Affinage

MACROH2A1

Core histone macro-H2A.1 · UniProt O75367

Length
369 aa
Mass
39.2 kDa
Annotated
2026-06-10
97 papers in source corpus 50 papers cited in narrative 50 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MacroH2A1 (H2AFY) is a tripartite histone variant whose H2A-like domain incorporates into nucleosomes while an appended macrodomain confers chromatin-regulatory and metabolite-sensing functions that shape gene expression, heterochromatin maintenance, and the DNA damage response (PMID:9634239, PMID:11772015). As a structural component of chromatin it produces nucleosomes resistant to DNase I and prone to internucleosomal interactions (PMID:11772015), is enriched on the inactive X chromosome and at H3K27me3-marked autosomal domains while being depleted from active gene bodies (PMID:9634239, PMID:16738309, PMID:20937776), and represses defined gene sets—including lipid metabolism genes, endogenous retroviruses, and rDNA—in vivo (PMID:17242180, PMID:18195046, PMID:24071584). Its two alternatively spliced isoforms diverge in the macrodomain: macroH2A1.1 binds NAD+-derived metabolites and poly(ADP-ribose), through which it suppresses basal PARP-1 activity to limit nuclear NAD+ consumption and sustain mitochondrial respiration and systemic energy metabolism (PMID:28991266, PMID:41134882), whereas macroH2A1.2 lacks this binding capacity (PMID:21844227, PMID:29339820). macroH2A1.1 is recruited to PARylated chromatin at double-strand breaks where it controls PAR dynamics, promotes NHEJ via PARP1/XRCC1 association, and supports DSB signaling (PMID:23031826, PMID:31636161, PMID:35511867); macroH2A1.2 instead promotes homologous-recombination-dependent processes such as ALT telomere maintenance under replication stress (PMID:30833786). Beyond repression, macroH2A1 cooperates with chromatin-modifying machinery—licensing CBP-mediated H2B acetylation through PARP-1 (PMID:25306110), partnering with EZH2 to deposit H3K27me2/3 (PMID:28992292), and controlling enhancer H3K27 acetylation during myogenesis (PMID:26832413). Its chromatin occupancy is dynamically regulated by ATRX, which restricts macroH2A association (PMID:22391447, PMID:30833786), by the FACT complex, which destabilizes macroH2A1.2 nucleosomes during transcription (PMID:39116874), and by multiple E3 ligases (CULLIN3/SPOP, SKP2, TRIM59) that govern its deposition and turnover (PMID:15897469, PMID:25818643, PMID:31488827). The protein carries diverse post-translational modifications including ubiquitination at K115/K116, mitotic S137 phosphorylation, and AMPKα-mediated S146 phosphorylation (PMID:16210244, PMID:16129414, PMID:18227505, PMID:39545415).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1998 High

    Established that macroH2A1 is a bona fide histone variant with an unusual non-histone extension and revealed its hallmark concentration on the inactive X chromosome, linking a histone variant directly to X inactivation.

    Evidence Gene cloning, protein characterization and immunofluorescence in female mammalian cells

    PMID:9634239

    Open questions at the time
    • Did not establish whether macroH2A1 is required for X inactivation versus merely a marker
    • Function of the macrodomain unknown at this stage
  2. 2000 High

    Resolved when and how macroH2A reaches the Xi by showing a non-chromatin centrosomal storage pool that redistributes to the Xi during differentiation, coincident with Xist stabilization, defining macroH2A deposition as a regulated post-initiation event.

    Evidence Immuno-RNA FISH and cell fractionation in differentiating ES cells, with centrosome co-purification in somatic cells

    PMID:10613899 PMID:10974005 PMID:11478850

    Open questions at the time
    • Mechanism targeting macroH2A specifically to the Xi not defined
    • Functional role of the centrosomal pool unresolved
  3. 2002 High

    Demonstrated that macroH2A1.2 can structurally substitute for canonical H2A in nucleosomes and alters their biophysical properties, providing the structural basis for its repressive chromatin function.

    Evidence In vitro nucleosome reconstitution with nuclease digestion and sedimentation assays

    PMID:11772015

    Open questions at the time
    • Did not connect altered nucleosome structure to specific transcriptional outcomes in vivo
    • Macrodomain contribution not isolated
  4. 2005 High

    Defined the macroH2A1 modification landscape and identified the CULLIN3/SPOP E3 ligase as a regulator of macroH2A1 deposition required for stable X inactivation, moving the field from localization to regulated control.

    Evidence Mass spectrometry of endogenous protein; RNAi knockdown with Xi reactivation and ubiquitination assays

    PMID:15897469 PMID:16129414 PMID:16210244

    Open questions at the time
    • Functional consequence of individual PTM sites not dissected
    • How ubiquitination alters macroH2A1 chromatin behavior unclear
  5. 2007 High

    Established macroH2A1 as a direct transcriptional repressor in vivo using knockout mice, showing derepression of macroH2A1-bound genes (notably lipid metabolism) and silencing of endogenous retroviruses linked to DNA methylation.

    Evidence MacroH2A1 knockout mice with expression arrays, ChIP, and bisulfite sequencing

    PMID:17242180 PMID:18195046

    Open questions at the time
    • Mechanism by which macroH2A1 enforces repression not fully resolved
    • Isoform-specific contributions not separated
  6. 2009 High

    Revealed that macroH2A1 occupancy is not uniformly repressive, mapping it to large H3K27me3 domains while showing it can positively regulate a subset of developmental and signaling genes within transcribed regions.

    Evidence Genome-wide ChIP-chip and ChIP-seq with siRNA functional validation in human cell lines and mouse liver

    PMID:20008927 PMID:20937776

    Open questions at the time
    • Determinants of activating versus repressive outcomes undefined
    • Isoform identity at activated loci not resolved
  7. 2008 Medium

    Identified mitosis-associated and interphase regulatory functions distinct from X inactivation through S137 phosphorylation and direct suppression of VRK1 kinase.

    Evidence Mass spectrometry, phospho-specific antibodies, NMR interaction mapping, and kinase activity assays

    PMID:18227505 PMID:22194607

    Open questions at the time
    • Kinase responsible for S137 phosphorylation not identified
    • VRK1 interaction characterized in a single lab without in vivo validation
  8. 2011 High

    Established isoform-specific, macrodomain-dependent functions in cancer by linking macroH2A1.1's NAD+/PAR-binding capacity to PARP-1 suppression and proliferation control, and demonstrated splicing regulation by QKI.

    Evidence Splicing microarrays, RNAi/overexpression with metabolite-binding mutants, proliferation assays across cancer types

    PMID:21844227

    Open questions at the time
    • Direct biochemical mechanism of PARP-1 level reduction not fully defined here
    • Did not address macroH2A1.2-specific functions
  9. 2012 High

    Identified ATRX as a negative regulator of macroH2A chromatin association and placed macroH2A1.1 in the DNA damage response as a PARP1-dependent reader of PARylated chromatin needed for 53BP1 recruitment and CHK2 signaling.

    Evidence Co-IP, ChIP-seq in ATRX-deficient cells, laser micro-irradiation with PARP inhibition and radiosensitivity assays

    PMID:22391447 PMID:23031826

    Open questions at the time
    • Mechanism of ATRX-mediated macroH2A eviction not detailed
    • Whether macroH2A acts catalytically or scaffold-wise at breaks unresolved
  10. 2014 High

    Connected macroH2A1.1's PARP-1 interaction to active chromatin by showing it licenses CBP-mediated H2B K12/K120 acetylation at target genes, a function lost in cancer.

    Evidence Co-IP, RNA-seq, ChIP, and in vitro acetylation assays with domain mutants in primary cells

    PMID:25306110

    Open questions at the time
    • Generality of the CBP cooperation across cell types unclear
    • How the same isoform balances repression and activation unresolved
  11. 2015 High

    Embedded macroH2A1 in senescence and cell-cycle control networks, showing it sustains a SASP positive-feedback loop subject to ATM-mediated removal and is a SKP2 substrate within a Skp2-macroH2A1-CDK8 tumorigenic axis.

    Evidence ChIP-seq, RNAi, pharmacological epistasis, ubiquitination assays, and mouse tumor models

    PMID:25818643 PMID:26300260

    Open questions at the time
    • Isoform specificity within these axes not fully separated
    • Direct chromatin targets driving these phenotypes incompletely defined
  12. 2017 High

    Defined the metabolic logic of macroH2A1.1 by showing its macrodomain inhibits basal PARP-1 activity to preserve NAD+ pools and mitochondrial respiration, and that it cooperates with EZH2 to drive differentiation programs.

    Evidence PARP and NAD+/NMN metabolite assays with macrodomain mutants, respiration assays, Co-IP, and ChIP in differentiating cells

    PMID:28991266 PMID:28992292

    Open questions at the time
    • EZH2 cooperation supported by single-lab Co-IP
    • Quantitative contribution of chromatin NAD+ buffering to whole-cell metabolism not bounded
  13. 2019 High

    Refined the DNA-repair model by showing macroH2A1.1 controls PAR accumulation kinetics to prevent NAD+ depletion and necrosis, while macroH2A1.2 supports HR-dependent ALT telomere maintenance under replication stress regulated by ATRX.

    Evidence Laser micro-irradiation, PAR/NAD+ measurements, cell death assays, telomere ChIP-seq and FISH with ATRX overexpression

    PMID:30833786 PMID:31636161

    Open questions at the time
    • Switch determining isoform deployment at distinct lesion types unclear
    • Structural basis of PAR protection by the macrodomain not resolved
  14. 2020 High

    Showed the two isoforms have opposing genome-stability roles, with macroH2A1.2 counteracting macroH2A1.1-promoted alt-EJ to preserve Xi integrity and female survival.

    Evidence Comparative proteomics, RNAi double-knockdown epistasis, anaphase-bridge FISH, and mouse genetics

    PMID:32649884

    Open questions at the time
    • Molecular basis for isoform antagonism at repair pathway choice undefined
    • Generality beyond the Xi not established
  15. 2021 High

    Expanded macroH2A1.1's functions to NHEJ promotion via exclusive PARP1/XRCC1 interaction and to transcriptional roles at active promoters and Pol II-paused genes, and tied isoform splicing to hematopoietic and neural differentiation programs.

    Evidence GFP-Trap LC-MS/MS, NHEJ reporter assays, KO mice, ChIP-seq/RNA-seq, and conditional KO with rescue

    PMID:34046991 PMID:34469727 PMID:35362516 PMID:35511867

    Open questions at the time
    • Mechanism switching macroH2A1.1 between repressive and pause-release roles unclear
    • Whether neural and B-cell effects are direct chromatin functions or downstream not fully resolved
  16. 2024 Medium

    Mechanistically detailed how macroH2A occupancy is set and read out: FACT destabilizes macroH2A1.2 nucleosomes via an S139 switch, macroH2A1 interacts with the MCM helicase to regulate Xi replication, ubiquitination releases active PARP-1 upon oxidative damage, and AMPKα/PD-L1 phosphorylate S146 to activate stress pathways.

    Evidence In vitro reconstitution with mutagenesis, ChIP-seq, Co-IP with domain mapping, ubiquitination/PARP activity assays, and phosphorylation assays

    PMID:39116874 PMID:39189450 PMID:39218869 PMID:39545415

    Open questions at the time
    • Several mechanisms rest on single-lab biochemistry without cross-validation
    • Integration of these regulatory inputs into a unified deposition/eviction model lacking
  17. 2024 Medium

    Provided isoform- and domain-resolved structural insight by showing both macroH2A1 domains independently override nucleosome positioning and destabilize chromatin in a heterologous yeast system, and proposed a PAR-dependent XRCC1 recruitment mechanism protecting against TOP1cc-induced damage.

    Evidence Histone replacement in yeast with domain-uncoupling constructs, nChIP-seq, Hi-C; single-cell TOP1cc visualization and pharmacogenomic screen (preprint)

    PMID:38990716

    Open questions at the time
    • Yeast findings require validation in mammalian chromatin context
    • TOP1cc protection mechanism reported in a preprint not yet peer-reviewed
  18. 2025 High

    Demonstrated in vivo that macroH2A1.1's metabolite-binding macrodomain links chromatin composition to systemic energy metabolism, with isoform-specific kidney pathology and metabolic shifts reversible by dietary intervention.

    Evidence Isoform-specific KO mice with metabolomics, RNA-seq, histopathology, and ketogenic-diet rescue

    PMID:41134882

    Open questions at the time
    • Tissue-specific chromatin targets driving systemic metabolic shifts not mapped
    • Causal chain from chromatin NAD+ handling to organ pathology incompletely defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the cell selects between macroH2A1.1 and macroH2A1.2 deposition at a given locus, and how their opposing functions in repair, transcription, and replication are coordinated, remains unresolved.
  • No unified model integrating splicing control, ATRX/FACT eviction, E3-ligase turnover, and PTMs into locus-specific isoform deployment
  • Structural basis of macrodomain reading of distinct NAD+ metabolites incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 4 GO:0005198 structural molecule activity 3 GO:0098772 molecular function regulator activity 3 GO:0042393 histone binding 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 3 GO:0005694 chromosome 2 GO:0005815 microtubule organizing center 2 GO:0005730 nucleolus 1
Pathway
R-HSA-4839726 Chromatin organization 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-73894 DNA Repair 3 R-HSA-1430728 Metabolism 2 R-HSA-1640170 Cell Cycle 2 R-HSA-8953897 Cellular responses to stimuli 1
Partners
ATRXEZH2HP1AMCM3PARP1SPOPVRK1XRCC1

Evidence

Reading pass · 50 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 MacroH2A1 (mH2A1) is a core histone variant whose amino-terminal third resembles histone H2A; the mH2A1.2 subtype is preferentially concentrated on the inactive X chromosome (Xi) of female mammals, linking X inactivation to a major alteration of the nucleosome. Immunofluorescence, gene cloning, protein characterization Nature High 9634239
1999 MacroH2A1.2 relocalization to the inactive X chromosome occurs after initiation and propagation of X-inactivation in differentiating murine ES cells (around day 7–9), in a synchronized wave, indicating it is not required for initiation of random X-inactivation but is precisely regulated. Immuno-RNA FISH on differentiating ES cells The Journal of cell biology High 10613899
2000 MacroH2A1 is stored at centrosomes in undifferentiated ES cells as a non-chromatin-associated pool, and upon differentiation of female ES cells, centrosomal macroH2A1 is dynamically redistributed to the Xi, coinciding with Xist RNA stabilization. Immunofluorescence, cell fractionation, nocodazole treatment The Journal of cell biology High 10974005
2001 MacroH2A1.2 co-localizes with HP1beta (M31) at the pseudoautosomal region (PAR) and at centromeric heterochromatin in male meiocytes, suggesting cooperation between these two proteins in meiotic sex chromosome inactivation. Immunofluorescence on surface-spread meiocytes from mouse testis and ovary Journal of cell science Medium 11591824
2001 MacroH2A1.2 associates stably with centrosomes in somatic cells (both XX and XY, interphase and mitosis) and co-purifies with centrosomes isolated from human lymphoblasts, indicating a centrosomal pool in addition to the chromatin-associated pool. Indirect immunofluorescence, biochemical centrosome purification and co-purification Experimental cell research Medium 11478850
2002 Recombinant macroH2A1.2 can substitute for both conventional H2A molecules in reconstituted nucleosomes; these macroH2A1.2-containing nucleosomes show increased resistance to DNase I cleavage at the nucleosomal midpoint and a greater tendency toward internucleosomal interactions. In vitro nucleosome reconstitution, sedimentation, micrococcal nuclease and DNase I digestion Biochemistry High 11772015
2002 The non-histone macrodomain of macroH2A1.2 binds directly to nuclear speckle protein SPOP through SPOP's MATH domain interacting with the leucine zipper-like region of macroH2A1.2. Yeast two-hybrid screen, GST pulldown with domain mapping Biochimica et biophysica acta Medium 12183056
2005 MacroH2A1.2 is monoubiquitinated in vivo at Lys115 (and Lys116) of its histone domain, and is additionally methylated at Lys17, Lys122, and Lys238, and phosphorylated at Thr128, as determined by mass spectrometry of GFP-tagged and endogenous protein. Tandem mass spectrometry of GFP-tagged and endogenous macroH2A1.2 Molecular & cellular proteomics High 16129414 16210244
2005 The CULLIN3/SPOP ubiquitin E3 ligase complex ubiquitinates macroH2A1 and the Polycomb protein BMI1; RNAi knockdown of CULLIN3 or SPOP causes loss of macroH2A1 from the Xi and promotes Xi reactivation in the presence of DNA methylation and HDAC inhibitors, demonstrating that CULLIN3/SPOP regulates macroH2A1 deposition and that macroH2A1 contributes to stable X inactivation. RNAi knockdown, immunofluorescence, Xi reactivation assay, ubiquitination assay Proceedings of the National Academy of Sciences High 15897469
2006 MacroH2A1 is depleted from transcribed regions of active genes and enriched on the inactive X chromosome in mouse liver chromatin; heterochromatin protein HP1beta co-purifies with macroH2A1-containing chromatin fragments. Thiol affinity chromatography of macroH2A1-containing chromatin, ChIP, co-purification Molecular and cellular biology Medium 16738309
2006 MacroH2A1 is preferentially deposited at methylated CpG-rich regions at imprinting control regions (ICRs) of multiple imprinted domains (Xist, Peg3, H19/Igf2, Gtl2/Dlk1, Gnas), showing allele-specific enrichment toward the inactive/methylated parental allele, indicating macroH2A1 is a component of ICR chromatin. ChIP with allele-specific analysis at multiple imprinted loci Human molecular genetics Medium 16421169
2007 MacroH2A1 knockout mice are viable and fertile; knockout liver shows increased expression of genes with macroH2A1-enriched nucleosomes on their coding/upstream regions, particularly lipid metabolism genes, demonstrating macroH2A1 functions as a direct transcriptional repressor of a specific gene set in adult liver. MacroH2A1 knockout mouse, gene expression arrays, ChIP Molecular and cellular biology High 17242180
2007 Multiple short sequences dispersed along the macroH2A1 histone domain (mapping to the macroH2A1/H2B dimer surface) are each individually sufficient to direct enrichment on the inactive X chromosome when introduced into canonical H2A. Chimeric H2A/macroH2A1 constructs expressed in female cells, immunofluorescence Journal of molecular biology Medium 17570398
2008 A phosphorylated subpopulation of macroH2A1 at Ser137 (S137ph) within the hinge region is excluded from the inactive X chromosome and enriched during mitosis in both male and female cells, suggesting a cell-cycle-specific function distinct from X inactivation. Mass spectrometry of purified endogenous macroH2A1, specific S137ph antibody, immunofluorescence Proceedings of the National Academy of Sciences High 18227505
2008 MacroH2A1 histone variants are required for silencing endogenous murine leukemia viruses (MLVs) in mouse liver; macroH2A1-enriched nucleosomes preferentially occupy the 5' end of pro-pol in MLV proviruses; absence of macroH2A1 also leads to localized loss of DNA methylation on MLV 5' ends. MacroH2A1 knockout mouse, RT-qPCR, ChIP, bisulfite sequencing Molecular and cellular biology High 18195046
2009 MacroH2A1 occupies large autosomal chromatin domains (>500 kb) marked by H3K27me3 repressive marks; however, when located in the transcribed regions of a subset of developmental and signaling genes, macroH2A1 positively regulates their expression, including augmenting serum starvation-responsive transcription. ChIP-chip (genome-wide), gene expression analysis, siRNA knockdown in IMR90 and MCF-7 cells Genes & development High 20008927
2010 Genome-wide mapping in mouse liver shows macroH2A1 nucleosomes are depleted from transcribed regions of active genes in sharply defined domains, uniformly enriched ~4-fold on the inactive X chromosome (absent from escape regions), and enriched on lipid metabolism genes that are repressed by macroH2A1. ChIP with high-throughput sequencing (ChIP-seq) in mouse liver Molecular and cellular biology High 20937776
2010 Deletion of macroH2A1 (H2afy) in female mice causes hepatic steatosis in ~50% of homozygous females; macroH2A1 is enriched at the Tbg promoter in wild-type females, and its absence leads to upregulation of X-linked Tbg gene, suggesting a direct sex-specific epigenetic regulation of lipid metabolism. Knockout mouse model, ChIP, RT-qPCR, histopathology Epigenetics & chromatin Medium 20359320
2010 MacroH2A1 knockdown, combined with DNA demethylation, significantly enhances reactivation of silenced tumor suppressor genes (p16/CDKN2A, MLH1, Timp3), demonstrating synergism between macroH2A1 occupancy and DNA methylation in maintaining epigenetic silencing. RNAi knockdown, 5-aza-dC treatment, RT-qPCR in cancer cell lines, ChIP Nucleic acids research Medium 21030442
2011 MacroH2A1.2 directly interacts with and suppresses VRK1 kinase during interphase, preventing premature histone H3 phosphorylation; this interaction was mapped by NMR spectroscopy and macroH2A1.2 levels are reduced in mitosis. NMR spectroscopy, co-immunoprecipitation, kinase activity assay, cell cycle analysis The Journal of biological chemistry Medium 22194607
2011 Female ES cells doubly deficient for both macroH2A1 and macroH2A2 readily execute and maintain X chromosome inactivation upon differentiation, demonstrating that macroH2A variants are not required for XCI initiation or maintenance. Stable shRNA knockdown of both macroH2A1 and macroH2A2 in female ES cells, differentiation assays, immunofluorescence PloS one Medium 21738686
2011 The RNA-binding protein QKI regulates alternative splicing of macroH2A1 pre-mRNA to increase macroH2A1.1 levels; macroH2A1.1 (but not macroH2A1.2) suppresses cancer cell proliferation in a manner requiring its ability to bind NAD+-derived metabolites (including poly(ADP-ribose)), and this suppression involves reduction of PARP-1 protein levels. RNAi, overexpression, RT-qPCR, proliferation assays, splicing microarray analysis in multiple cancer types Molecular and cellular biology High 21844227
2012 ATRX (SWI/SNF helicase) interacts with macroH2A and acts as a negative regulator of macroH2A's chromatin association; in ATRX-deficient human erythroleukemic cells, macroH2A accumulates at the HBA gene cluster, coinciding with loss of α-globin expression. Co-immunoprecipitation, ChIP-seq, ATRX-deficient cell lines Genes & development High 22391447
2012 MacroH2A1.2 (but not macroH2A1.1) interacts with HER-2 protein in cancer cells through the macro domain of macroH2A1.2 (specifically the -EIS- insertion); macroH2A1.2 overexpression increases HER-2 expression and ERBB2 promoter occupancy, promoting tumorigenicity. Co-immunoprecipitation, domain mapping, ChIP, overexpression assays in cancer cell lines The Journal of biological chemistry Medium 22589551
2012 MacroH2A1.1 is recruited to DNA double-strand breaks (DSBs) via a mechanism requiring PARP1 activity; it is not incorporated into nucleosomes at DSBs but associates with PARylated chromatin; cells lacking macroH2A1 show defective 53BP1 recruitment, impaired CHK2 activation, and increased radiosensitivity. Laser micro-irradiation, immunofluorescence, PARP1 inhibitor treatment, PARP1 knockdown, radiosensitivity assay, CHK2 phosphorylation assay FEBS letters High 23031826
2013 MacroH2A1 is present at the promoter of methylated rDNA genes and represses rDNA transcription; its knockdown causes up to 5-fold increase in pre-rRNA levels with increased RNA polymerase I and UBF loading; inhibition of RNA Pol I transcription induces macroH2A1 recruitment to rDNA and nucleolar relocalization. RNAi knockdown, RT-qPCR, ChIP, RNA Pol I inhibition (actinomycin D), immunofluorescence in HeLa, HepG2, and mouse ES cells Nucleic acids research Medium 24071584
2014 MacroH2A1.1, through interaction with PARP-1 (via its PAR-binding macrodomain), promotes CBP-mediated acetylation of H2B at K12 and K120, which regulates expression of macroH2A1-target genes; this regulation is specific to macroH2A1-containing acetylated chromatin and is commonly lost in cancer cells. Co-immunoprecipitation, RNA-seq, ChIP, in vitro acetylation assay, domain mutant analysis in primary human cells Nature structural & molecular biology High 25306110
2015 MacroH2A1 is a critical component of the positive feedback loop maintaining SASP gene expression during oncogene-induced senescence; it undergoes genome-wide relocalization during OIS; ATM (activated by SASP-induced ER stress and reactive oxygen species) mediates removal of macroH2A1 from SASP gene chromatin, creating a negative feedback loop. ChIP-seq, RNAi, ATM inhibition, ER stress induction, OIS model in primary cells Molecular cell High 26300260
2015 MacroH2A1 is a substrate of the SKP2 SCF E3 ubiquitin ligase complex; SKP2-mediated degradation of macroH2A1 promotes CDK8 gene and protein expression; CDK8 in turn regulates p27 via facilitating SKP2-mediated p27 ubiquitination, establishing a Skp2-macroH2A1-CDK8 axis controlling G2/M transition and tumorigenesis. Co-immunoprecipitation, ubiquitination assay, overexpression/knockdown, mouse tumor models (xenograft and transgenic) Nature communications High 25818643
2016 MacroH2A1.2 is required for activation of the myogenic gene regulatory network and muscle cell differentiation; it regulates H3K27 acetylation at prospective muscle enhancers and is required for recruitment of the transcription factor Pbx1 to these enhancers. RNAi knockdown, ChIP-seq, RNA-seq, differentiation assays in C2C12 cells Cell reports High 26832413
2017 MacroH2A1.1 inhibits basal PARP-1 activity through direct binding (via its NAD+-metabolite-binding macrodomain), limiting nuclear NAD+ consumption; this increases the NAD+ precursor NMN, maintaining mitochondrial NAD+ pools critical for respiration; macroH2A1.1 is induced during myogenic differentiation via alternative splicing switch. PARP activity assay, NAD+/NMN metabolite measurement, macrodomain-mutant analysis, macroH2A1.1 KD/KO in differentiating myotubes, Seahorse respiration assay Nature structural & molecular biology High 28991266
2017 MacroH2A1.1 cooperates with EZH2 to promote adipogenesis by directly interacting with EZH2 (requiring intact macrodomain residues G224 and G314), leading to H3K27me2/me3 accumulation on Wnt gene promoters and suppression of Wnt/β-catenin signaling. Co-immunoprecipitation, ChIP, macrodomain point mutant analysis, siRNA knockdown, overexpression in 3T3-L1 cells Journal of molecular cell biology Medium 28992292
2018 MacroH2A1.2 physically interacts with EZH2 and elevates H3K27me3 levels at the LOX gene promoter in breast cancer cells to repress LOX expression and secretion, thereby inhibiting breast cancer-induced osteoclastogenesis. Co-immunoprecipitation, ChIP, gene expression analysis, osteoclastogenesis functional assay Cell reports Medium 29972783
2018 MacroH2A1.2 interacts directly with HP1α and H1.2, requiring both to maintain the inactive state of the LTβ gene in prostate cancer cells, thereby inhibiting osteoclastogenesis; HP1α and H1.2 alone have intrinsic anti-osteoclastogenic activity in a macroH2A1.2-dependent manner. Co-immunoprecipitation, ChIP, knockdown/overexpression, osteoclastogenesis assay Oncogene Medium 29925860
2018 MacroH2A1.1 suppresses EMT induction in mammary epithelial cells in an isoform-specific and stage-specific manner that depends on the ability of its macrodomain to bind PAR; macroH2A1.2 (which lacks PAR-binding) does not suppress EMT. Overexpression of macroH2A1.1 vs 1.2 (and PAR-binding mutant), flow cytometry for stem cell markers, morphological assays in HMLE cells Scientific reports Medium 29339820
2019 EGFR-activated CDK5 phosphorylates TRIM59 at Ser308, recruiting PIN1 for cis-trans isomerization, leading to TRIM59 nuclear translocation via importin α5; nuclear TRIM59 ubiquitinates and degrades macroH2A1, leading to STAT3 signaling activation and GBM tumorigenicity. Co-immunoprecipitation, in vitro kinase assay, ubiquitination assay, nuclear fractionation, rescue experiments, intracranial tumor models Nature communications High 31488827
2019 MacroH2A1.1 is recruited to DNA DSBs through direct association with PARylated chromatin (PARP1-dependent); macroH2A1 regulates kinetics of PAR accumulation after acute DNA damage by both suppressing PARP activity and protecting PAR from degradation, thereby preventing NAD+ depletion and necrotic cell death, and promoting efficient repair of oxidative DNA damage. Laser micro-irradiation, PARP inhibition, macroH2A1 KD/KO, PAR immunofluorescence/ELISA, NAD+ measurement, cell death assays Molecular and cellular biology High 31636161
2019 MacroH2A1.2 is highly enriched at ALT telomeres and transiently lost during acute replication stress to facilitate DSB formation required for ALT; re-deposition occurs in a DNA damage response-dependent manner to promote HR-associated ALT; ectopic ATRX expression prevents this loss, establishing ATRX as a negative regulator of macroH2A1.2 at telomeres. ChIP-seq, telomere FISH, ATRX overexpression, replication stress induction, HR assay Nature structural & molecular biology High 30833786
2020 MacroH2A1.2 is required for Xi integrity and female survival; it counteracts macroH2A1.1's role in promoting alternative end-joining (alt-EJ), which causes anaphase defects when macroH2A1.2 is absent; simultaneous depletion of macroH2A1.1 or alt-EJ factors rescues Xi genomic instability in macroH2A1.2-deficient cells. Comparative proteomics, RNAi double-knockdown, flow cytometry, FISH for anaphase bridges, mouse genetics Molecular cell High 32649884
2021 MacroH2A1.1 overexpression exclusively (not macroH2A1.2) enhances nonhomologous end joining (NHEJ) DNA repair and iPSC reprogramming efficiency; macroH2A1.1 interacts exclusively with PARP1 and XRCC1 (not macroH2A1.2), identified by GFP-Trap pull-down and LC-MS/MS. GFP-Trap pull-down with LC-MS/MS, U2OS-GFP-NHEJ reporter assay, macroH2A1.1 KO mice, iPSC reprogramming efficiency assay Stem cells High 35511867
2021 MacroH2A1.1 genome-wide localization in breast cancer cells (MDA-MB-231) shows binding to active promoters and enhancers in addition to heterochromatin; it regulates Pol II-paused genes through two mechanisms: mitigating excess transcription at genes where it occupies promoter+gene body, and stimulating Pol II pause-release at paused genes where it occupies only the TSS. ChIP-seq of endogenous macroH2A1.1, selective knockdown, RNA-seq, 3D genome analysis Journal of cell science Medium 35362516
2021 MacroH2A1.2 deficiency impairs neural stem cell differentiation in mice, enhances neural progenitor proliferation, and reduces differentiation; NKX2.2 is identified as a direct downstream effector whose expression is reduced upon macroH2A1.2 loss; NKX2.2 overexpression rescues neuronal abnormalities, and macroH2A1.2-deficient mice display autism-like behaviors. Conditional mouse KO, in vitro differentiation assays, overexpression rescue, behavior tests EMBO reports Medium 34046991
2021 Mutant U2AF1(S34F)-induced alternative splicing reduces H2afy1.1 (macroH2A1.1) expression, which decreases EBF1 (early B cell factor 1) transcription factor expression; macroH2A1 is enriched at the EBF1 promoter; re-expression of macroH2A1.1 rescues EBF1 expression and B cell numbers in vivo. Mouse genetic model (U2AF1 S34F), ChIP, RT-qPCR, induced expression rescue, in vivo B cell counting Cell reports High 34469727
2024 FACT (facilitates chromatin transcription) complex destabilizes macroH2A1.2-containing nucleosomes and promotes their depletion during transcription; residue S139 in macroH2A1.2 is a critical switch modulating FACT's function; FACT-mediated macroH2A1 depletion controls macroH2A genomic distribution and stimulation-induced transcription in macrophages. In vitro nucleosome reconstitution, FACT activity assay, S139 mutagenesis, ChIP-seq, genome-wide macroH2A distribution analysis Molecular cell High 39116874
2024 MacroH2A1.1, through its PAR-binding macrodomain, establishes a TOP1-permissive chromatin environment by facilitating PAR-dependent recruitment of XRCC1 (TOP1cc repair effector) to protect from ssDNA damage caused by transcription-induced topological stress; macroH2A1.2 (lacking PAR-binding) cannot provide this protection. Single-cell visualization of TOP1ccs, XRCC1 recruitment assay, macroH2A1.1 inactivation, pharmacogenomic screen in breast cancer cells bioRxivpreprint Medium
2024 MacroH2A1 overexpression is toxic in yeast (failing to complement replication-coupled H2A), and both its histone fold domain and macro domain independently override native nucleosome positioning; macroH2A1 expression leads to lower nucleosome occupancy, decreased short-range chromatin interactions, disrupted centromeric clustering, and increased chromosome instability. Histone replacement in yeast, domain uncoupling constructs, nChIP-seq, Hi-C, chromosome instability assay Cell reports Medium 38990716
2024 MacroH2A1 (mH2A1) regulates replication origin firing on the inactive X chromosome by interacting with the replicative MCM helicase complex (mapped to a phenylalanine in macroH2A1 interacting with the C-terminus of Mcm3), enhancing pre-replication complex licensing during G1; macroH2A1-containing nucleosomes slow replication progression rate on the Xi. KD/KO of macroH2A1 isoforms, replication fork imaging, nChIP-seq, Co-IP with MCM helicase, domain mapping Nucleic acids research Medium 39189450
2024 Nuclear PD-L1, phosphorylated by AMPKα, cooperates with AMPKα to directly phosphorylate macroH2A1 at Ser146, epigenetically activating senescence-associated, JAK/STAT, and Hippo signaling pathway genes. Nuclear PD-L1 enforced expression, AMPKα inhibition/activation, phosphorylation assay, gene expression analysis The Journal of clinical investigation Medium 39545415
2024 Upon oxidative DNA damage, macroH2A1 (mH2A) is ubiquitinated, causing release and activation of PARP-1 from the mH2A1 nucleosome complex; in the undamaged state, mH2A nucleosome-associated PARP-1 is inactive; in vivo-induced ubiquitination of mH2A without DNA damage is sufficient to release PARP-1; this pathway is specific to oxidative damage (not alkylation or doxorubicin). In vivo ubiquitination induction, PARP-1 activity assay, Co-IP of PARP-1 with mH2A nucleosomes, cell survival assay, damage-type comparison BMC biology Medium 39218869
2025 Loss of macroH2A1.1 (but not macroH2A1.2 or macroH2A2) in mice causes kidney histopathological changes associated with systemic shifts in nutrient metabolization: reduced lipid oxidation, increased glycolysis, and altered NAD+ metabolism; a ketogenic diet overrides these metabolic phenotypes and prevents kidney abnormalities, indicating macroH2A1.1's metabolite-binding macrodomain links chromatin composition to systemic energy metabolism. Isoform-specific KO mice, metabolomics, RNA-seq, histopathology, glucose tolerance test, dietary intervention Science advances High 41134882

Source papers

Stage 0 corpus · 97 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 Histone macroH2A1 is concentrated in the inactive X chromosome of female mammals. Nature 479 9634239
2005 Stable X chromosome inactivation involves the PRC1 Polycomb complex and requires histone MACROH2A1 and the CULLIN3/SPOP ubiquitin E3 ligase. Proceedings of the National Academy of Sciences of the United States of America 270 15897469
2015 MacroH2A1 and ATM Play Opposing Roles in Paracrine Senescence and the Senescence-Associated Secretory Phenotype. Molecular cell 173 26300260
2009 The histone variant macroH2A1 marks repressed autosomal chromatin, but protects a subset of its target genes from silencing. Genes & development 149 20008927
1999 Histone macroH2A1.2 relocates to the inactive X chromosome after initiation and propagation of X-inactivation. The Journal of cell biology 134 10613899
2011 QKI-mediated alternative splicing of the histone variant MacroH2A1 regulates cancer cell proliferation. Molecular and cellular biology 132 21844227
2000 Histone macroH2A1 is concentrated in the inactive X chromosome of female preimplantation mouse embryos. Development (Cambridge, England) 127 10804171
2012 ATRX-mediated chromatin association of histone variant macroH2A1 regulates α-globin expression. Genes & development 112 22391447
2014 MacroH2A1.1 and PARP-1 cooperate to regulate transcription by promoting CBP-mediated H2B acetylation. Nature structural & molecular biology 98 25306110
2007 Developmental changes in histone macroH2A1-mediated gene regulation. Molecular and cellular biology 98 17242180
1997 Developmental and tissue expression patterns of histone macroH2A1 subtypes. Journal of cellular biochemistry 97 9138085
2015 Skp2-macroH2A1-CDK8 axis orchestrates G2/M transition and tumorigenesis. Nature communications 93 25818643
1999 Messenger RNAs encoding mouse histone macroH2A1 isoforms are expressed at similar levels in male and female cells and result from alternative splicing. Nucleic acids research 81 10471737
2000 Dynamic relocalization of histone MacroH2A1 from centrosomes to inactive X chromosomes during X inactivation. The Journal of cell biology 80 10974005
2016 DNA Hypomethylation and Histone Variant macroH2A1 Synergistically Attenuate Chemotherapy-Induced Senescence to Promote Hepatocellular Carcinoma Progression. Cancer research 75 26772755
2000 Histone macroH2A1.2 is concentrated in the XY-body by the early pachytene stage of spermatogenesis. Experimental cell research 75 10896776
2012 Differential regulation and predictive potential of MacroH2A1 isoforms in colon cancer. The American journal of pathology 72 22542848
2005 Mapping post-translational modifications of the histone variant MacroH2A1 using tandem mass spectrometry. Molecular & cellular proteomics : MCP 62 16210244
2012 The histone variant macroH2A1.1 is recruited to DSBs through a mechanism involving PARP1. FEBS letters 60 23031826
2013 Immunopositivity for histone macroH2A1 isoforms marks steatosis-associated hepatocellular carcinoma. PloS one 59 23372727
2001 M31 and macroH2A1.2 colocalise at the pseudoautosomal region during mouse meiosis. Journal of cell science 58 11591824
2019 CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity. Nature communications 57 31488827
2010 Genome-wide distribution of macroH2A1 histone variants in mouse liver chromatin. Molecular and cellular biology 56 20937776
2010 Histone variant macroH2A1 deletion in mice causes female-specific steatosis. Epigenetics & chromatin 55 20359320
2014 SIRT1-metabolite binding histone macroH2A1.1 protects hepatocytes against lipid accumulation. Aging 53 24473773
2017 MacroH2A1.1 regulates mitochondrial respiration by limiting nuclear NAD+ consumption. Nature structural & molecular biology 52 28991266
2006 macroH2A1 histone variants are depleted on active genes but concentrated on the inactive X chromosome. Molecular and cellular biology 51 16738309
2008 A phosphorylated subpopulation of the histone variant macroH2A1 is excluded from the inactive X chromosome and enriched during mitosis. Proceedings of the National Academy of Sciences of the United States of America 47 18227505
2008 Weak but uniform enrichment of the histone variant macroH2A1 along the inactive X chromosome. Molecular and cellular biology 47 18936163
2016 The Histone Variant MacroH2A1.2 Is Necessary for the Activation of Muscle Enhancers and Recruitment of the Transcription Factor Pbx1. Cell reports 44 26832413
2018 Histone variant macroH2A1 rewires carbohydrate and lipid metabolism of hepatocellular carcinoma cells towards cancer stem cells. Epigenetics 42 30165787
2013 macroH2A1 histone variant represses rDNA transcription. Nucleic acids research 42 24071584
2019 MacroH2A1 Regulation of Poly(ADP-Ribose) Synthesis and Stability Prevents Necrosis and Promotes DNA Repair. Molecular and cellular biology 41 31636161
2020 Epigenetic Regulation of DNA Repair Pathway Choice by MacroH2A1 Splice Variants Ensures Genome Stability. Molecular cell 40 32649884
2019 The macroH2A1.2 histone variant links ATRX loss to alternative telomere lengthening. Nature structural & molecular biology 40 30833786
2012 The atypical histone macroH2A1.2 interacts with HER-2 protein in cancer cells. The Journal of biological chemistry 39 22589551
2010 Synergism between DNA methylation and macroH2A1 occupancy in epigenetic silencing of the tumor suppressor gene p16(CDKN2A). Nucleic acids research 39 21030442
2014 MacroH2A1 isoforms are associated with epigenetic markers for activation of lipogenic genes in fat-induced steatosis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 38 25526730
2011 X chromosome inactivation and differentiation occur readily in ES cells doubly-deficient for macroH2A1 and macroH2A2. PloS one 38 21738686
2020 Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4+CD25+FoxP3+ regulatory T cells activation. Theranostics 37 31903159
2017 MacroH2A1.1 cooperates with EZH2 to promote adipogenesis by regulating Wnt signaling. Journal of molecular cell biology 37 28992292
2016 ZEB1-induced tumourigenesis requires senescence inhibition via activation of DKK1/mutant p53/Mdm2/CtBP and repression of macroH2A1. Gut 36 27965283
2011 Macro histone H2A1.2 (macroH2A1) protein suppresses mitotic kinase VRK1 during interphase. The Journal of biological chemistry 36 22194607
2008 macroH2A1-dependent silencing of endogenous murine leukemia viruses. Molecular and cellular biology 36 18195046
2006 Allele-specific deposition of macroH2A1 in imprinting control regions. Human molecular genetics 36 16421169
2018 Regulation of Breast Cancer-Induced Osteoclastogenesis by MacroH2A1.2 Involving EZH2-Mediated H3K27me3. Cell reports 35 29972783
2016 Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis. Epigenetics & chromatin 34 27800025
2015 MacroH2A1 downregulation enhances the stem-like properties of bladder cancer cells by transactivation of Lin28B. Oncogene 33 26028027
2017 Histone MacroH2A1: A Chromatin Point of Intersection between Fasting, Senescence and Cellular Regeneration. Genes 30 29206173
2000 Histone macroH2A1.2 is concentrated in the XY compartment of mammalian male meiotic nuclei. Cytogenetics and cell genetics 30 10894952
2002 Reconstitution of nucleosomes with histone macroH2A1.2. Biochemistry 29 11772015
2018 Histone Variant MacroH2A1 Plays an Isoform-Specific Role in Suppressing Epithelial-Mesenchymal Transition. Scientific reports 28 29339820
2002 MacroH2A1.2 binds the nuclear protein Spop. Biochimica et biophysica acta 28 12183056
2020 MacroH2A1 Immunoexpression in Breast Cancer. Frontiers in oncology 27 32974186
2018 MacroH2A1.2 inhibits prostate cancer-induced osteoclastogenesis through cooperation with HP1α and H1.2. Oncogene 27 29925860
2019 Deficiency and haploinsufficiency of histone macroH2A1.1 in mice recapitulate hematopoietic defects of human myelodysplastic syndrome. Clinical epigenetics 26 31439048
2002 Xist expression and macroH2A1.2 localisation in mouse primordial and pluripotent embryonic germ cells. Differentiation; research in biological diversity 26 11841480
2007 The histone domain of macroH2A1 contains several dispersed elements that are each sufficient to direct enrichment on the inactive X chromosome. Journal of molecular biology 25 17570398
2005 Histone variant macroH2A1.2 is mono-ubiquitinated at its histone domain. Biochemical and biophysical research communications 25 16129414
2020 Loss of macroH2A1 decreases mitochondrial metabolism and reduces the aggressiveness of uveal melanoma cells. Aging 24 32401230
2022 Histone Variant macroH2A1.1 Enhances Nonhomologous End Joining-dependent DNA Double-strand-break Repair and Reprogramming Efficiency of Human iPSCs. Stem cells (Dayton, Ohio) 21 35511867
2019 H2AFY promoter deletion causes PITX1 endoactivation and Liebenberg syndrome. Journal of medical genetics 21 30711920
2021 Systemic depletion of histone macroH2A1.1 boosts hippocampal synaptic plasticity and social behavior in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20 34320234
2021 Mutant U2AF1-induced alternative splicing of H2afy (macroH2A1) regulates B-lymphopoiesis in mice. Cell reports 19 34469727
2018 The MacroH2A1.1 - PARP1 Axis at the Intersection Between Stress Response and Metabolism. Frontiers in genetics 19 30356649
2021 MacroH2A1.2 deficiency leads to neural stem cell differentiation defects and autism-like behaviors. EMBO reports 18 34046991
2016 QKI5-mediated alternative splicing of the histone variant macroH2A1 regulates gastric carcinogenesis. Oncotarget 18 27092877
2022 Evolution, structure and function of divergent macroH2A1 splice isoforms. Seminars in cell & developmental biology 17 35422391
2019 Histone variant MacroH2A1 is downregulated in prostate cancer and influences malignant cell phenotype. Cancer cell international 17 31164793
2001 Centrosomal association of histone macroH2A1.2 in embryonic stem cells and somatic cells. Experimental cell research 16 11478850
2004 Localisation of histone macroH2A1.2 to the XY-body is not a response to the presence of asynapsed chromosome axes. Journal of cell science 15 14676273
2022 The histone variant macroH2A1.1 regulates RNA polymerase II-paused genes within defined chromatin interaction landscapes. Journal of cell science 14 35362516
2024 Nuclear PD-L1 compartmentalization suppresses tumorigenesis and overcomes immunocheckpoint therapy resistance in mice via histone macroH2A1. The Journal of clinical investigation 11 39545415
2022 Next-generation proteomics of serum extracellular vesicles combined with single-cell RNA sequencing identifies MACROH2A1 associated with refractory COVID-19. Inflammation and regeneration 11 36451245
2021 Phosphorylation within Intrinsic Disordered Region Discriminates Histone Variant macroH2A1 Splicing Isoforms-macroH2A1.1 and macroH2A1.2. Biology 11 34356514
2020 The Histone Variant MacroH2A1 Regulates Key Genes for Myogenic Cell Fusion in a Splice-Isoform Dependent Manner. Cells 11 32365743
2018 The histone variant macroH2A1 is a splicing-modulated caretaker of genome integrity and tumor growth. Molecular & cellular oncology 11 30250894
2023 MacroH2A1.1 as a crossroad between epigenetics, inflammation and metabolism of mesenchymal stromal cells in myelodysplastic syndromes. Cell death & disease 8 37852977
2023 Deficiency of histone variant macroH2A1.1 is associated with sexually dimorphic obesity in mice. Scientific reports 8 37926763
2007 MacroH2A1 knockdown effects on the Peg3 imprinted domain. BMC genomics 8 18166131
2022 Analysis of histone variant constraint and tissue expression suggests five potential novel human disease genes: H2AFY2, H2AFZ, H2AFY, H2AFV, H1F0. Human genetics 7 35072799
2018 H2AFY is a novel fusion partner of MECOM in acute myeloid leukemia. Cancer genetics 6 29666008
2010 The Sgp3 locus derived from the 129 strain is responsible for enhanced endogenous retroviral expression in macroH2A1-deficient mice. Journal of autoimmunity 6 20833509
2024 FACT mediates the depletion of macroH2A1.2 to expedite gene transcription. Molecular cell 5 39116874
2024 CYB561 promotes HER2+ breast cancer proliferation by inhibiting H2AFY degradation. Cell death discovery 4 38245506
2024 macroH2A1 drives nucleosome dephasing and genome instability in histone humanized yeast. Cell reports 4 38990716
2024 Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma. The Journal of clinical investigation 4 39255035
2023 Genome-wide identification of mammalian cell-cycle invariant and mitotic-specific macroH2A1 domains. Bioscience trends 4 37778979
2024 Histone variant macroH2A1 regulates synchronous firing of replication origins in the inactive X chromosome. Nucleic acids research 3 39189450
2024 Identification of a novel DNA oxidative damage repair pathway, requiring the ubiquitination of the histone variant macroH2A1.1. BMC biology 2 39218869
2023 Integrative CUT&Tag-RNA-Seq analysis of histone variant macroH2A1-dependent orchestration of human induced pluripotent stem cell reprogramming. Epigenomics 2 37846557
2025 Loss of histone macroH2A1.1 causes kidney abnormalities secondary to a change in nutrient metabolization. Science advances 1 41134882
2023 Human macroH2A1 drives nucleosome dephasing and genome instability in histone-humanized yeast. bioRxiv : the preprint server for biology 1 37205538
2023 Recruitment of the Histone Variant MacroH2A1 to the Pericentric Region Occurs upon Chromatin Relaxation and Is Responsible for Major Satellite Transcriptional Regulation. Cells 1 37681907
2026 A ∼18 kb upstream deletion of H2AFY is associated with the feathered leg trait in Yanying chickens. Poultry science 0 42102759
2026 H2AFY regulates autophagy-dependent ferroptosis through ITM2A in hepatocellular carcinoma progression. Archives of biochemistry and biophysics 0 42140467
2025 Regional Conservation and Transcriptional Regulation of Tumor-Associated Genes by macroH2A1 Deposition in Mammalian Cells. Biomolecules 0 41154614

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