Affinage

ATF7IP

Activating transcription factor 7-interacting protein 1 · UniProt Q6VMQ6

Length
1270 aa
Mass
136.4 kDa
Annotated
2026-06-09
34 papers in source corpus 25 papers cited in narrative 25 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

ATF7IP (MCAF1) is an obligate nuclear cofactor of the histone H3K9 methyltransferase SETDB1 that drives genome-wide H3K9me3-dependent heterochromatin silencing of endogenous retroviruses, transposable elements, and specific gene loci (PMID:27732843, PMID:33256805). Its central function is to control SETDB1 localization and stability: ATF7IP binds the N-terminal region of SETDB1 harboring its nuclear export signals and forms a 1:2 hetero-trimeric complex in which ATF7IP coiled-coil motifs directly compete with Crm1 for the SETDB1 NES, blocking nuclear export and retaining SETDB1 in the nucleus in a ubiquitinated, enzymatically active form (PMID:31576654, PMID:40339988); loss of ATF7IP triggers proteasomal degradation of nuclear SETDB1 and phenocopies SETDB1 loss in H3K9me3 deposition and transgene silencing (PMID:27732843). This requirement for ATF7IP as a SETDB1 nuclear-localization cofactor is conserved from Drosophila (Windei/Eggless) (PMID:19750210). Beyond positioning SETDB1, ATF7IP acts as a recruitment and regulatory hub: its C-terminal fibronectin type-III domain binds co-repressors including ZMYM2 and MGA to direct SETDB1-mediated silencing, with MGA targeting SETDB1 to meiosis-related genes (PMID:33256805, PMID:40727931); G9a/GLP tri-methylation of ATF7IP at an H3K9-like lysine recruits the HUSH-component reader MPP8 to promote provirus silencing (PMID:30286792); and SUMOylation-dependent interaction with MBD1 links DNA methylation to H3K9me3 heterochromatin (PMID:16757475). Through SETDB1-mediated H3K9me3, ATF7IP represses immune and developmental loci, silencing Il2 and Il7r in T cells to shape effector, memory and exhaustion responses (PMID:31217192, PMID:35110421, PMID:41973040), maintaining hematopoietic progenitor expansion and thymic homing (PMID:36577070, PMID:40670340), and restraining tumor-antigen and ERV expression so that its loss triggers type I interferon responses and T-cell infiltration (PMID:34462284). ATF7IP also has SETDB1-independent activities, acting as a co-activator of Sp1-dependent transcription including at TERT/TERC to support telomerase (PMID:19106100).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2005 Medium

    Established ATF7IP/MCAF1 as a transcriptional bridging factor, showing it can act as a positive co-activator by linking Sp1 to viral transcription factors, framing it initially as a context-dependent coactivator rather than a silencer.

    Evidence Yeast two-hybrid, Co-IP, reporter assays and ChIP defining an Sp1-MCAF1-Rta complex (EBV context)

    PMID:16314315

    Open questions at the time
    • Co-activator role characterized only in viral transcription factor context
    • Does not address H3K9 methylation or heterochromatin function
  2. 2006 High

    Connected MCAF1 to heterochromatin maintenance by showing SUMO-dependent recruitment to MBD1, linking DNA methylation readers to H3K9me3/HP1 foci.

    Evidence Binding assays, reciprocal Co-IP, SUMO siRNA knockdown and immunofluorescence in cells

    PMID:16757475

    Open questions at the time
    • SUMO target and acceptor sites not fully mapped
    • Functional silencing consequences at specific loci not tested
  3. 2008 High

    Demonstrated a gene-activating role at the telomerase genes, showing MCAF1 promotes active Pol II occupancy and TERT/TERC expression via Sp1.

    Evidence siRNA knockdown, TRAP telomerase assay, ChIP at TERT, Co-IP and domain mapping

    PMID:19106100

    Open questions at the time
    • Relationship between this activating role and SETDB1-mediated silencing unresolved
    • Direct vs indirect recruitment to Pol II machinery not separated
  4. 2009 High

    Identified the SETDB1 cofactor function via the Drosophila homolog Windei, establishing that the ATF7IP family is required for H3K9 methyltransferase nuclear localization in vivo.

    Evidence Drosophila genetic loss-of-function, Co-IP domain mapping, immunofluorescence in germline

    PMID:19750210

    Open questions at the time
    • Mechanism of nuclear retention not biochemically defined here
    • Conservation to mammalian SETDB1 inferred, not directly shown in this study
  5. 2016 High

    Defined the core biochemical relationship: ATF7IP is required for nuclear SETDB1 stability against proteasomal degradation, and reconstitution showed the binary complex modulates SETDB1 catalytic activity.

    Evidence ATF7IP KO cells with proteasome rescue, genome-wide H3K9me3 ChIP-seq, RNA-seq; plus in vitro 1:1 complex purification with kinetic and SAMDI/radiometric assays

    PMID:26813693 PMID:27732843

    Open questions at the time
    • How ATF7IP stabilizes SETDB1 mechanistically not fully resolved in 2016
    • Apparent 1:1 in vitro vs cellular complex stoichiometry not reconciled until later
  6. 2019 High

    Resolved the localization mechanism, showing ATF7IP binds the SETDB1 N-terminal NES region to inhibit Crm1-mediated export and enrich a ubiquitinated, active nuclear SETDB1 pool.

    Evidence Co-IP, nuclear/cytoplasmic fractionation, NES deletion/mutation, ubiquitination assays

    PMID:31576654

    Open questions at the time
    • Direct competition with Crm1 not yet demonstrated biochemically
    • Ubiquitin ligase responsible for SETDB1 activation not identified
  7. 2025 High

    Provided the structural and stoichiometric mechanism, establishing a 1:2 SETDB1:ATF7IP hetero-trimer in which ATF7IP coiled-coils directly outcompete Crm1 for the SETDB1 NES.

    Evidence AlphaFold2 prediction, biochemical reconstitution, native mass spectrometry, Co-IP, direct competition binding assays

    PMID:40339988

    Open questions at the time
    • No experimental high-resolution structure of the full complex
    • How multimer resolution upon SETDB1 binding is regulated in cells not addressed
  8. 2018 High

    Revealed a regulatory layer on ATF7IP itself: G9a/GLP methylation of an H3K9-like lysine creates a docking site for the HUSH reader MPP8, accelerating provirus silencing independent of the ATF7IP-SETDB1 interaction.

    Evidence Substrate screen, in vitro methylation, chromodomain binding, un-methylatable mutant rescue in Atf7ip KO mESCs

    PMID:30286792

    Open questions at the time
    • Genome-wide impact of ATF7IP methylation not mapped
    • Dynamics/turnover of the methyl mark not characterized
  9. 2020 High

    Dissected ATF7IP domains, separating the SETDB1-interaction region (required for SETDB1 nuclear localization and silencing) from the FNIII domain that acts as a co-repressor binding hub for ZMYM2 and MGA.

    Evidence Truncation rescue in Atf7ip KO mESCs, retroviral reporter silencing, RNA-seq, AP-MS interactome, ZMYM2 knockdown

    PMID:33256805

    Open questions at the time
    • Mechanistic contribution of each FNIII partner to silencing not fully separated
    • Whether FNIII partners target distinct loci not resolved
  10. 2014 Medium

    Linked the ATF7IP-MBD1-SETDB1 axis to physiological gene programs, showing it is co-opted by Aire for tissue-specific antigen expression and contributes to X-inactivation maintenance.

    Evidence Co-IP, Mbd1 KO mice with autoimmune phenotype; siRNA Atf7ip knockdown in MEFs with Xi reporter reactivation and epistasis

    PMID:24464130 PMID:25028596

    Open questions at the time
    • XCI evidence primarily siRNA-based in a single system
    • How a silencing complex supports Aire-dependent activation mechanistically unclear
  11. 2022 High

    Established ATF7IP as a physiological repressor of immune and hematopoietic gene programs through locus-specific H3K9me3 at transposable-element-associated regulatory regions.

    Evidence T cell-specific and zebrafish Atf7ip KO, H3K9me3 ChIP-seq at Il2/Il7r and hematopoietic loci, infection/differentiation phenotypes

    PMID:31217192 PMID:35110421 PMID:36577070

    Open questions at the time
    • Selectivity of locus targeting versus genome-wide silencing not fully explained
    • Contribution of innate-immune retrotransposon derepression vs direct gene silencing to phenotypes not always separated
  12. 2021 Medium

    Demonstrated therapeutic relevance in tumor immunity, showing ATF7IP/SETDB1 loss derepresses ERVs and tumor antigens to trigger interferon responses and T-cell infiltration.

    Evidence CRISPR-Cas9 suppressor screen in syngeneic tumor model, ERV/IFN and T-cell infiltration readouts

    PMID:34462284

    Open questions at the time
    • Mechanism inferred from screen without biochemical dissection
    • Direct vs interferon-mediated effects on immune escape not separated
  13. 2025 Medium

    Extended the silencing role to specific developmental and recruitment contexts and to non-canonical functions, including MGA-directed SETDB1 recruitment to meiotic genes, T-cell exhaustion control, thymic homing, and ferroptosis resistance in HCC.

    Evidence Co-IP and ChIP-seq in mESCs (MGA), conditional KO T-cell and hematopoiesis models, ferroptosis assays with CYB5R2 silencing and PARK7 stabilization

    PMID:40670340 PMID:40716153 PMID:40727931 PMID:41973040

    Open questions at the time
    • Several arms (ferroptosis, exhaustion, MGA recruitment) come from single recent studies not independently replicated
    • PARK7 stabilization mechanism is SETDB1-independent and mechanistically unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ATF7IP and SETDB1 achieve locus selectivity across such diverse contexts, and how the FNIII co-repressor hub, ATF7IP methylation, SUMO/MBD1 inputs, and co-factor recruitment are integrated to direct silencing to particular targets, remains unresolved.
  • No unified model of locus targeting
  • Quantitative contribution of each regulatory input to silencing at endogenous loci unknown
  • Roles in DNA repair (ssDI) and DUX4/D4Z4 silencing rest on low-confidence screen/reporter data

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0060090 molecular adaptor activity 3 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 3 GO:0005694 chromosome 1
Pathway
R-HSA-168256 Immune System 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-392499 Metabolism of proteins 2 R-HSA-4839726 Chromatin organization 2
Partners
MBD1MGAMPP8PARK7SETDB1SP1SUMO-2/3ZMYM2
Complex memberships
HUSH complex (functional association)SETDB1-ATF7IP complex

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2016 ATF7IP is essential for SETDB1 stability: nuclear SETDB1 protein is degraded by the proteasome upon ablation of ATF7IP. Loss of ATF7IP phenocopies loss of SETDB1, with near-identical defects in global H3K9me3 deposition and similar transcriptome dysregulation, including failure of HUSH complex-mediated transgene silencing. ATF7IP knockout cells, proteasome inhibitor rescue, genome-wide H3K9me3 ChIP-seq, RNA-seq Cell reports High 27732843
2019 ATF7IP mediates retention of SETDB1 in the nucleus by binding to the N-terminal region of SETDB1 that harbors nuclear export signal (NES) motifs, thereby inhibiting Crm1-mediated nuclear export and promoting nuclear import. Nuclear SETDB1 accumulates in a more ubiquitinated, enzymatically active form. Co-immunoprecipitation, nuclear/cytoplasmic fractionation, NES deletion/mutation analysis, ubiquitination assays EMBO reports High 31576654
2025 One copy of Setdb1 and two copies of ATF7IP form a 1:2 hetero-trimeric complex in vitro and in cells. ATF7IP self-associates into multimers that are resolved upon Setdb1 binding. ATF7IP binds the Setdb1 NES motifs via coiled-coil interactions and directly competes with Crm1 for these sites, blocking Crm1-mediated nuclear export of Setdb1. AlphaFold2 structural prediction, biochemical reconstitution, native mass spectrometry, Co-IP in cells, competition binding assays The Journal of biological chemistry High 40339988
2016 SETDB1 and ATF7IP form a 1:1 stoichiometric complex in vitro. The SETDB1:ATF7IP complex efficiently catalyzes mono- and di-methylation of H3K9 peptides, but the binary complex shows 4-fold lower activity than SETDB1 alone due to a decreased kcat with comparable substrate KM. ATF7IP does not affect the distributive mechanism of H3K9 methylation by SETDB1. Co-expression and purification of 1:1 complex, radiometric flashplate assay, SAMDI mass spectrometry, kinetic analysis Biochemistry High 26813693
2006 MCAF1 (ATF7IP) directly interacts with SUMO-2/3 and SUMO-1. SUMOylation of MBD1 facilitates the interaction between MBD1 and MCAF1. In cells, MCAF1 co-localizes with MBD1 in heterochromatin regions enriched in H3K9me3, HP1β, and HP1γ. Knockdown of SUMO-2/3 or SUMO-1 dissociates MCAF1, H3K9me3, and HP1 from MBD1-containing heterochromatin foci. Protein-binding assays, co-immunoprecipitation, siRNA knockdown, immunofluorescence/confocal microscopy The Journal of biological chemistry High 16757475
2018 G9a/GLP tri-methylates ATF7IP at a histone H3K9-like lysine mimic. The chromodomain protein MPP8, a known H3K9me3-reader and component of the HUSH silencing complex, recognizes methylated ATF7IP via its chromodomain. Induction of SETDB1/MPP8-mediated provirus silencing is delayed in mESCs expressing only an un-methylatable ATF7IP mutant, but the ATF7IP–SETDB1 interaction itself does not depend on ATF7IP methylation. Comprehensive substrate screen in mESCs, in vitro methylation assays, chromodomain binding assay, un-methylatable mutant rescue in Atf7ip KO mESCs, reporter-provirus silencing assay Epigenetics & chromatin High 30286792
2020 The SETDB1-interaction region within ATF7IP is essential for SETDB1 nuclear localization and silencing of ERVs and integrated retroviral transgenes. The C-terminal fibronectin type-III (FNIII) domain of ATF7IP is dispensable for SETDB1 nuclear localization but contributes to efficient SETDB1 complex-mediated silencing; it acts as a binding hub for additional interacting proteins including ZMYM2 and MGA (via a consensus FAM motif). ZMYM2 was shown to be involved in efficient transgene silencing. Truncation mutants in Atf7ip KO mESCs, retroviral reporter silencing assay, RNA-seq, proteomics (AP-MS) of FNIII domain interactors, siRNA knockdown of ZMYM2 Epigenetics & chromatin High 33256805
2009 Windei (Wde), the Drosophila homolog of MCAF1/ATF7IP, is an essential cofactor of the H3K9 methyltransferase dSETDB1/Eggless required for its nuclear localization and function in female germ line cells. Deletion analysis combined with co-immunoprecipitation identified the regions in Wde and Egg necessary and sufficient for their interaction. Genetic loss-of-function in Drosophila, deletion analysis, co-immunoprecipitation, immunofluorescence PLoS genetics High 19750210
2008 MCAF1 (ATF7IP) interacts directly with Sp1 and the general transcriptional apparatus through two evolutionarily conserved domains. Depletion of MCAF1 or Sp1 down-regulates TERT and TERC genes, reducing telomerase activity. MCAF1 promotes occupancy of active RNA Pol II and ERCC3 at the TERT promoter. siRNA knockdown, telomerase activity assay (TRAP), ChIP at TERT promoter, co-immunoprecipitation, domain deletion analysis The Journal of biological chemistry High 19106100
2014 ATF7IP and MBD1 form a complex that is co-opted by the transcriptional regulator Aire for targeting and activating loci encoding tissue-specific antigens in thymic epithelial cells. Mbd1-/- mice develop autoimmunity and have a defect in Aire-dependent thymic expression of TSA genes. Co-immunoprecipitation (Aire-ATF7IP/MBD1 interaction), Mbd1 knockout mice, gene expression analysis Nature immunology High 24464130
2014 The Mbd1-Atf7ip-Setdb1 pathway contributes to maintenance of X chromosome inactivation (XCI) in somatic cells. siRNA-mediated knockdown of Atf7ip in MEFs induces reactivation of Xi-linked reporter genes, an effect strongly enhanced by additional inhibition of DNA methylation or Xist. Depletion of MBD1 or SETDB1, but not unrelated H3K9 methyltransferases, similarly reactivates Xi-linked reporters. siRNA knockdown in MEFs, Xi reporter reactivation assay, genetic epistasis with DNA methylation inhibitors and Xist depletion Epigenetics & chromatin Medium 25028596
2019 ATF7ip represses Il2 gene expression in T cells through deposition of H3K9me3 at the Il2-Il21 intergenic region. T cell-specific deletion of Atf7ip leads to aberrant overproduction of IL-2 upon TCR stimulation, impaired Th17 differentiation, and resistance to colitis in vivo. T cell-specific Atf7ip conditional KO mice, ChIP-seq (H3K9me3 at Il2 locus), cytokine measurements, in vivo colitis model The Journal of experimental medicine High 31217192
2022 ATF7ip targets transposable elements for H3K9me3 deposition at the Il7r locus and Il2-Il21 intergenic region in CD8+ T cells, repressing Il7r and Il2 expression. T cell-specific deletion of Atf7ip enhances IL-7R and IL-2 expression, leading to enhanced CD8+ T cell effector and memory responses. T cell-specific Atf7ip KO mice, ChIP-seq (H3K9me3), gene expression analysis, viral infection memory model Journal of immunology High 35110421
2021 Disruption of Atf7ip or Setdb1 in tumor cells restores tumor antigen expression, elevates endogenous retroviral (ERV) antigen levels and mRNA intron retention, triggers a type I interferon response, and increases T-cell infiltration. This was identified via a CRISPR-Cas9 suppressor screen in a syngeneic immune escape tumor model. CRISPR-Cas9 suppressor screen, syngeneic transplantable tumor model, ERV expression analysis, IFN response assay, T cell infiltration measurement Cancer immunology research Medium 34462284
2022 In zebrafish, Atf7ip regulates hematopoiesis through Setdb1-mediated H3K9me3 modification of hematopoietic regulatory genes including cebpβ and cdkn1a, preventing premature myeloid differentiation and maintaining HSPC expansion. Loss of Atf7ip or Setdb1 also derepresses retrotransposons, activating Mda5/RLR innate immune signaling and driving stress myelopoiesis. Zebrafish atf7ip/setdb1 mutants, H3K9me3 ChIP, ChIP-seq, gene expression analysis, retrotransposon derepression assay, innate immune signaling measurement PNAS High 36577070
2025 MGA, a scaffolding component of PRC1.6, directly recruits SETDB1 to meiosis-related genes in mouse ESCs via its interaction with ATF7IP, depositing H3K9me3 and establishing a robustly repressed chromatin state beyond that achieved by PRC1/PRC2 alone. Co-immunoprecipitation (MGA-ATF7IP-SETDB1), ChIP-seq (H3K9me3 at meiosis-related genes), genetic KO of MGA/ATF7IP in mESCs iScience Medium 40727931
2025 In zebrafish, Atf7ip interacts with Setdb1 to catalyze H3K9me3 modification of the bach2b gene, derepressing ccr9a and irf4a expression and promoting lymphoid progenitor thymic homing and T cell differentiation. Depletion of ATF7IP in mice (CAG-CreERT2 and Mx1-iCre) impedes hematopoietic progenitor migration to the thymus, reducing T lymphopoiesis. Zebrafish atf7ip/setdb1 mutants, H3K9me3 ChIP at bach2b, rescue experiments (irf4a overexpression, bach2b knockdown), conditional KO in mice Nature communications High 40670340
2005 MCAF1 (ATF7IP) interacts with both the EBV transcription factor Rta and Sp1, forming a trimeric Sp1-MCAF1-Rta complex at Sp1 binding sites that activates Sp1-dependent transcription. The Rta-MCAF1 interaction is prevented when Rta is bound to an Rta-response element (RRE), restricting MCAF1's co-activator role to Sp1-dependent (non-RRE) promoters. Yeast two-hybrid, co-immunoprecipitation, transient transfection reporter assays, ChIP Nucleic acids research Medium 16314315
2010 MCAF1 (ATF7IP) acts as an intermediary enabling Rta and Zta (EBV transcription factors) to form a trimeric complex at Zta response elements (ZRE) in vitro and in cells, allowing synergistic transcriptional activation of EBV lytic genes. The interaction between Rta and Zta in vitro requires the region between amino acids 562–816 of MCAF1. In vitro complex formation, co-immunoprecipitation, ChIP, confocal microscopy, MCAF1 siRNA knockdown, domain deletion analysis Nucleic acids research Medium 20385599
2025 ATF7IP promotes H3K9me3 deposition at the Il7r locus and Il2-Il21 intergenic region in CD8+ T cells, facilitating terminal T cell exhaustion. Loss of Atf7ip in CD8+ T cells decreases terminal exhaustion and increases progenitor-exhausted cell numbers in chronic viral infection and cancer models. T cell-specific Atf7ip KO, ChIP-seq, chronic viral infection model, tumor models, exhaustion marker analysis Cancer immunology research Medium 41973040
2025 ATF7IP inhibits ferroptosis in hepatocellular carcinoma cells by two mechanisms: (1) interacting with SETDB1 to epigenetically silence CYB5R2 transcription, thereby reducing cellular Fe2+ levels; and (2) stabilizing the antioxidant protein PARK7, preserving the transsulfuration pathway for glutathione production. ATF7IP knockdown, Co-IP (ATF7IP-SETDB1), ChIP at CYB5R2 locus, glutathione measurement, lipid peroxidation assay, PARK7 protein stability assay, in vivo xenograft Redox biology Medium 40716153
2023 Atf7ip contributes to nuclear localization of Setdb1 in osteoblasts (MC3T3-E1 cells) but does not affect Setdb1 expression levels. Atf7ip negatively regulates Sp7 (Osterix) expression; Sp7 knockdown attenuates the pro-differentiation effect of Atf7ip deletion, placing Sp7 downstream of Atf7ip in osteoblast differentiation. Osteoblast-specific Atf7ip KO mice show increased bone formation. Atf7ip overexpression and KO in MC3T3-E1 cells, conditional KO mice (Oc-Cre;Atf7ip), µ-CT and histomorphometry, nuclear fractionation, siRNA epistasis (Sp7) International journal of molecular sciences Medium 36901736
2015 The ATF7IP-PDGFRB fusion protein constitutively activates PDGFRB kinase and downstream AKT and MAPK signaling, transforming Ba/F3 cells to cytokine-independent growth. Tyrosine-to-phenylalanine mutations at MAPK adaptor binding sites in the PDGFRB portion abolish transformation, indicating MAPK signaling is critical for ATF7IP-PDGFRB-mediated cell transformation. Ba/F3 transformation assay, site-directed mutagenesis of PDGFRB signaling residues, phospho-Western blotting, tyrosine kinase inhibitor treatment, MEK inhibitor selectivity assay Experimental hematology Medium 26703895
2025 SETDB1/ATF7IP (heterodimer) and the downstream HUSH complex are negative regulators of the homology-directed repair sub-pathway ssDI (single-stranded DNA incorporation) specifically at transgenic reporter loci and HUSH-regulated single-copy genes, but not at other endogenous loci. This was identified in a genome-wide CRISPR KO screen. Genome-wide CRISPR KO screen, ssDI reporter assay, epistasis with HUSH complex components Epigenetics & chromatin Low 41656257
2025 SETDB1, ATF7IP, SIN3A/B, and LRIF1 are necessary for epigenetic silencing activity conferred by a discrete D4Z4 fragment adjacent to a constitutively-driven reporter, establishing these factors as required components of D4Z4-mediated epigenetic repression of DUX4. D4Z4 fragment reporter assay, siRNA/KD of individual factors, p38 inhibitor enhancement assay bioRxiv (preprint)preprint Low bio_10.1101_2025.02.19.639175

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 Variants near DMRT1, TERT and ATF7IP are associated with testicular germ cell cancer. Nature genetics 278 20543847
1998 Interaction of BTG1 and p53-regulated BTG2 gene products with mCaf1, the murine homolog of a component of the yeast CCR4 transcriptional regulatory complex. The Journal of biological chemistry 126 9712883
2016 ATF7IP-Mediated Stabilization of the Histone Methyltransferase SETDB1 Is Essential for Heterochromatin Formation by the HUSH Complex. Cell reports 114 27732843
2006 Involvement of SUMO modification in MBD1- and MCAF1-mediated heterochromatin formation. The Journal of biological chemistry 79 16757475
2014 The transcriptional regulator Aire coopts the repressive ATF7ip-MBD1 complex for the induction of immunotolerance. Nature immunology 73 24464130
2014 The Mbd1-Atf7ip-Setdb1 pathway contributes to the maintenance of X chromosome inactivation. Epigenetics & chromatin 71 25028596
2019 ATF7IP regulates SETDB1 nuclear localization and increases its ubiquitination. EMBO reports 66 31576654
2005 Activation of Sp1-mediated transcription by Rta of Epstein-Barr virus via an interaction with MCAF1. Nucleic acids research 62 16314315
2018 Tri-methylation of ATF7IP by G9a/GLP recruits the chromodomain protein MPP8. Epigenetics & chromatin 50 30286792
2008 MCAF1/AM is involved in Sp1-mediated maintenance of cancer-associated telomerase activity. The Journal of biological chemistry 50 19106100
2009 Windei, the Drosophila homolog of mAM/MCAF1, is an essential cofactor of the H3K9 methyl transferase dSETDB1/Eggless in germ line development. PLoS genetics 44 19750210
2021 Targeting the Atf7ip-Setdb1 Complex Augments Antitumor Immunity by Boosting Tumor Immunogenicity. Cancer immunology research 37 34462284
2010 MCAF1 and synergistic activation of the transcription of Epstein-Barr virus lytic genes by Rta and Zta. Nucleic acids research 27 20385599
2014 ATF7IP as a novel PDGFRB fusion partner in acute lymphoblastic leukaemia in children. British journal of haematology 25 24628626
2022 Atf7ip and Setdb1 interaction orchestrates the hematopoietic stem and progenitor cell state with diverse lineage differentiation. Proceedings of the National Academy of Sciences of the United States of America 24 36577070
2020 The fibronectin type-III (FNIII) domain of ATF7IP contributes to efficient transcriptional silencing mediated by the SETDB1 complex. Epigenetics & chromatin 19 33256805
2016 Characterization of the Enzymatic Activity of SETDB1 and Its 1:1 Complex with ATF7IP. Biochemistry 17 26813693
2019 The epigenetic regulator ATF7ip inhibits Il2 expression, regulating Th17 responses. The Journal of experimental medicine 14 31217192
2015 Ph-like ALL-related novel fusion kinase ATF7IP-PDGFRB exhibits high sensitivity to tyrosine kinase inhibitors in murine cells. Experimental hematology 14 26703895
2017 Acute Lymphoblastic Leukemia Patient with Variant ATF7IP/PDGFRB Fusion and Favorable Response to Tyrosine Kinase Inhibitor Treatment: A Case Report. The American journal of case reports 13 29133777
2024 Genome-Wide CRISPR/Cas9 Screening Unveils a Novel Target ATF7IP-SETDB1 Complex for Enhancing Difficult-to-Express Protein Production. ACS synthetic biology 12 38240694
2022 Methyltransferase Setdb1 Promotes Osteoblast Proliferation by Epigenetically Silencing Macrod2 with the Assistance of Atf7ip. Cells 11 36010655
2014 MCAF1 and Rta-activated BZLF1 transcription in Epstein-Barr virus. PloS one 11 24598729
2013 Genome-wide association study identifies loci at ATF7IP and KLK2 associated with percentage of circulating free PSA. Neoplasia (New York, N.Y.) 10 23359319
2022 ATF7ip Targets Transposable Elements for H3K9me3 Deposition to Modify CD8+ T Cell Effector and Memory Responses. Journal of immunology (Baltimore, Md. : 1950) 8 35110421
2023 Atf7ip Inhibits Osteoblast Differentiation via Negative Regulation of the Sp7 Transcription Factor. International journal of molecular sciences 6 36901736
2025 MGA directly recruits SETDB1/ATF7IP for histone H3K9me3 mark on meiosis-related genes in mouse embryonic stem cells. iScience 3 40727931
2025 ATF7IP inhibits Sorafenib-induced ferroptosis in hepatocellular carcinoma cells by inhibiting CYB5R2 transcription and stabilizing PARK7 protein. Redox biology 2 40716153
2025 Setdb1 and Atf7IP form a hetero-trimeric complex that blocks Setdb1 nuclear export. The Journal of biological chemistry 1 40339988
2025 ATF7IP/SETDB1-mediated epigenetic programming regulates thymic homing and T lymphopoiesis of hematopoietic progenitors during embryogenesis. Nature communications 1 40670340
2022 Mutational Alterations of DNA Methylation-related Genes CTCF, ZFP57, and ATF7IP Genes in Colon Cancers. Applied immunohistochemistry & molecular morphology : AIMM 1 35175239
2026 SETDB1/ATF7IP regulate the precise genome engineering of HUSH-regulated genes. Epigenetics & chromatin 0 41656257
2026 ATF7ip inhibits the tumor immune response by promoting terminal CD8+ T cell Exhaustion. Cancer immunology research 0 41973040
2025 Circ-ATF7IP promotes IL13RA1 dependent M2 polarization of macrophage via sponging MiR-488-3p in papillary thyroid carcinoma. Biochimica et biophysica acta. General subjects 0 40945694

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