Affinage

HELLS

Lymphoid-specific helicase · UniProt Q9NRZ9

Length
838 aa
Mass
97.1 kDa
Annotated
2026-04-28
100 papers in source corpus 41 papers cited in narrative 41 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HELLS (LSH) is an SNF2-family chromatin remodeling ATPase that functions as the catalytic subunit of a bipartite nucleosome remodeling complex with CDCA7 to control DNA methylation, histone variant deposition, and DNA repair across multiple chromatin contexts. HELLS lacks autonomous remodeling activity; CDCA7 is required for its chromatin loading and nucleosome sliding, and this complex enables access of both de novo (DNMT3A/3B) and maintenance (DNMT1/UHRF1) DNA methyltransferases to nucleosomal DNA, thereby establishing and maintaining CpG methylation at repetitive elements, developmental gene promoters, and imprinted loci (PMID:29339483, PMID:16395332, PMID:33170271, PMID:29140247). Beyond methylation, HELLS deposits the histone variant macroH2A in an ATP-dependent manner to silence repeats and protect stalled replication forks through RAD51 loading, promotes DNA double-strand break repair via both NHEJ (through CDCA7-Ku70/Ku80 interaction) and homologous recombination (through CtIP-mediated end resection), and is recruited by PRDM9 to open chromatin at meiotic recombination hotspots, where its loss causes sterility due to DSB mis-targeting (PMID:33159050, PMID:34112784, PMID:30307408, PMID:31802118, PMID:32001511). HELLS also cooperates with E2F3 and histone-modifying enzymes (HDACs, G9a) as a transcriptional regulator at developmental and cell-cycle gene promoters, and its loss causes premature senescence, proliferative failure in lymphocytes, and centromere dysfunction in oocyte meiosis (PMID:22157815, PMID:21149390, PMID:15105378, PMID:32900989). Biallelic mutations in HELLS cause ICF syndrome type 4, an immunodeficiency disorder linked to disruption of these chromatin regulatory functions (PMID:29339483, PMID:33159050).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2000 High

    Initial characterization established that HELLS is required for lymphocyte proliferative expansion, answering whether this SNF2-family member has a non-redundant role in cell division.

    Evidence Lsh knockout mice with hematopoietic reconstitution showing T cell apoptosis and proliferative failure

    PMID:10781083

    Open questions at the time
    • Molecular mechanism of proliferative failure unknown
    • Whether remodeling activity underlies the lymphocyte phenotype untested
    • No connection to DNA methylation yet established
  2. 2003 High

    Localization and loss-of-function studies revealed that HELLS concentrates at pericentromeric heterochromatin and its absence causes global hypomethylation-associated mitotic defects, establishing it as a chromatin-associated factor controlling genome stability through epigenetic mechanisms.

    Evidence GFP-fusion imaging, deletion mapping, HDAC inhibitor treatment, Lsh-/- MEF centrosome/spindle analysis, 5-azacytidine epistasis

    PMID:12907649 PMID:14517253 PMID:14612388

    Open questions at the time
    • Whether HELLS has intrinsic nucleosome remodeling activity unknown
    • Mechanism connecting HELLS to DNA methyltransferase recruitment not established
  3. 2004 High

    HELLS knockout mice displayed premature aging with global hypomethylation and derepression of repetitive elements, demonstrating HELLS is essential for genome-wide DNA methylation and repeat silencing in vivo.

    Evidence Gene disruption, whole-genome methylation, repeat transcription, p16/Bmi-1 expression in PASG-/- mice; ChIP at repeat loci

    PMID:15105378 PMID:15448183

    Open questions at the time
    • Whether HELLS directly engages DNA methyltransferases or acts indirectly not resolved
    • Mechanism at specific locus classes (imprinted, developmental) not explored
  4. 2005 High

    HELLS was shown to directly occupy specific imprinted loci and developmental gene promoters, establishing it acts locus-specifically rather than solely as a global heterochromatin factor.

    Evidence ChIP for Lsh at Cdkn1c DMR with allele-specific methylation analysis in Lsh-/- embryos

    PMID:15647320

    Open questions at the time
    • Whether HELLS recruits DNMTs to these specific loci untested
    • Generality across imprinted loci unclear given selective effects
  5. 2006 High

    Two studies resolved that HELLS functions specifically in de novo methylation by physically associating with DNMT3A/3B, and that it is essential for meiotic chromosome synapsis and retrotransposon silencing in germ cells.

    Evidence Episomal methylation assay, Co-IP with DNMT3A/3B in Lsh-/- fibroblasts; Lsh KO oocyte cytology with bisulfite methylation

    PMID:16395332 PMID:17115026

    Open questions at the time
    • Whether HELLS ATPase activity is required for DNMT recruitment not tested
    • Mechanism of HELLS action during meiotic synapsis not distinguished from methylation role
  6. 2007 High

    HELLS was established as a transcriptional repressor that cooperates with DNMT1, DNMT3B, HDAC1/2, and Polycomb components at developmental (Hox) gene loci, revealing a repressive hub linking DNA methylation, histone deacetylation, and Polycomb silencing.

    Evidence Promoter-targeting reporter assay, DNMT knockout cell epistasis, ChIP at Hox loci for Lsh/Dnmt3b/PRC1

    PMID:17726103 PMID:17967891

    Open questions at the time
    • Whether HELLS directly recruits HDACs or PRC1 versus indirect chromatin effects unresolved
    • Structural basis of HELLS-DNMT-HDAC cooperation unknown
  7. 2009 High

    HELLS was shown to repress p16INK4a via HDAC1/2 recruitment and to enable DNMT3B-mediated silencing of stem cell genes during differentiation, defining its roles in cellular senescence and developmental gene regulation.

    Evidence Co-IP of Lsh with HDAC1/2, ChIP at p16 promoter with TSA epistasis; Dnmt3b ChIP at Oct4 locus in Lsh-/- differentiating ES cells

    PMID:19561196 PMID:19650037

    Open questions at the time
    • Whether HELLS ATPase activity is required for HDAC recruitment unknown
    • Genome-wide extent of HELLS-HDAC senescence regulation not mapped
  8. 2010 High

    Genome-wide methylation profiling revealed HELLS cooperates with G9a/GLP histone methyltransferase for developmentally programmed DNA methylation, establishing a chromatin-modification cascade requiring HELLS.

    Evidence Promoter methylation arrays in Hells-/- MEFs, G9a ChIP epistasis

    PMID:21149390

    Open questions at the time
    • Whether HELLS directly recruits G9a or acts through chromatin remodeling not distinguished
    • Extent of overlap between HELLS-G9a and HELLS-DNMT3B programs not fully defined
  9. 2011 High

    HELLS was discovered to interact with E2F3 and bind active gene promoters genome-wide, revealing an unexpected role in transcriptional activation alongside its silencing functions, and was confirmed essential for male meiotic progression.

    Evidence Mass spectrometry, Co-IP, ChIP-seq for HELLS/E2F3; ectopic testis grafting of Hells-null tissue

    PMID:21349825 PMID:22157815

    Open questions at the time
    • How HELLS switches between activating and repressive functions at different loci unexplained
    • Whether E2F3 cooperation requires HELLS ATPase activity untested
  10. 2012 High

    HELLS ATPase activity was shown to be required for efficient γH2AX formation and DDR signaling (MDC1, 53BP1, CHK2) after DNA double-strand breaks, establishing HELLS as a chromatin remodeler in the DNA damage response.

    Evidence ATPase-dead mutant, γH2AX/53BP1/MDC1 foci, IR survival assay

    PMID:22946062

    Open questions at the time
    • Whether HELLS remodels nucleosomes directly at DSB sites or acts indirectly unknown
    • Relationship to specific repair pathways (NHEJ vs HR) not resolved
  11. 2015 High

    Definitive demonstration that HELLS ATPase activity is required for de novo DNA methylation: ATP-mutant HELLS fails to promote DNMT3B association with repeat loci and cannot restore normal nucleosome occupancy, establishing remodeling as the mechanism enabling methyltransferase access.

    Evidence ATPase-dead Lsh rescue in KO ES cells, DNMT3b ChIP, MNase nucleosome occupancy

    PMID:25578963

    Open questions at the time
    • Whether HELLS directly slides/evicts nucleosomes or acts through an intermediate not resolved
    • No structural model of HELLS-nucleosome engagement
  12. 2017 High

    Comparative genomics in Arabidopsis and mouse demonstrated that HELLS/DDM1 enables methylation of nucleosome-wrapped DNA genome-wide, showing the remodeler determines the nucleosomal versus linker DNA methylation pattern.

    Evidence Whole-genome bisulfite sequencing in DDM1 and Lsh mutants with double-mutant epistasis

    PMID:29140247

    Open questions at the time
    • Precise remodeling mechanism (sliding vs eviction vs unwrapping) at nucleosomal substrates unknown
    • Whether linker histone H1 and HELLS compete at the same nucleosome sites in mammals not tested
  13. 2018 High

    Two landmark studies resolved that HELLS requires CDCA7 as an obligate partner for nucleosome remodeling and chromatin loading, and that the HELLS-CDCA7 axis promotes NHEJ through Ku70/Ku80 interaction — with ICF mutations disrupting both functions.

    Evidence Xenopus extract reconstitution of HELLS-CDCA7 remodeling; Co-IP of CDCA7 with Ku proteins, NHEJ reporter, live Ku80 imaging at laser damage

    PMID:29339483 PMID:30307408

    Open questions at the time
    • Structural basis of CDCA7-HELLS assembly unknown
    • How CDCA7 activates HELLS ATPase mechanistically not determined
    • Whether HELLS-CDCA7 complex directly remodels nucleosomes at DSB sites during NHEJ untested
  14. 2019 High

    HELLS was shown to remodel nucleosomes at enhancers and regulatory regions independently of DNA methylation, and to regulate transcription factor access — answering whether HELLS acts solely through methylation or has methylation-independent chromatin functions.

    Evidence Auxin-inducible degron for acute Lsh depletion, MNase-seq, TF ChIP after depletion

    PMID:30861354

    Open questions at the time
    • Extent to which methylation-independent remodeling contributes to developmental phenotypes vs methylation-dependent functions not quantified
  15. 2020 High

    A burst of discoveries established that HELLS: (1) facilitates DNMT1 maintenance methylation via UHRF1 chromatin association; (2) deposits macroH2A in an ATP-dependent manner; (3) forms a pioneer complex with PRDM9 at meiotic hotspots; (4) promotes class-switch recombination end-joining in B cells; (5) regulates kinetochore function in oocytes; and (6) prevents R-loop accumulation at repeats.

    Evidence Co-IP/chromatin fractionation for UHRF1; CIP tethering and ChIP-seq for macroH2A; ATAC-seq/ChIP-seq in Hells KO spermatocytes; conditional KO B cell CSR assays; super-resolution kinetochore imaging in KO oocytes; DRIP-seq and iPOND in ICF cells

    PMID:32001511 PMID:32727902 PMID:32900989 PMID:33047671 PMID:33082427 PMID:33159050 PMID:33170271

    Open questions at the time
    • How HELLS is differentially directed to maintenance methylation vs de novo methylation targets unknown
    • Structural mechanism of macroH2A deposition not resolved
    • Whether kinetochore and meiotic hotspot functions use the CDCA7 partner not tested
  16. 2020 High

    HELLS was shown to promote homologous recombination by interacting with CtIP and facilitating end resection at DSBs within heterochromatin, resolving its specific role in HR pathway choice.

    Evidence Co-IP of HELLS-CtIP, HR reporter assay, ATPase-dead mutant, G2 cell cycle staging

    PMID:31802118

    Open questions at the time
    • Whether HELLS remodels heterochromatic nucleosomes to expose DNA ends for CtIP not directly shown
    • Interplay between HELLS-CDCA7 NHEJ function and HELLS-CtIP HR function at heterochromatic DSBs not resolved
  17. 2021 High

    The macroH2A deposition activity of HELLS was linked to replication fork protection: HELLS/macroH2A deficiency impairs RAD51 loading through perturbed BRCA1/53BP1 balance and H4K20 methylation, leading to MRE11/EXO1-dependent nascent DNA degradation.

    Evidence DNA fiber fork protection assay, RAD51/BRCA1/53BP1 foci, H4K20me ChIP, macroH2A rescue, nuclease inhibitor epistasis

    PMID:34112784

    Open questions at the time
    • Whether macroH2A deposition at forks is constitutive or induced by replication stress unknown
    • Direct visualization of macroH2A at stalled forks lacking
  18. 2023 Medium

    HELLS protein stability was shown to be regulated by competing ubiquitin ligase (CRL4-DCAF8) and deubiquitinase (USP5, USP11) systems, with functional consequences for ferroptosis resistance and cancer biology.

    Evidence CRL4-DCAF8 reconstitution and degradation assay; USP5/USP11 Co-IP and ubiquitination assays in HCC/CRC cells

    PMID:33288900 PMID:37414755 PMID:37492786

    Open questions at the time
    • Physiological contexts governing HELLS stability regulation beyond cancer not explored
    • Whether stability regulation affects all HELLS functions equally unknown
    • Independent replication of each DUB-LSH axis in other labs lacking

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of the HELLS-CDCA7 remodeling complex, how HELLS switches between its diverse chromatin substrates (methylation, macroH2A, DSB repair, kinetochore), and the molecular basis of ICF4 pathogenesis beyond methylation loss.
  • No cryo-EM or crystal structure of HELLS or HELLS-CDCA7 complex
  • Mechanism by which CDCA7 activates HELLS ATPase unknown
  • How HELLS is recruited to different genomic contexts (repeats, DSBs, meiotic hotspots, kinetochores) remains poorly understood
  • Relative contributions of methylation loss, macroH2A loss, and repair defects to ICF4 immunodeficiency not dissected

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140657 ATP-dependent activity 5 GO:0140110 transcription regulator activity 3 GO:0042393 histone binding 2 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005694 chromosome 3 GO:0005634 nucleus 2
Pathway
R-HSA-1474165 Reproduction 5 R-HSA-1266738 Developmental Biology 4 R-HSA-1640170 Cell Cycle 3 R-HSA-4839726 Chromatin organization 3 R-HSA-73894 DNA Repair 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-168256 Immune System 2
Partners
CDCA7DNMT3ADNMT3BE2F3HDAC1HDAC2PRDM9UHRF1
Complex memberships
HELLS-CDCA7 nucleosome remodeling complex

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 HELLS and CDCA7 form a stoichiometric bipartite nucleosome remodeling complex on chromatin. HELLS alone lacks nucleosome remodeling activity, but the HELLS-CDCA7 complex possesses nucleosome remodeling activity. CDCA7 is essential for loading HELLS onto chromatin, and ICF patient mutations in CDCA7 abolish chromatin recruitment of the complex. Xenopus egg extract proteomics, reconstitution of nucleosome remodeling activity, chromatin fractionation, functional analysis of ICF patient mutations Proceedings of the National Academy of Sciences of the United States of America High 29339483
2006 Lsh is directly involved in de novo DNA methylation: it associates with Dnmt3a and Dnmt3b (but not Dnmt1) in embryonic cells and is required for acquisition of new methylation patterns on episomal vectors in Lsh-/- fibroblasts, while maintenance of pre-existing methylation does not require Lsh. Episomal methylation assay in Lsh-/- fibroblasts, co-immunoprecipitation, ES cell knockdown, retroviral silencing assays The EMBO journal High 16395332
2007 LSH functions as a transcriptional repressor when targeted to a promoter; it cooperates with DNMT1, DNMT3B, HDAC1, and HDAC2 to silence transcription. LSH is present mostly as a monomeric protein in nuclear extracts and is not found in a large multisubunit complex. Interactions with HDACs and transcriptional repression are lost in DNMT1/DNMT3B knockout cells, but DNMT enzymatic activity is not required for LSH-mediated silencing. Promoter-targeting reporter assay, native co-immunoprecipitation, DNMT knockout cell lines, HDAC inhibitor experiments Molecular and cellular biology High 17967891
2010 LSH cooperates with the G9a/GLP histone methyltransferase complex for developmentally programmed DNA methylation at specific gene promoters. In the absence of LSH, G9a recruitment is compromised at affected loci, and methylation and gene silencing are impaired. Genome-wide promoter methylation profiling in Hells-/- MEFs, ChIP for G9a, comparison with DNMT and ES cell methylation patterns Genome research High 21149390
2015 The ATP-binding/hydrolysis activity of Lsh is required for de novo DNA methylation at repeat sequences and for normal nucleosome density. ATP-mutant Lsh fails to promote stable association of DNMT3b with repeat loci and cannot restore nucleosome occupancy in KO ES cells. ATPase-dead Lsh mutant rescue in KO ES cells, DNMT3b ChIP, MNase nucleosome occupancy assay Nucleic acids research High 25578963
2020 LSH facilitates DNA methylation by DNMT1 through promoting UHRF1 chromatin association and UHRF1-catalyzed H3 ubiquitination in an ATPase-dependent manner, which recruits DNMT1 to the replication fork. LSH interacts with UHRF1 but not with DNMT1 directly. A feed-forward loop exists where UHRF1 also enhances LSH association with the replication fork. Co-immunoprecipitation, UHRF1 chromatin fractionation, H3 ubiquitination assay, replication fork ChIP, ATPase-dead mutant analysis Nucleic acids research High 33170271
2020 LSH induces macroH2A1.2 and macroH2A2 deposition at chromatin in an ATP-dependent manner, and this macroH2A deposition mediates transcriptional repression. LSH is a major genome-wide regulator of macroH2A distribution. ICF4 patient mutations in LSH fail to induce macroH2A deposition, and ICF4 patient cells show reduced macroH2A enrichment. Chemical-induced proximity (CIP) tethering to engineered locus, siRNA knockdown, ChIP-seq for macroH2A, ICF4 patient cell analysis, ATPase-dead mutant Nature communications High 33159050
2021 LSH protects stalled replication forks from nascent DNA degradation via macroH2A-dependent RAD51 filament formation. LSH/macroH2A deficiency impairs RAD51 loading by perturbing BRCA1/53BP1 balance at stalled forks through abnormal H4K20 methylation. MRE11 and EXO1 mediate the nascent DNA degradation in LSH-deficient cells. DNA fiber assay (fork protection), RAD51 ChIP/foci, BRCA1/53BP1 foci, H4K20me ChIP, macroH2A overexpression rescue, MRE11/EXO1 inhibitor epistasis Nature communications High 34112784
2003 Lsh accumulates at pericentromeric heterochromatin in an exclusively nuclear localization, with the N-terminal region containing the nuclear localization domain and internal/C-terminal regions required for chromatin association. Histone deacetylase inhibitor treatment that disrupts heterochromatin organization causes dissociation of Lsh from pericentromeric heterochromatin, indicating intact heterochromatin structure is required for Lsh recruitment. GFP-fusion live imaging, subcellular fractionation, deletion mutant mapping, HDAC inhibitor treatment, immunofluorescence Molecular and cellular biology High 14612388
2003 Loss of Lsh results in accumulation of di- and tri-methylated H3K4 at pericentromeric DNA and repetitive sequences, while H3K9me2/3 and HP1 distribution appear unchanged. Chemical DNA demethylation with 5-azacytidine recapitulates the H3K4me increase, supporting a model where Lsh-dependent CpG methylation loss antecedes H3K4 hypermethylation. ChIP with H3K4me and H3K9me antibodies in Lsh-/- mice, 5-azacytidine demethylation experiment The EMBO journal High 14517253
2004 Lsh directly associates with repetitive genomic sequences (pericentromeric repeats, retroviral LTR elements) by ChIP, and its deletion leads to increased histone acetylation and transcriptional reactivation at these repeat loci without major effects on single-copy genes. Chromatin immunoprecipitation, microarray transcriptome analysis, histone acetylation ChIP Nucleic acids research High 15448183
2012 LSH ATPase activity is required for efficient H2AX phosphorylation (γH2AX formation) in response to DNA double-strand breaks, and LSH-deficient cells show impaired MDC1 and 53BP1 recruitment to DSBs and compromised CHK2 phosphorylation. LSH-deficient cells repair DSBs less efficiently and show reduced viability after ionizing radiation. ATPase-dead LSH mutant, γH2AX foci quantification, ionizing radiation survival, 53BP1/MDC1 foci, CHK2 phosphorylation assay Journal of cell science High 22946062
2020 HELLS and PRDM9 form a pioneer complex at meiotic recombination hot spots. HELLS is recruited to hot spots by PRDM9 and is necessary for histone modifications (PRDM9-dependent H3K4me3 and H3K36me3) and DNA accessibility at hot spots. In male mice lacking HELLS, DSBs are retargeted to other open chromatin sites, leading to germ cell death and sterility. ATAC-seq for chromatin accessibility, ChIP-seq for histone modifications and PRDM9, DSB mapping in Hells knockout mice, spermatocyte phenotyping Genes & development High 32001511
2020 HELLS is required for PRDM9 binding and DSB formation at PRDM9-specified recombination hot spots during male meiosis, but not for DSB activity at PRDM9-independent sites. HELLS is also essential for 5-hydroxymethylcytosine (5hmC) enrichment at PRDM9 hot spots, which occurs downstream of PRDM9 binding and histone modification but independent of DSB catalysis. Proteomic identification of PRDM9 partners, ChIP-seq for PRDM9 binding, DSB mapping, 5hmC profiling in Hells KO and SPO11/PRDM9 mutant mice eLife High 33047671
2018 CDCA7 and HELLS deficiency compromises canonical non-homologous end joining (C-NHEJ): Ku80 and Ku70 co-immunoprecipitate with CDCA7, HELLS-deficient and CDCA7-deficient HEK293 cells show delayed Ku80 accumulation at DNA damage sites and impaired C-NHEJ activity. ICF3 mutations in CDCA7 that impair chromatin binding abrogate the co-IP with Ku proteins. Co-immunoprecipitation, NHEJ reporter assay, live-cell imaging of Ku80 recruitment to laser-induced damage, γH2AX quantification, ICF patient lymphoblastoid cell analysis The Journal of clinical investigation High 30307408
2020 HELLS promotes end resection to facilitate homologous recombination at two-ended DSBs and contributes to DSB repair within heterochromatin during G2. HELLS interacts with CtIP and facilitates CtIP accumulation at IR-induced foci. The ATPase domain of HELLS is required for this HR-promoting function. Co-immunoprecipitation of HELLS-CtIP, CtIP foci quantification, HR reporter assay, ATPase-dead mutant analysis, cell cycle staging Nucleic acids research High 31802118
2011 HELLS interacts with E2F3A in vivo and cooperates with E2F3 transcriptional activity. HELLS binds promoters of active genes genome-wide and co-regulates E2F3-dependent genes including MLL1. Depletion of HELLS perturbs E2F-target gene induction and impairs cell-cycle re-entry. Mass spectrometric identification of E2F3B interaction partners, co-immunoprecipitation, ChIP-seq for HELLS and E2F3A/B, siRNA knockdown with cell cycle and transcription readouts The EMBO journal High 22157815
2006 Lsh is essential for meiotic chromosome synapsis and transcriptional silencing of retrotransposons in female germ cells. Lsh knockout oocytes show demethylation of transposable elements and tandem repeats at pericentric heterochromatin, incomplete chromosome synapsis with persistent RAD51 foci, γH2AX phosphorylation, failure to load crossover-associated foci, and absence of ovarian follicle formation. Lsh knockout mouse analysis, immunofluorescence for synapsis markers and RAD51/γH2AX, bisulfite methylation analysis, nuclear compartmentalization of Lsh in germ line Nature cell biology High 17115026
2011 Lymphoid-specific helicase (HELLS/LSH) is essential for meiotic progression in male spermatocytes: HELLS-null grafted testes show arrest at mid-pachytene stage with abnormal chromosome synapsis and reduced spermatogonial proliferation. Ectopic testis tissue grafting into immunodeficient mice, BrdU incorporation, meiotic chromosome spread analysis Biology of reproduction High 21349825
2007 Lsh can associate with Hox gene loci and regulates Dnmt3b binding and DNA methylation at selected Hox genes during development. Lsh can also associate with PRC1 components and influences PRC-mediated histone modifications at Hox genes, placing Lsh in a feedback loop reinforcing both DNA methylation and Polycomb silencing. ChIP for Lsh, Dnmt3b, and PRC1 components at Hox loci; methylation analysis in Lsh-/- embryos; Hox gene expression profiling Proceedings of the National Academy of Sciences of the United States of America High 17726103
2009 Lsh represses p16(INK4a) to delay cellular senescence by recruiting HDAC1 and HDAC2 to the p16 promoter. Lsh interacts with HDAC1 and HDAC2 in vivo, and HDAC inhibitor treatment (TSA) blocks the repressive effect of Lsh and reverses histone H3 deacetylation at the p16 promoter. Co-immunoprecipitation of Lsh with HDAC1/2, ChIP for Lsh and acetylated H3 at p16 promoter, TSA treatment, senescence assays Nucleic acids research High 19561196
2017 DDM1 (plant ortholog) and Lsh (mouse) enable DNA methylation of nucleosomal DNA; genetic inactivation of these remodelers biases methylation toward inter-nucleosomal linker DNA, indicating that nucleosome-wrapped DNA (not naked/linker DNA) is the preferred substrate of eukaryotic methyltransferases in vivo when the remodeler is present. Whole-genome bisulfite sequencing in Arabidopsis DDM1 mutants and mouse Lsh mutants, simultaneous DDM1/H1 double mutant analysis eLife High 29140247
2019 HELLS alters nucleosome occupancy at transcriptional regulatory regions (putative enhancers characterized by DNase I hypersensitivity and H3 tail modifications). This nucleosome remodeling activity is independent of DNA methylation level and involves reduced H3 occupancy. LSH-mediated nucleosome positioning prevents binding of tissue-specific transcription factors, and LSH depletion increases binding of ectopically expressed transcription factors to their sites. MNase-seq for nucleosome occupancy, auxin-inducible degron for acute Lsh depletion, transcription factor binding ChIP after depletion Epigenetics High 30861354
2005 Lsh directly associates with the 5' DMR at the Cdkn1c promoter (by ChIP) and is required for CpG methylation at this site and silencing of the paternal Cdkn1c allele (imprinting), but Lsh is not required for maintenance of imprinting marks at H19, Igf2, Igf2r, Zac1, or Meg9. ChIP for Lsh at imprinted loci, bisulfite methylation analysis, allelic expression analysis in Lsh-/- embryos Development (Cambridge, England) High 15647320
2009 Lsh is required for establishment of DNA methylation at stem cell-specific gene promoters (e.g., Oct4) during ES cell differentiation, in part by regulating access of Dnmt3b to its genomic targets. Lsh depletion prevents complete silencing of stem cell gene expression during differentiation. Bisulfite methylation analysis, Dnmt3b ChIP at stem cell gene loci in Lsh-/- cells, differentiation assays with gene expression monitoring Stem cells (Dayton, Ohio) High 19650037
2016 LSH binds the FH (fumarate hydratase) promoter and recruits the epigenetic silencer G9a to repress FH transcription, thereby modulating TCA cycle intermediates and promoting EMT in nasopharyngeal carcinoma. ChIP for LSH and G9a at FH promoter, RNAi knockdown of FH, TCA intermediate measurement, EMT phenotype assays Cancer research Medium 27302170
2020 LSH depletion leads to increased transcription of pericentromeric repeat sequences and formation of aberrant DNA:RNA hybrids (R-loops) at these repeats. The CDCA7/HELLS complex is required for accumulation of DNMT1/UHRF1 maintenance methylation machinery on nascent DNA. Ectopic expression of RNASEH1 reduces DNA damage accumulation in ICF mutant cells. DRIP-seq for R-loops, iPOND for nascent DNA proteomics, RNASEH1 rescue, pericentromeric repeat transcription quantification in ICF mutant cells Scientific reports High 33082427
2020 LSH is required for B lymphocyte development and immunoglobulin class switch recombination (CSR): conditional Lsh knockout B cells initiate CSR normally (normal germline transcripts and DSBs) but show impaired canonical end-joining at CSR junctions, indicating LSH promotes the end-joining step of CSR. Conditional Lsh KO (Mx1- and Vav-Cre), bone marrow transplantation, biotin-labeling DNA break assay, End-seq, digestion-circularization PCR, chromosomal break repair assay Proceedings of the National Academy of Sciences of the United States of America High 32727902
2017 Lsh/HELLS is required for self-renewal and proliferation of neural stem/progenitor cells; its ablation alters epigenetic states (H3K4me1 and DNA methylation) at enhancer regions of the cell cycle regulator Cdkn1a and stem cell regulator Bmp4, altering their expression. Lsh-/- neural stem cell culture, RNA-seq, ChIP for H3K4me1 and methylation at Cdkn1a and Bmp4 enhancers, apoptosis and self-renewal assays Scientific reports Medium 28442710
2023 USP5 (ubiquitin-specific protease 5) acts as a deubiquitinase for LSH, interacting with LSH and stabilizing it by removing ubiquitin modifications through a deubiquitylation activity-dependent process, which promotes HCC tumor progression. Co-immunoprecipitation, ubiquitination assay, USP5 inhibitor (degrasyn), knockdown/overexpression functional assays in HCC cells MedComm Medium 37492786
2020 CRL4DCAF8 is a bona fide E3 ubiquitin ligase for LSH that promotes its degradation; WDR76 antagonizes DCAF8-targeted LSH proteolysis through competitive inhibition of the holo-CRL4DCAF8-LSH complex. This opposing regulatory system controls LSH stability during ferroptosis. CRL4-DCAF8 complex reconstitution, degradation assay, competitive inhibition analysis, transcriptomic epistasis in ferroptosis Cell death and differentiation Medium 33288900
2020 LSH regulates kinetochore function in oocyte meiosis: LSH is enriched at meiotic kinetochores and the inner centromere, and its deletion causes increased histone H3T3 phosphorylation, HDAC2 and DNMT1 reduction at centromeres, accumulation of major satellite transcripts, centromere fusions, ectopic kinetochore formation, and abnormal chromosome segregation. Super-resolution chromatin immunofluorescence, H3T3ph ChIP/immunostaining, centromere transcript quantification, LSH conditional KO oocyte analysis Nature communications High 32900989
2000 Lsh is expressed primarily in lymphoid tissue (highest in thymocytes) in adults and is induced by T cell receptor crosslinking plus CD28 costimulation correlating with S phase entry. Lsh-/- T cells undergo apoptosis and show severely suppressed proliferation after polyclonal activation, while cytokine production and V(D)J recombination remain normal. Lsh gene knockout by homologous recombination, hematopoietic reconstitution in Rag2-/- mice, proliferation assay, apoptosis assay, cytokine measurement Proceedings of the National Academy of Sciences of the United States of America High 10781083
2003 Lsh-/- murine embryonal fibroblasts show severe proliferative defects, early senescence, and abnormal mitosis characterized by high centrosome numbers, multipolar spindles, micronuclei, and elevated DNA content. Similar centrosome abnormalities are induced in wild-type cells by 5-azacytidine (a demethylating agent), suggesting hypomethylation drives the mitotic defects. MEF culture from Lsh-/- embryos, centrosome immunostaining, mitotic spindle analysis, 5-azacytidine treatment epistasis Cancer research High 12907649
2004 Disruption of PASG/Lsh causes global DNA hypomethylation, developmental growth retardation, and a premature aging phenotype in mice. PASG mutant fibroblasts show replicative senescence and markedly increased p16(INK4a) expression associated with down-regulation of bmi-1 (a negative regulator of p16), independent of promoter methylation changes. Targeted gene disruption, whole-genome methylation analysis, senescence assays, p16/bmi-1 expression analysis in PASG-/- mice Genes & development High 15105378
2019 HELLS interacts with E2F3 and MYC transcription factors in glioblastoma stem cells (GSCs) to regulate gene expression critical to GSC proliferation and maintenance; HELLS targeting disrupts GSC proliferation, survival, and self-renewal with induction of replication stress and DNA damage. Co-immunoprecipitation of HELLS with E2F3 and MYC, HELLS knockdown with proliferation/self-renewal/DNA damage readouts JCI insight Medium 30779712
2019 LSH interacts with and stabilizes GINS4 mRNA by binding to its 3' UTR region, increasing GINS4 expression at the post-transcriptional level in non-small cell lung cancer cells. Co-immunoprecipitation, RNA immunoprecipitation assay, GINS4 3'UTR binding analysis Journal of experimental & clinical cancer research Low 31253190
2019 The lncRNA GIAT4RA promotes LSH ubiquitination and proteasomal degradation by binding the 227-589 AA region of LSH and counteracting the interaction between LSH and the deubiquitinase Uchl3, thereby reducing Uchl3-mediated LSH stabilization. Co-immunoprecipitation, ubiquitination assay, domain mapping of GIAT4RA-LSH interaction, Uchl3 competitive inhibition analysis Oncogene Medium 31417184
2023 USP11 deubiquitinates and stabilizes LSH protein; this interaction is disrupted by erastin treatment. Stabilized LSH then binds the CYP24A1 promoter, promotes nucleosome eviction and reduces H3K27me3 occupancy at this locus, activating CYP24A1 transcription to inhibit ferroptosis in colorectal cancer. Co-immunoprecipitation, ubiquitination assay, ChIP for LSH and H3K27me3 at CYP24A1 promoter, MNase nucleosome assay, ferroptosis phenotype assays Cell death & disease Medium 37414755
2019 LSH inhibits p53 ubiquitination (specifically K11- and K48-linked polyubiquitin chains), preventing proteasomal degradation of p53. LSH also forms a complex with PKM2, and this LSH-PKM2 complex transactivates p53-mediated lipid metabolism gene expression. The LSH-PKM2 interaction is mediated by the PKM2 C-terminal region and the coiled-coil/ATP-binding domains of LSH. Co-immunoprecipitation, ubiquitination assay with linkage-specific antibodies, domain mapping, p53 transcriptional activity assay Epigenetics & chromatin Medium 31594538
2023 CDCA7 and HELLS show strong coevolutionary presence-absence patterns with DNMT1 and UHRF1 across eukaryotes. Almost all CDCA7-harboring eukaryote species also have HELLS and a maintenance methyltransferase (DNMT1 or DNMT5), supporting that the CDCA7-HELLS complex has a specialized conserved role in HELLS-dependent DNA methylation maintenance inherited from the last eukaryotic common ancestor. Phylogenetic coevolution analysis (CoPAP), genome database survey across eukaryotic clades eLife Low 37769127

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 The Ity/Lsh/Bcg locus: natural resistance to infection with intracellular parasites is abrogated by disruption of the Nramp1 gene. The Journal of experimental medicine 483 7650477
1991 Type 1 diabetes in mice is linked to the interleukin-1 receptor and Lsh/Ity/Bcg genes on chromosome 1. Nature 182 1832743
2011 ΔNp63α is an oncogene that targets chromatin remodeler Lsh to drive skin stem cell proliferation and tumorigenesis. Cell stem cell 173 21295273
2015 Mutations in CDCA7 and HELLS cause immunodeficiency-centromeric instability-facial anomalies syndrome. Nature communications 149 26216346
1996 The Bcg/Ity/Lsh locus: genetic transfer of resistance to infections in C57BL/6J mice transgenic for the Nramp1 Gly169 allele. Infection and immunity 145 8757814
2004 Growth retardation and premature aging phenotypes in mice with disruption of the SNF2-like gene, PASG. Genes & development 143 15105378
2006 Lsh is involved in de novo methylation of DNA. The EMBO journal 138 16395332
1984 Expression of the natural resistance gene Lsh in resident liver macrophages. Infection and immunity 130 6698599
2007 LSH cooperates with DNA methyltransferases to repress transcription. Molecular and cellular biology 120 17967891
1995 Natural resistance to infection with intracellular parasites: molecular genetics identifies Nramp1 as the Bcg/Ity/Lsh locus. Journal of leukocyte biology 118 7561513
2003 Divalent cation transport and susceptibility to infectious and autoimmune disease: continuation of the Ity/Lsh/Bcg/Nramp1/Slc11a1 gene story. Immunology letters 116 12527228
1982 Inbred mouse strain resistance to Mycobacterium lepraemurium follows the Ity/Lsh pattern. Immunology 111 6749659
2018 HELLS and CDCA7 comprise a bipartite nucleosome remodeling complex defective in ICF syndrome. Proceedings of the National Academy of Sciences of the United States of America 106 29339483
1995 Nramp transfection transfers Ity/Lsh/Bcg-related pleiotropic effects on macrophage activation: influence on oxidative burst and nitric oxide pathways. Molecular medicine (Cambridge, Mass.) 105 8529105
2006 Lsh is required for meiotic chromosome synapsis and retrotransposon silencing in female germ cells. Nature cell biology 103 17115026
2004 Lsh, an epigenetic guardian of repetitive elements. Nucleic acids research 102 15448183
2010 LSH and G9a/GLP complex are required for developmentally programmed DNA methylation. Genome research 99 21149390
2016 Chromatin Remodeling Factor LSH Drives Cancer Progression by Suppressing the Activity of Fumarate Hydratase. Cancer research 93 27302170
2017 DDM1 and Lsh remodelers allow methylation of DNA wrapped in nucleosomes. eLife 92 29140247
1994 Genetic regulation of leishmanial and mycobacterial infections: the Lsh/Ity/Bcg gene story continues. Immunology letters 92 7737696
2000 Lsh, an SNF2/helicase family member, is required for proliferation of mature T lymphocytes. Proceedings of the National Academy of Sciences of the United States of America 86 10781083
1999 Genetic regulation of macrophage activation: understanding the function of Nramp1 (=Ity/Lsh/Bcg). Immunology letters 83 10065630
2014 Genome-wide DNA methylation patterns in LSH mutant reveals de-repression of repeat elements and redundant epigenetic silencing pathways. Genome research 81 25170028
2010 Downstream targets of FOXM1: CEP55 and HELLS are cancer progression markers of head and neck squamous cell carcinoma. Oral oncology 79 20400365
2003 Lsh, a modulator of CpG methylation, is crucial for normal histone methylation. The EMBO journal 79 14517253
2011 Lsh, chromatin remodeling family member, modulates genome-wide cytosine methylation patterns at nonrepeat sequences. Proceedings of the National Academy of Sciences of the United States of America 77 21427231
2001 Lsh, a SNF2 family member, is required for normal murine development. Biochimica et biophysica acta 76 11325543
2018 CDCA7 and HELLS mutations undermine nonhomologous end joining in centromeric instability syndrome. The Journal of clinical investigation 73 30307408
1991 Genetic regulation of macrophage priming/activation: the Lsh gene story. Immunology letters 73 1757110
2011 The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation. The EMBO journal 70 22157815
1994 Induction of early-response genes KC and JE by mycobacterial lipoarabinomannans: regulation of KC expression in murine macrophages by Lsh/Ity/Bcg (candidate Nramp). Infection and immunity 69 8132324
2000 Proliferation-associated SNF2-like gene (PASG): a SNF2 family member altered in leukemia. Cancer research 65 10910076
2015 The ATP binding site of the chromatin remodeling homolog Lsh is required for nucleosome density and de novo DNA methylation at repeat sequences. Nucleic acids research 64 25578963
2018 Comparative methylome analysis of ICF patients identifies heterochromatin loci that require ZBTB24, CDCA7 and HELLS for their methylated state. Human molecular genetics 63 29659838
1997 Nramp1 transfection transfers Ity/Lsh/Bcg-related pleiotropic effects on macrophage activation: influence on antigen processing and presentation. Infection and immunity 63 9009286
2007 Lsh controls Hox gene silencing during development. Proceedings of the National Academy of Sciences of the United States of America 62 17726103
2019 HELLS Regulates Chromatin Remodeling and Epigenetic Silencing of Multiple Tumor Suppressor Genes in Human Hepatocellular Carcinoma. Hepatology (Baltimore, Md.) 60 30516846
2009 Lsh participates in DNA methylation and silencing of stem cell genes. Stem cells (Dayton, Ohio) 60 19650037
2005 Lsh controls silencing of the imprinted Cdkn1c gene. Development (Cambridge, England) 60 15647320
2003 Association of Lsh, a regulator of DNA methylation, with pericentromeric heterochromatin is dependent on intact heterochromatin. Molecular and cellular biology 60 14612388
2020 A role for LSH in facilitating DNA methylation by DNMT1 through enhancing UHRF1 chromatin association. Nucleic acids research 55 33170271
2017 Chromatin Remodeling Factor LSH is Upregulated by the LRP6-GSK3β-E2F1 Axis Linking Reversely with Survival in Gliomas. Theranostics 55 28042322
2012 The SNF2 family ATPase LSH promotes phosphorylation of H2AX and efficient repair of DNA double-strand breaks in mammalian cells. Journal of cell science 55 22946062
2005 Lsh, a guardian of heterochromatin at repeat elements. Biochemistry and cell biology = Biochimie et biologie cellulaire 53 16094458
2003 Lsh-deficient murine embryonal fibroblasts show reduced proliferation with signs of abnormal mitosis. Cancer research 52 12907649
1993 The murine homologue of the human interleukin-8 receptor type B maps near the Ity-Lsh-Bcg disease resistance locus. Genomics 52 8288247
2020 HELLS and PRDM9 form a pioneer complex to open chromatin at meiotic recombination hot spots. Genes & development 51 32001511
1993 An RFLP map for 2q33-q37 from multicase mycobacterial and leishmanial disease families: no evidence for an Lsh/Ity/Bcg gene homologue influencing susceptibility to leprosy. Annals of human genetics 51 7910002
2013 Lsh regulates LTR retrotransposon repression independently of Dnmt3b function. Genome biology 50 24367978
1989 Influence of Lsh, H-2, and an H-11-linked gene on visceralization and metastasis associated with Leishmania mexicana infection in mice. Infection and immunity 49 2917789
2020 The human HELLS chromatin remodelling protein promotes end resection to facilitate homologous recombination and contributes to DSB repair within heterochromatin. Nucleic acids research 48 31802118
1987 Variable expression of the murine natural resistance gene Lsh in different macrophage populations infected in vitro with Leishmania donovani. Parasite immunology 46 3431902
2019 LSH interacts with and stabilizes GINS4 transcript that promotes tumourigenesis in non-small cell lung cancer. Journal of experimental & clinical cancer research : CR 44 31253190
1990 A genetic map of mouse chromosome 1 near the Lsh-Ity-Bcg disease resistance locus. Genomics 44 1970800
2019 Chromatin remodeler HELLS maintains glioma stem cells through E2F3 and MYC. JCI insight 42 30779712
2019 GIAT4RA functions as a tumor suppressor in non-small cell lung cancer by counteracting Uchl3-mediated deubiquitination of LSH. Oncogene 42 31417184
1994 Interaction with extracellular matrix proteins influences Lsh/Ity/Bcg (candidate Nramp) gene regulation of macrophage priming/activation for tumour necrosis factor-alpha and nitrite release. Immunology 42 8045593
2009 Senescence delay and repression of p16INK4a by Lsh via recruitment of histone deacetylases in human diploid fibroblasts. Nucleic acids research 40 19561196
2015 Senescence-associated Long Non-coding RNA (SALNR) Delays Oncogene-induced Senescence through NF90 Regulation. The Journal of biological chemistry 38 26491010
2014 CG hypomethylation in Lsh-/- mouse embryonic fibroblasts is associated with de novo H3K4me1 formation and altered cellular plasticity. Proceedings of the National Academy of Sciences of the United States of America 37 24711395
2010 Lsh mediated RNA polymerase II stalling at HoxC6 and HoxC8 involves DNA methylation. PloS one 36 20161795
2017 Metabolic pathway for a new strain Pseudomonas synxantha LSH-7': from chemotaxis to uptake of n-hexadecane. Scientific reports 35 28051099
2020 LSH mediates gene repression through macroH2A deposition. Nature communications 34 33159050
2017 Lsh/HELLS regulates self-renewal/proliferation of neural stem/progenitor cells. Scientific reports 34 28442710
2023 The ubiquitin-specific protease 5 mediated deubiquitination of LSH links metabolic regulation of ferroptosis to hepatocellular carcinoma progression. MedComm 33 37492786
2020 CDCA7 and HELLS suppress DNA:RNA hybrid-associated DNA damage at pericentromeric repeats. Scientific reports 33 33082427
1988 Acquisition of cell-mediated immunity to Leishmania. II. LSH gene regulation of accessory cell function. Immunology 33 3141269
2014 Chromatin remodelers HELLS and UHRF1 mediate the epigenetic deregulation of genes that drive retinoblastoma tumor progression. Oncotarget 32 25338120
2023 USP11-mediated LSH deubiquitination inhibits ferroptosis in colorectal cancer through epigenetic activation of CYP24A1. Cell death & disease 31 37414755
2020 Chromatin remodeling protein HELLS is critical for retinoblastoma tumor initiation and progression. Oncogenesis 31 32071286
2011 Lymphoid-specific helicase (HELLS) is essential for meiotic progression in mouse spermatocytes. Biology of reproduction 31 21349825
1992 Melatonin decreases estrogen receptor expression in the medial preoptic area of inbred (LSH/SsLak) golden hamsters. Biology of reproduction 31 1493172
1988 Differences in Lsh gene control over systemic Leishmania major and Leishmania donovani or Leishmania mexicana mexicana infections are caused by differential targeting to infiltrating and resident liver macrophage populations. Infection and immunity 31 3356462
2008 DNA hypomethylation caused by Lsh deletion promotes erythroleukemia development. Epigenetics 30 18487951
2021 The epigenetic regulator LSH maintains fork protection and genomic stability via MacroH2A deposition and RAD51 filament formation. Nature communications 28 34112784
2020 HELLS, a chromatin remodeler is highly expressed in pancreatic cancer and downregulation of it impairs tumor growth and sensitizes to cisplatin by reexpressing the tumor suppressor TGFBR3. Cancer medicine 28 33280236
2020 CRL4DCAF8 dependent opposing stability control over the chromatin remodeler LSH orchestrates epigenetic dynamics in ferroptosis. Cell death and differentiation 28 33288900
2011 Hell's Gate globin I: an acid and thermostable bacterial hemoglobin resembling mammalian neuroglobin. FEBS letters 28 21925500
2004 Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer. International journal of cancer 28 15305370
1995 Involvement of CD4+ T lymphocytes in induction of severe destructive Lyme arthritis in inbred LSH hamsters. Infection and immunity 28 7591141
2020 Lsh/HELLS is required for B lymphocyte development and immunoglobulin class switch recombination. Proceedings of the National Academy of Sciences of the United States of America 26 32727902
2022 The Chromatin Remodeler HELLS: A New Regulator in DNA Repair, Genome Maintenance, and Cancer. International journal of molecular sciences 24 36012581
2019 Downregulation of the Helicase Lymphoid-Specific (HELLS) Gene Impairs Cell Proliferation and Induces Cell Cycle Arrest in Colorectal Cancer Cells. OncoTargets and therapy 24 32063710
2016 The SNF2 family ATPase LSH promotes cell-autonomous de novo DNA methylation in somatic cells. Nucleic acids research 24 27179028
2004 TP53 in gastric cancer: mutations in the l3 loop and LSH motif DNA-binding domains of TP53 predict poor outcome. Journal of cellular physiology 24 15254976
2020 Identification and validation of HELLS (Helicase, Lymphoid-Specific) and ICAM1 (Intercellular adhesion molecule 1) as potential diagnostic biomarkers of lung cancer. PeerJ 23 32195055
2020 PRDM9 activity depends on HELLS and promotes local 5-hydroxymethylcytosine enrichment. eLife 23 33047671
2019 The chromatin remodeling protein Lsh alters nucleosome occupancy at putative enhancers and modulates binding of lineage specific transcription factors. Epigenetics 23 30861354
2019 DNA methylation modifier LSH inhibits p53 ubiquitination and transactivates p53 to promote lipid metabolism. Epigenetics & chromatin 22 31594538
2018 Aryl hydrocarbon receptor activated by benzo (a) pyrene promotes SMARCA6 expression in NSCLC. American journal of cancer research 22 30094095
2016 The LSH/DDM1 Homolog MUS-30 Is Required for Genome Stability, but Not for DNA Methylation in Neurospora crassa. PLoS genetics 22 26771905
2011 Linking expression of FOXM1, CEP55 and HELLS to tumorigenesis in oropharyngeal squamous cell carcinoma. The Laryngoscope 22 22109759
1985 Genetic control of systemic Leishmania major infections: dissociation of intrahepatic amastigote replication from control by the Lsh gene. Infection and immunity 21 4055035
2019 Upregulation of the chromatin remodeler HELLS is mediated by YAP1 in Sonic Hedgehog Medulloblastoma. Scientific reports 20 31541170
2022 Efficient biodegradation of phenanthrene using Pseudomonas stutzeri LSH-PAH1 with the addition of sophorolipids: Alleviation of biotoxicity and cometabolism studies. Environmental pollution (Barking, Essex : 1987) 19 35182655
2020 Helicase LSH/Hells regulates kinetochore function, histone H3/Thr3 phosphorylation and centromere transcription during oocyte meiosis. Nature communications 19 32900989
2016 Chromatin remodeling factor LSH affects fumarate hydratase as a cancer driver. Chinese journal of cancer 18 27473869
1994 Influence of macrophage resistance gene Lsh/Ity/Bcg (candidate Nramp) on Toxoplasma gondii infection in mice. Clinical and experimental immunology 18 8033407
2023 Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases. eLife 17 37769127
2017 The LSH/HELLS homolog Irc5 contributes to cohesin association with chromatin in yeast. Nucleic acids research 17 28383696