 BLM helicase facilitates RNA polymerase I-mediated ribosomal RNA transcription. Human molecular genetics 50 22106380
2006 BLM is an early responder to DNA double-strand breaks. Biochemical and biophysical research communications 50 16876111
2013 TopBP1 controls BLM protein level to maintain genome stability. Molecular cell 49 24239288
2007 BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination. The Journal of cell biology 47 17591918
2017 SELF-BLM: Prediction of drug-target interactions via self-training SVM. PloS one 46 28192537
2004 Clinical features of Bloom syndrome and function of the causative gene, BLM helicase. Expert review of molecular diagnostics 46 15137905
2014 The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair. DNA repair 45 25150915
2021 EXO5-DNA structure and BLM interactions direct DNA resection critical for ATR-dependent replication restart. Molecular cell 41 34197737
2020 Heterozygous germline BLM mutations increase susceptibility to asbestos and mesothelioma. Proceedings of the National Academy of Sciences of the United States of America 41 33318203
2003 Chromosome instability and tumor predisposition inversely correlate with BLM protein levels. DNA repair 39 14642567
2024 BLM helicase unwinds lagging strand substrates to assemble the ALT telomere damage response. Molecular cell 34 38593805
2021 USP37 regulates DNA damage response through stabilizing and deubiquitinating BLM. Nucleic acids research 34 34606619
2019 Single-molecule visualization of human BLM helicase as it acts upon double- and single-stranded DNA substrates. Nucleic acids research 34 31544923
2009 Association between polymorphisms in RMI1, TOP3A, and BLM and risk of cancer, a case-control study. BMC cancer 34 19432957
2020 Human RPA activates BLM's bidirectional DNA unwinding from a nick. eLife 33 32101168
2014 Association of BLM and BRCA1 during Telomere Maintenance in ALT Cells. PloS one 33 25084169
2002 Characterization and potential function of a novel testis-specific nucleoporin BS-63. Molecular reproduction and development 33 11774384
2019 Helicases FANCJ, RTEL1 and BLM Act on Guanine Quadruplex DNA in Vivo. Genes 32 31683575
2018 BLM prevents instability of structure-forming DNA sequences at common fragile sites. PLoS genetics 32 30496191
2012 Collaborating functions of BLM and DNA topoisomerase I in regulating human rDNA transcription. Mutation research 32 23261817
2015 The risk for developing cancer in Israeli ATM, BLM, and FANCC heterozygous mutation carriers. Cancer genetics 31 26778106
2014 RECQL5 and BLM exhibit divergent functions in cells defective for the Fanconi anemia pathway. Nucleic acids research 31 25520194
2008 The fission yeast BLM homolog Rqh1 promotes meiotic recombination. Genetics 31 18562672
2019 PLK1 facilitates chromosome biorientation by suppressing centromere disintegration driven by BLM-mediated unwinding and spindle pulling. Nature communications 30 31253795
2018 BS-Seeker3: ultrafast pipeline for bisulfite sequencing. BMC bioinformatics 30 29614954
2018 RUNX Poly(ADP-Ribosyl)ation and BLM Interaction Facilitate the Fanconi Anemia Pathway of DNA Repair. Cell reports 30 30110632
2012 Multimeric BLM is dissociated upon ATP hydrolysis and functions as monomers in resolving DNA structures. Nucleic acids research 30 22885301
2009 BLM helicase stimulates the ATPase and chromatin-remodeling activities of RAD54. Journal of cell science 30 19671661
2009 Colorectal cancer and polymorphisms in DNA repair genes WRN, RMI1 and BLM. Carcinogenesis 30 19945966
2020 Phosphorylation of the RecQ Helicase Sgs1/BLM Controls Its DNA Unwinding Activity during Meiosis and Mitosis. Developmental cell 29 32504558
2014 DNA helicase HIM-6/BLM both promotes MutSγ-dependent crossovers and antagonizes MutSγ-independent interhomolog associations during caenorhabditis elegans meiosis. Genetics 28 25053665
2025 Irinotecan alleviates chemoresistance to anthracyclines through the inhibition of AARS1-mediated BLM lactylation and homologous recombination repair. Signal transduction and targeted therapy 27 40634292
2022 A POLD3/BLM dependent pathway handles DSBs in transcribed chromatin upon excessive RNA:DNA hybrid accumulation. Nature communications 27 35440629
2017 RecQ helicase BLM regulates prostate cancer cell proliferation and apoptosis. Oncology letters 26 28943928
2023 BLM helicase protein negatively regulates stress granule formation through unwinding RNA G-quadruplex structures. Nucleic acids research 25 37503837
2018 BLM can regulate cataract progression by influencing cell vitality and apoptosis. Experimental eye research 25 30227115
2017 Structural Insight into BLM Recognition by TopBP1. Structure (London, England : 1993) 25 28919440
2016 BLM promotes the activation of Fanconi Anemia signaling pathway. Oncotarget 25 27083049
2015 Mre11 and Blm-Dependent Formation of ALT-Like Telomeres in Ku-Deficient Ustilago maydis. PLoS genetics 24 26492073
2023 Fraxetin alleviates BLM-induced idiopathic pulmonary fibrosis by inhibiting NCOA4-mediated epithelial cell ferroptosis. Inflammation research : official journal of the European Histamine Research Society ... [et al.] 23 37798541
2011 Chromosome breakage is regulated by the interaction of the BLM helicase and topoisomerase IIalpha. Cancer research 23 21224348
2023 BLM overexpression as a predictive biomarker for CHK1 inhibitor response in PARP inhibitor-resistant BRCA-mutant ovarian cancer. Science translational medicine 22 37343085
2021 Ellagic Acid Attenuates BLM-Induced Pulmonary Fibrosis via Inhibiting Wnt Signaling Pathway. Frontiers in pharmacology 22 33912053
2013 A common nonsense mutation of the BLM gene and prostate cancer risk and survival. Gene 22 24096176
2001 Selective cleavage of BLM, the bloom syndrome protein, during apoptotic cell death. The Journal of biological chemistry 22 11154689
2018 BLM Potentiates c-Jun Degradation and Alters Its Function as an Oncogenic Transcription Factor. Cell reports 21 30044990
2025 MRN-CtIP, EXO1, and DNA2-WRN/BLM act bidirectionally to process DNA gaps in PARPi-treated cells without strand cleavage. Genes & development 19 40127955
2022 The CDK1-TOPBP1-PLK1 axis regulates the Bloom's syndrome helicase BLM to suppress crossover recombination in somatic cells. Science advances 19 35119917
2019 Inherited Variants in BLM and the Risk and Clinical Characteristics of Breast Cancer. Cancers 19 31614901
2007 Functional interactions between BLM and XRCC3 in the cell. The Journal of cell biology 19 17923529

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