Affinage

TRIM28

Transcription intermediary factor 1-beta · UniProt Q13263

Length
835 aa
Mass
88.5 kDa
Annotated
2026-04-28
100 papers in source corpus 50 papers cited in narrative 50 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TRIM28 (KAP1/TIF1β) is a multifunctional scaffold protein that acts as a universal transcriptional co-repressor, SUMO E3 ligase, and ubiquitin E3 ligase, integrating chromatin regulation, DNA damage signaling, innate immunity, and autophagy. Recruited to specific genomic loci by KRAB-zinc finger proteins via a structurally defined coiled-coil interface, TRIM28 nucleates heterochromatin through SETDB1-mediated H3K9me3 deposition and HP1 spreading, silencing endogenous retroviruses, imprinting control regions, and lineage-specific genes (PMID:31289231, PMID:36341546, PMID:20221260, PMID:22055183, PMID:23293284). Its tandem PHD-bromodomain functions as an intramolecular SUMO E3 ligase and a chromatin reader of hypo-acetylated H4 tails, coupling RNA Pol II pausing to CDK9-dependent pause release, while also SUMOylating diverse substrates including CDK9, Vps34, NLRP3, ACSL4, and viral nucleocapsid proteins to regulate transcription, autophagy, inflammasome assembly, ferroptosis, and innate immune evasion (PMID:18488044, PMID:25173174, PMID:32402252, PMID:30652970, PMID:34373456, PMID:38172120, PMID:39875520). TRIM28 activity is dynamically controlled by phosphorylation at Ser824 (by ATM/Chk2, triggering heterochromatin relaxation for DNA repair) and Ser473 (by PKCδ, p38, and RIPK3, disrupting HP1 binding to derepress target genes), establishing a phosphorylation-SUMOylation switch that tunes its repressor function in response to DNA damage, metabolic stress, and necroptotic signaling (PMID:17942393, PMID:18590578, PMID:27364555, PMID:34419074).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2005 High

    Establishing that TRIM28 operates beyond KRAB-ZFP co-repression as a p53 regulator: TRIM28 cooperates with MDM2 to promote p53 ubiquitination and degradation and recruits HDAC1 to inhibit p53 acetylation, linking TRIM28 to the DNA damage-apoptosis decision.

    Evidence Co-IP, RNAi, ubiquitination/acetylation assays, transcriptional reporters in human cell lines

    PMID:16107876

    Open questions at the time
    • Whether TRIM28 directly ubiquitinates p53 or only facilitates MDM2-mediated ubiquitination
    • Structural basis of the KAP1-MDM2 interaction
  2. 2007 High

    Defining the phosphorylation-SUMOylation switch: ATM phosphorylates TRIM28 at Ser824 after DNA damage, which reduces SUMOylation and relieves transcriptional repression of pro-apoptotic genes, establishing a post-translational toggle that converts a damage signal into chromatin derepression.

    Evidence Site-directed mutagenesis (S824A/D), ATM inhibition, SUMOylation and ChIP assays

    PMID:17942393

    Open questions at the time
    • How SENP1-mediated deSUMOylation feeds back to regulate Ser824 phosphorylation in vivo
    • Whether the switch operates identically at heterochromatic versus euchromatic loci
  3. 2008 High

    Two key structural and regulatory discoveries converged: the PHD-bromodomain was shown to function as an intramolecular SUMO E3 ligase (via NMR structure), and Ser473 phosphorylation by PKCδ was shown to disrupt HP1 binding, establishing the two principal post-translational regulatory axes of TRIM28.

    Evidence NMR structure of PHD-bromodomain with UBC9 binding and mutagenesis; ChIP, phospho-specific antibodies, S473A/E mutagenesis, PKCδ pathway inhibition

    PMID:18488044 PMID:18590578

    Open questions at the time
    • Full-length structural model integrating the SUMO ligase cassette with the TRIM domain
    • Whether other kinases besides PKCδ target Ser473 in vivo
  4. 2010 High

    Demonstrating the long-range mechanism of KRAB-ZFP/TRIM28 repression: H3K9me3 and HP1β spread linearly from TRIM28 binding sites over tens of kilobases, blocking RNA Pol II recruitment at distal promoters, establishing a spreading model for TRIM28-mediated silencing.

    Evidence Ectopic repressor tethering, multi-locus ChIP for H3K9me3/HP1/Pol II, endogenous ZFP gene cluster analysis

    PMID:20221260

    Open questions at the time
    • Factors that limit heterochromatin spreading boundaries
    • Whether spreading requires continuous TRIM28 occupancy
  5. 2011 High

    Multiple studies expanded TRIM28 function into genomic imprinting, HIV restriction, DNA repair, and T cell regulation: TRIM28 protects imprinting control regions from demethylation via ZFP57, deacetylates HIV-1 integrase via HDAC1 recruitment, and an HP1-KAP1 axis regulates DNA repair kinetics in heterochromatin.

    Evidence ZFP57/KAP1 KO ES cells with methylation analysis; Co-IP with acetylated HIV integrase and viral infectivity assay; HP1-KO and phospho-mutant cell lines with γH2AX resolution

    PMID:21669397 PMID:22055183 PMID:22205726

    Open questions at the time
    • Whether TRIM28 directly recruits DNMTs or acts through an intermediate
    • Structural basis of acetylated integrase recognition
  6. 2013 High

    TRIM28 was established as a SUMO E3 ligase for non-self substrates (Vps34), a regulator of ERV silencing through SETDB1, a controller of erythropoiesis via a KRAB-ZFP/miRNA cascade, and a dual-function factor in ES cells cooperating with PRC1.

    Evidence Vps34 SUMOylation at K840, HSP70 KO MEFs, autophagy assay; KAP1 KO ES cells with ERV methylation; conditional hematopoietic KO with anemia; PRC1 Co-IP with domain mutants in ES cells

    PMID:23293284 PMID:23493425 PMID:23569248 PMID:24687849

    Open questions at the time
    • Whether other autophagy kinases are TRIM28 SUMO substrates
    • How PRC1 and KRAB-ZFP recruitment pathways are coordinated at shared loci
  7. 2014 High

    TRIM28 was revealed as a global regulator of RNA Pol II promoter-proximal pausing, extending its function beyond heterochromatic silencing to active transcriptional regulation genome-wide.

    Evidence In vitro transcription reconstitution at HSPA1B, genome-wide ChIP-seq of Pol II occupancy upon TRIM28 depletion

    PMID:25173174

    Open questions at the time
    • How TRIM28 distinguishes pausing targets from silencing targets
    • Identity of the kinase mediating transcription-coupled TRIM28 phosphorylation for pause release
  8. 2016 High

    Ser473 phosphorylation was linked to metabolic stress signaling through p38/ROS, controlling mitochondrial dynamics via MFN2, expanding TRIM28's regulatory scope to organelle morphology.

    Evidence Live-cell imaging, S473A mutant, MFN2 expression analysis, xenograft model in glucose-starved breast cancer cells

    PMID:27364555

    Open questions at the time
    • Whether TRIM28 directly regulates MFN2 transcription or acts through an intermediate repressor
    • Generalizability beyond breast cancer cells
  9. 2018 High

    TRIM28 was shown to associate with replication fork components (PCNA, MCM3, MCM6) and to catalyze E3 ubiquitin ligase activity toward BCL2A1 at mitochondria, establishing its dual roles in heterochromatin maintenance during S-phase and mitochondrial apoptosis regulation.

    Evidence Endogenous Co-IP/PLA of PCNA-KAP1-Suv39h1 complex with S-phase phosphorylation; endogenous Co-IP at mitochondria with ubiquitination assay and TRIM17 competition

    PMID:29955894 PMID:30042493

    Open questions at the time
    • Whether KAP1-PCNA interaction is direct or mediated by chromatin
    • Structural basis of TRIM17 competition for BCL2A1 binding
  10. 2019 High

    Two major structural and enzymatic advances: the crystal structure of the TRIM domain revealed the antiparallel dimer architecture and KRAB-binding interface, and TRIM28 was shown to SUMOylate CDK9 with SUMO4, inhibiting P-TEFb and promoting HIV-1 latency.

    Evidence X-ray crystallography of TRIM domain with structure-guided mutagenesis and silencing assays; global SUMO-MS identifying CDK9 sites, kinase activity assay

    PMID:30652970 PMID:31289231

    Open questions at the time
    • Full-length structure of TRIM28 with all domains resolved
    • Whether SUMO4-specific CDK9 modification occurs outside HIV latency contexts
  11. 2020 High

    The chromatin reader function of TRIM28 was mechanistically resolved: the PHD-bromodomain reads hypo-acetylated H4 tails at promoters, enabling TRIM28 to dock on chromatin, associate with Pol II, and recruit pathway-specific factors like SMAD2 for CDK9-dependent pause release.

    Evidence Reader domain biochemistry, Co-IP, ChIP-seq, CDK9 kinase assay, SMAD2 recruitment assay

    PMID:32402252

    Open questions at the time
    • Whether other signal-responsive transcription factors use the same TRIM28-Pol II docking mechanism
    • Structural detail of the H4 tail–bromodomain interaction
  12. 2021 High

    TRIM28 was established as an NLRP3 SUMO E3 ligase stabilizing the inflammasome, and RIPK3-mediated Ser473 phosphorylation was shown to derepress inflammatory gene programs during necroptosis, connecting TRIM28 to innate immune activation.

    Evidence NLRP3 SUMOylation/ubiquitination assays with Trim28 KO mice and inflammasome readout; TAP-MS identification and RNA-seq upon RIPK3-phosphorylated TRIM28

    PMID:34373456 PMID:34419074

    Open questions at the time
    • Whether TRIM28 SUMOylation of NLRP3 competes with specific ubiquitin E3 ligases
    • In vivo validation of RIPK3-TRIM28 axis in tissue-specific necroptosis
  13. 2022 High

    The atomic-resolution KRAB-TRIM28 interface was defined by co-crystal structure with ZNF93, and TRIM28-dependent SUMOylation was shown to maintain ovarian identity by preventing female-to-male sex reversal.

    Evidence Crystal structure of KAP1 TRIM–ZNF93 KRAB complex validated by mutagenesis and genome-wide H3K9me3 ChIP-seq; conditional Trim28 KO ovary with SUMOylation profiling and sex-reversal phenotype

    PMID:35906245 PMID:36341546

    Open questions at the time
    • Whether the ZNF93-defined interface generalizes to all ~350 human KRAB-ZFPs
    • Identity of the specific ovarian transcription factors SUMOylated by TRIM28
  14. 2023 High

    TRIM28's E3 ubiquitin ligase activity was extended to MAVS (K48-linked, degradation), RIPK1 (K63-linked, NF-κB activation), and TFE3 (degradation), with RING domain catalytic residues mapped, establishing TRIM28 as a bona fide ubiquitin E3 ligase for multiple substrates across immune and autophagy pathways.

    Evidence RING domain C65/C68 mutagenesis with site-specific ubiquitination of MAVS; K63 ubiquitination assay for RIPK1 with syngeneic tumor models; TFE3 ubiquitination and ChIP

    PMID:36935008 PMID:37119745 PMID:37865804

    Open questions at the time
    • Whether RING-dependent and PHD-dependent E3 activities are mutually exclusive
    • Structural basis of substrate selectivity for ubiquitin versus SUMO modification
  15. 2024 High

    TRIM28 SUMOylation of the SARS-CoV-2 nucleocapsid protein at Lys65 promotes viral phase separation and immune evasion, demonstrating that pathogens co-opt TRIM28 SUMO ligase activity.

    Evidence Site-specific SUMOylation, LLPS assay, interfering peptide blocking TRIM28-NP interaction, viral replication assay

    PMID:38172120

    Open questions at the time
    • Whether other coronaviral proteins are TRIM28 SUMO substrates
    • Therapeutic potential of the interfering peptide in vivo
  16. 2025 High

    TRIM28 SUMOylation of ACSL4 at Lys532 blocks its autophagic degradation and drives ferroptosis after spinal cord injury, revealing a SUMO-ubiquitin crosstalk mechanism regulating neuronal cell death.

    Evidence K532 mutagenesis, SUMO3/K63-Ub crosstalk assays, conditional Trim28 KO mouse with motor phenotype, SENP3 competition

    PMID:39875520

    Open questions at the time
    • Whether TRIM28-ACSL4 axis operates in other ferroptosis-sensitive tissues
    • Structural basis of ACSL4 recognition by TRIM28

Open questions

Synthesis pass · forward-looking unresolved questions
  • No full-length structure of TRIM28 integrating the RING-B-box-coiled-coil, HP1-binding, PHD-bromodomain, and SUMO ligase modules has been determined; how TRIM28 switches between co-repressor, co-activator, SUMO ligase, and ubiquitin ligase modes at different genomic loci remains mechanistically unresolved.
  • Full-length structural model
  • Mechanism distinguishing repressive versus activating modes at specific loci
  • How substrate selectivity for SUMO versus ubiquitin E3 activity is determined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016874 ligase activity 8 GO:0140110 transcription regulator activity 7 GO:0140096 catalytic activity, acting on a protein 4 GO:0003677 DNA binding 3 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 6 GO:0005694 chromosome 4 GO:0005739 mitochondrion 1
Pathway
R-HSA-4839726 Chromatin organization 7 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4 R-HSA-392499 Metabolism of proteins 4 R-HSA-73894 DNA Repair 4 R-HSA-1643685 Disease 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-9612973 Autophagy 2 R-HSA-69306 DNA Replication 1
Partners
CDK9EZH2HP1MAVSMDM2NLRP3PCNASETDB1
Complex memberships
KAP1-HP1 heterochromatin complexKAP1-PCNA-Suv39h1 replication complexKRAB-ZFP/KAP1/SETDB1 silencing complexMDM2-KAP1-p53 complex

Evidence

Reading pass · 50 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 The tandem PHD finger-bromodomain of KAP1/TRIM28 functions as an intramolecular SUMO E3 ligase; NMR solution structure revealed the PHD finger and bromodomain form a unified scaffold, and mutation-based structure-function analysis showed this unit facilitates lysine SUMOylation required for KAP1 co-repressor activity in gene silencing, with UBC9 binding mapped to the PHD-bromodomain interface. NMR structure determination, mutation-based structure-function analysis, UBC9 binding assay, transcriptional repression assay Nature structural & molecular biology High 18488044
2019 Crystal structure of the KAP1 TRIM domain revealed it forms antiparallel dimers that assemble into higher-order oligomers; the KRAB domain-binding site was mapped to the coiled-coil domain near the dimer dyad, and structure-guided mutations at this interface abolished KRAB binding and transcriptional silencing of retrotransposons. X-ray crystallography, biophysical oligomerization assays, structure-guided mutagenesis, transcriptional silencing assay Proceedings of the National Academy of Sciences of the United States of America High 31289231
2022 Crystal structure of the KAP1 TRIM domain in complex with the KRAB domain of ZNF93 defined the molecular interface; structure-guided mutations abolished KRAB binding and eliminated genome-wide H3K9me3 deposition at thousands of KAP1/KRAB-ZFP target loci. X-ray crystallography, structure-guided mutagenesis, epigenetic silencing assay, ChIP-seq The EMBO journal High 36341546
2011 ZFP57 and its cofactor KAP1/TRIM28 bind selectively to the H3K9me3-bearing, DNA-methylated allele of imprinting control regions (ICRs) in ES cells; KAP1 deletion induces loss of heterochromatin marks at ICRs, and ZFP57/KAP1 associate with DNMTs and the hemimethylated DNA-binding protein NP95 to protect ICRs against DNA demethylation. The methylated TGCCGC hexanucleotide was identified as the ZFP57 recognition motif. Co-immunoprecipitation, ChIP, KAP1/ZFP57 knockout ES cells, DNA methylation analysis Molecular cell High 22055183
2010 KRAB-ZFP/KAP1 mediates long-range transcriptional repression through spreading of H3K9me3 and HP1β from the repressor binding site to promoters located up to tens of kilobases away, blocking RNA Pol II recruitment and transcriptional initiation. Ectopic repressor assay, ChIP (H3K9me3, H3K-acetylation, RNA Pol II), lentiviral gene trap, KAP1-dependent endogenous ZFP gene cluster analysis PLoS genetics High 20221260
2005 MDM2 interacts with KAP1/TRIM28 via the N-terminal coiled-coil domain of KAP1 and the central acidic domain of MDM2; KAP1 stimulates the p53-HDAC1 complex, inhibits p53 acetylation, and cooperates with MDM2 to promote p53 ubiquitination and degradation. ARF competes with KAP1 for MDM2 binding. RNAi depletion of KAP1 stimulates p53 transcriptional activity and sensitizes cells to DNA damage-induced apoptosis. Co-immunoprecipitation, RNAi knockdown, ubiquitination assay, acetylation assay, transcriptional reporter assay The EMBO journal High 16107876
2007 ATM phosphorylates KAP1 at Ser-824 in response to DNA damage (doxorubicin), and this phosphorylation reduces KAP1 SUMOylation; the S824A mutation increases KAP1 SUMOylation and represses p21 transcription, whereas S824D mimics constitutive phosphorylation, decreases SUMOylation and stimulates p21 transcription. SENP1 deSUMOylase regulates basal KAP1 Ser-824 phosphorylation. This phosphorylation/sumoylation switch controls KAP1-mediated transcriptional repression of p21, Gadd45α, Bax, Puma, and Noxa. Site-directed mutagenesis, ATM inhibition/siRNA, SUMOylation assay, ChIP, transcriptional reporter assay The Journal of biological chemistry High 17942393
2011 KAP1/TRIM28 is phosphorylated by ATM at Ser-824 in response to DNA damage; HP1α associates with unmodified KAP1 at heterochromatic loci, and loss of HP1 prevents discrete pKAP1-S824 foci formation while elevating total pKAP1 levels. KAP1 is also phosphorylated at Ser-473 in response to DNA damage, and HP1 association tempers both phosphorylation events and slows resolution of γH2AX foci, establishing an HP1-KAP1 axis that regulates DNA repair in heterochromatin. Immunofluorescence, ChIP, live-cell imaging at heterochromatic transgene loci, HP1-knockout and KAP1 phospho-mutant cell lines Molecular cancer research : MCR High 22205726
2014 TRIM28 regulates RNA Pol II promoter-proximal pausing and pause release: TRIM28 depletion attenuates Pol II pausing at HSPA1B in vitro in an HSF1-dependent manner and de-represses paused Pol II-regulated genes in vivo. Genome-wide ChIP-seq revealed a global role for TRIM28 in Pol II pausing, and mechanistic studies indicate transcription-coupled phosphorylation regulates Pol II pause release by TRIM28. In vitro transcription assay, ChIP-seq, siRNA knockdown, genome-wide Pol II occupancy analysis Nature structural & molecular biology High 25173174
2020 KAP1/TRIM28 uses a chromatin reader cassette to bind hypo-acetylated histone H4 tails at promoters; upon chromatin docking it associates with RNA Pol II and then recruits pathway-specific transcription factor SMAD2 in response to TGFβ, enabling CDK9-dependent pause release of Pol II. This coupling mechanism sustains transcriptional programs dysregulated in cancer. Chromatin reader domain characterization, Co-IP, ChIP-seq, CDK9 kinase assay, SMAD2 recruitment assay Molecular cell High 32402252
2007 KAP1 binds E2F1 in a pRb-independent manner, stimulates formation of an E2F1-HDAC1 complex, and inhibits E2F1 acetylation and transcriptional/apoptotic activity; RNAi depletion of KAP1 in pRb-deficient cells increases E2F1 acetylation, stimulates E2F1-dependent transcription, and sensitizes cells to apoptosis. Co-immunoprecipitation, RNAi knockdown, acetylation assay, transcriptional reporter assay, apoptosis assay The Journal of biological chemistry High 17704056
2013 KAP1/TRIM28 acts as an E3 SUMO ligase for Vps34: acetylated HSP70 binds the Beclin-1-Vps34 complex and recruits KAP1, which SUMOylates Vps34 at Lys840, increasing Vps34 activity and promoting autophagosome formation. HSP70 knockdown abolishes Beclin-1-Vps34 complex formation and KAP1 binding. Co-immunoprecipitation, SUMOylation assay, HSP70 knockout MEFs, autophagy (AV formation) readout Proceedings of the National Academy of Sciences of the United States of America High 23569248
2021 TRIM28 acts as an E3 SUMO ligase for NLRP3: it binds NLRP3, promotes SUMO1/2/3 modification, inhibits NLRP3 ubiquitination and proteasomal degradation, thereby stabilizing NLRP3 and facilitating inflammasome assembly and activation. Trim28 deficiency attenuates NLRP3 inflammasome activation in vitro and in vivo. Co-immunoprecipitation, SUMOylation assay, ubiquitination assay, Trim28-knockout cells and mice, inflammasome activation assay Nature communications High 34373456
2019 TRIM28 suppresses HIV-1 transcription by SUMOylating CDK9 (P-TEFb catalytic subunit) at Lys44, Lys56, and Lys68 with SUMO4, thereby inhibiting CDK9 kinase activity and/or blocking CDK9-CyclinT1 assembly, and consequently inhibiting viral transcriptional elongation to promote HIV-1 latency. Global site-specific SUMO mass spectrometry, serial SUMOylation assay, CDK9 kinase activity assay, Co-immunoprecipitation eLife High 30652970
2011 KAP1/TRIM28 binds acetylated HIV-1 integrase and induces its deacetylation through recruitment of HDAC1 into a protein complex, thereby restricting HIV-1 integration and viral infectivity. Co-immunoprecipitation with acetylated integrase, modulation of KAP1 levels in T cells and other cell types, viral infectivity assay Cell host & microbe High 21669397
2008 Phosphorylation of TIF1β/KAP1 at Ser473 (mediated by PKCδ) disrupts the TIF1β-HP1 interaction by interfering with the HP1-box (PXVXL motif), thereby relieving transcriptional repression of cell-cycle genes (cyclin A2, Cdc2, Cdc25A); non-phosphorylated TIF1β/Ser473 permits HP1β association and promoter occupancy correlated with gene repression. ChIP, phospho-specific antibodies, site-directed mutagenesis (S473A/S473E), co-immunoprecipitation, PKCδ pathway inhibition BMC molecular biology High 18590578
2016 Metabolic stress induces ROS/p38-dependent phosphorylation of KAP1 at Ser473, which limits mitochondrial hyperfusion in glucose-starved breast cancer cells by downregulating MFN2, leading to mitochondrial fragmentation and reduced oxidative phosphorylation. Phosphorylation-defective KAP1 S473A mutant fails to restrict hyperfusion. Live-cell imaging, phospho-defective mutants, MFN2 expression analysis, xenograft model Cancer research High 27364555
2021 Activated RIPK3 phosphorylates TRIM28 at Ser473, inhibiting its chromatin-binding activity, thereby derepressing NF-κB and SOX9 transcription factors, leading to elevated cytokine expression and dendritic cell maturation during necroptosis. TAP-MS identified TRIM28 as the relevant co-repressor. Tandem-affinity purification mass spectrometry (TAP-MS), biochemical phosphorylation assays, RNA-seq, chromatin binding assays Molecular cancer High 34419074
2018 TRIM28 interacts with TRIM24 to prevent SPOP-mediated ubiquitination and degradation of TRIM24; TRIM28 also facilitates TRIM24 chromatin occupancy and augments androgen receptor (AR) signaling in prostate cancer cells. Co-immunoprecipitation, ubiquitination assay, chromatin occupancy assay (ChIP), xenograft tumor growth Nature communications High 30479348
2016 TRIM28 stabilizes alpha-synuclein and tau, promoting their nuclear accumulation and toxicity; reduction of TRIM28 rescues neurodegeneration in Drosophila and C. elegans models of tau- and alpha-synuclein-mediated toxicity. A screen identified TRIM28 as a shared post-translational regulator of both proteins. Genetic screen, TRIM28 loss-of-function in Drosophila and C. elegans models, protein level analysis, nuclear fractionation eLife Medium 27779468
2013 In embryonic stem cells, KAP1/TRIM28 represses endogenous retroviruses (ERVs) through SETDB1/ESET-mediated H3K9 trimethylation, and is required for de novo DNA methylation of introduced ERV sequences in a mechanism requiring a sequence-recognizing KRAB-ZFP. KAP1 knockout in early embryos affects ERV methylation genome-wide. KAP1 and KRAB-ZFP knockout/knockdown in ES cells, de novo methylation assay, ChIP, in vivo embryo analysis Development (Cambridge, England) High 23293284
2013 A KRAB-ZFP/KAP1-miRNA cascade controls erythropoiesis: hematopoietic-specific KAP1 deletion in mice causes hypoproliferative anemia by preventing induction of mitophagy-associated genes due to persistent expression of microRNAs targeting mitophagy transcripts; stage-specific KRAB-ZFPs normally repress these miRNAs through KAP1. Hematopoietic-restricted Kap1 conditional knockout mice, RNA-seq, miRNA profiling, mitophagy assay Science (New York, N.Y.) High 23493425
2018 KAP1/TRIM28 associates with DNA replication factors PCNA, MCM3, and MCM6; these interactions are promoted by KAP1 phosphorylation at Ser473 during S phase. KAP1 forms a complex with PCNA and the histone methyltransferase Suv39h1 to reinstate H3K9me3-marked heterochromatin after DNA replication. Co-immunoprecipitation, cell fractionation, proximity ligation assay, S-phase phosphorylation analysis Nucleic acids research High 29955894
2015 The nuclear oncogene SET interacts with KAP1 and its overexpression results in sustained retention of KAP1 and HP1 on chromatin near double-strand breaks, impairing HR-mediated DNA repair by inhibiting DNA end resection. Co-immunoprecipitation, ChIP, SET overexpression/depletion, HR repair assay, radiomimetic drug sensitivity Cell reports Medium 25818296
2007 KAP1 interacts with STAT3 in vivo; siRNA-mediated reduction of KAP1 enhances IL-6-induced STAT3-dependent transcription and leads to marked nuclear accumulation of STAT3 phosphorylated at Ser727, establishing KAP1 as a negative regulator of the IL-6/STAT3 signaling pathway. Yeast two-hybrid screening, endogenous Co-immunoprecipitation, siRNA knockdown, transcriptional reporter assay, phospho-STAT3 analysis Oncogene Medium 18037959
2012 In T cells, TRIM28 is phosphorylated upon TCR stimulation and is required for global regulation of CD4+ T cells; conditional T cell-specific deletion of TRIM28 causes lymphopenia, defective IL-2 production, incomplete cell-cycle progression, and derepression of TGF-β3 leading to accumulation of autoreactive TH17 and Foxp3+ T cells with impaired suppressor function. Conditional T cell-specific TRIM28 knockout mouse, TCR stimulation assays, cytokine profiling, flow cytometry Nature immunology High 22544392
2013 KAP1 represses differentiation-inducible genes in ES cells through cooperative binding with PRC1 (polycomb repressive complex 1) mediated by the KAP1 coiled-coil region; conversely, KAP1 binds transcribed and flanking sequences of pluripotency genes without enhancing PRC1 binding and derepresses their transcription. The coiled-coil-mediated PRC1 interaction is specifically required for repression of differentiation genes. Conditional KAP1 knockout in ES cells, Co-immunoprecipitation, ChIP, domain-deletion mutants, RNA-seq Molecular and cellular biology High 24687849
2021 HP1β is phosphorylated at Ser89 by CK2 during stem cell differentiation, creating a binding site for KAP1; this phosphorylation-dependent sequestration of KAP1 in heterochromatin compartments downregulates pluripotency factors and triggers pluripotency exit. Ubiquitination-deficient KAP1 knockout cells show enhanced differentiation, suggesting KAP1 regulates pluripotency via its ubiquitination activity. HP1β-/- ES cells, CK2 kinase assay, Co-immunoprecipitation, proximity ligation, KAP1-/- cells with ubiquitination-deficient mutants Nucleic acids research High 34214177
2016 KAP1 interacts with c-Raf and maintains c-Raf phosphorylation at Ser259 (inhibitory site); KAP1 knockout decreases pSer259-Raf and increases pSer338-Raf, thereby activating the MEK-ERK pathway. This places KAP1 as a negative regulator of the Raf-MEK-ERK axis in lung cancer cells. Functional proteomics screening (Co-IP), KAP1 knockout, phospho-Raf/MEK/ERK analysis, xenograft model Molecular carcinogenesis Medium 29917268
2020 TRIM28 promotes sequential ubiquitination of p53 by acting upstream of RLIM and MDM2 ubiquitin ligases; TRIM28 overexpression in lung cancer cells increases p53 degradation, proliferation, migration, and invasion. Ubiquitination assay, TRIM28 overexpression/knockdown, xenograft models Cell death and differentiation Medium 33328571
2018 TRIM28 acts as an E3 ubiquitin ligase for BCL2A1 at the mitochondria: endogenous TRIM28 and BCL2A1 interact at the mitochondria, and TRIM28 knockdown decreases BCL2A1 ubiquitination. TRIM17 stabilizes BCL2A1 by blocking TRIM28 from binding and ubiquitinating BCL2A1. GSK3 phosphorylation of BCL2A1 also inhibits its degradation. Co-immunoprecipitation of endogenous proteins at mitochondria, ubiquitination assay, TRIM28 knockdown, TRIM17 competition assay Cell death and differentiation High 30042493
2023 TRIM28 directly binds and stabilizes PD-L1 by inhibiting its ubiquitination and promoting its SUMOylation; additionally, TRIM28 promotes K63 polyubiquitination of TBK1, activating TBK1-IRF1 and TBK1-mTOR pathways to enhance PD-L1 transcription in gastric cancer cells. CRISPR-Cas9 genome-wide screen, Co-immunoprecipitation, ubiquitination and SUMOylation assays, TBK1 K63 ubiquitination assay Signal transduction and targeted therapy High 37357254
2023 TRIM28 promotes K63-linked ubiquitination of RIPK1 through its E3 ligase activity, sustaining NF-κB pathway activation and upregulation of CXCL1, which recruits CXCR2-expressing MDSCs to the tumor microenvironment; E3 ligase domain mutagenesis abolished NF-κB activation. Co-immunoprecipitation, K63 ubiquitination assay, E3 ligase domain mutagenesis, syngeneic tumor models, flow cytometry Journal of experimental & clinical cancer research : CR High 37865804
2023 TRIM28 functions as a negative regulator of the RLR innate immune pathway by targeting MAVS for K48-linked polyubiquitination and proteasomal degradation; the RING domain cysteine residues C65 and C68 are critical for this activity, and TRIM28 ubiquitinates MAVS at K7, K10, K371, K420, and K500. Co-immunoprecipitation, K48 ubiquitination assay, RING domain mutagenesis, TRIM28 overexpression/knockdown, IFN production assay The Journal of biological chemistry High 37119745
2024 TRIM28 catalyzes SUMOylation of the SARS-CoV-2 nucleocapsid protein (SARS2-NP) at Lys65, which promotes NP homo-oligomerization, RNA association, and liquid-liquid phase separation (LLPS), thereby suppressing innate antiviral immunity. An interfering peptide blocking the TRIM28-NP interaction abolishes NP SUMOylation and reduces viral replication. SUMOylation assay with site mutagenesis, LLPS assay, Co-immunoprecipitation, interfering peptide, viral replication assay Nature communications High 38172120
2022 TRIM28-dependent SUMOylation of ovarian-specific transcription factors is required to prevent female-to-male sex reversal of the mouse ovary; TRIM28 is recruited to chromatin near FOXL2 binding sites and its E3-SUMO ligase activity maintains the sex-specific SUMOylation profile necessary to repress testicular genes. Conditional Trim28 knockout mouse ovary, ChIP, SUMOylation profiling, transcriptomics, lineage tracing Nature communications High 35906245
2017 Nearly 10,000 primate-specific ERVs act as docking platforms for TRIM28 in human neural progenitor cells; TRIM28 binding establishes local H3K9me3 heterochromatin at ERVs and consequently represses neighboring protein-coding genes important for brain development. ChIP-seq (TRIM28, H3K9me3) in human neural progenitor cells, RNA-seq, correlation of TRIM28 binding with gene expression Cell reports High 28052240
2013 The lncRNA Paupar directly binds KAP1 and promotes KAP1 chromatin occupancy and H3K9me3 deposition at distal target genes through a ribonucleoprotein complex containing Paupar, KAP1, and PAX6 transcription factor; both Paupar and Kap1 loss-of-function disrupt olfactory bulb neurogenesis in vivo. RNA-protein pulldown, Co-immunoprecipitation, ChIP-seq (KAP1, H3K9me3), Paupar/Kap1 in vivo knockdown, neurogenesis assay The EMBO journal High 29661885
2013 FOXP3-interacting KRAB domain protein (FIK) bridges FOXP3 to KAP1/TRIM28 in a chromatin-remodeling complex in human regulatory T cells; disruption of the FOXP3-FIK-KAP1 complex restores expression of FOXP3 target genes and abrogates Treg suppressor activity. Co-immunoprecipitation, yeast two-hybrid, siRNA disruption, Treg suppression functional assay Journal of immunology (Baltimore, Md. : 1950) Medium 23543754
2017 TRIM28 interacts with EZH2 in a complex distinct from PRC2, together with SWI/SNF subunits; this TRIM28-EZH2 complex activates (rather than represses) a gene set associated with stem cell maintenance and mammosphere formation in breast cancer. TRIM28 depletion represses EZH2 chromatin recruitment and mammosphere formation, and EZH2 rescue requires the pre-SET domain TRIM28-interaction region. Co-immunoprecipitation, mass spectrometry of EZH2 interactome, RNA-seq, ChIP, mammosphere formation assay, domain-specific rescue Oncogene High 28068325
2016 URI recruits PP2A phosphatase to interact with KAP1, and this URI-KAP1-PP2A complex decreases KAP1 phosphorylation. URI also contributes to retrotransposon (LINE-1, L1PA2) repression in a manner similar to the KAP1-SETDB1 complex. Co-immunoprecipitation, mass spectrometry, microarray analysis of transposons, URI/KAP1 knockdown The Journal of biological chemistry Medium 27780869
2019 ZFP30, a KRAB-ZFP, recruits KAP1 to a retrotransposon-derived Pparg2 enhancer to activate (not repress) adipogenesis; mechanistic studies show KAP1 acts as a co-activator of ZFP30 in this adipogenic context, demonstrating a non-repressive function for the KZFP-KAP1 axis. ChIP-seq, murine and human adipogenesis models, Co-immunoprecipitation, in vivo adipogenesis assay Nature communications High 31000713
2021 In myeloid/microglial cells, KAP1 represses HIV-1 gene expression by interacting with and promoting proteasomal degradation of the viral transactivator Tat; KAP1 also binds and cooperates with the epigenetic silencer CTIP2 at the latent HIV-1 promoter, and Tat and CTIP2 compete for KAP1 binding. Co-immunoprecipitation, proteasome inhibition assay, ChIP, KAP1 depletion in myeloid HIV-1 latency models Scientific reports Medium 33514850
2023 TRIM28 promotes ubiquitination and proteasome-mediated degradation of TFE3 in renal cells, restraining TFE3-driven autophagic gene expression; TFE3 interacts with and recruits KDM6A (H3K27 demethylase) to increase H3K4me3 (not H3K27 demethylation) at autophagic gene promoters. Co-immunoprecipitation, ubiquitination assay, ChIP, TFE3/TRIM28 knockdown, cancer cell proliferation assay The Journal of biological chemistry Medium 36935008
2025 TRIM28 binds ACSL4 and promotes SUMO3 modification at Lys532, inhibiting K63-linked ubiquitination and thereby suppressing OPTN-dependent autophagic degradation of ACSL4, which drives neuronal ferroptosis after spinal cord injury. SENP3 acts as the deSUMOylation enzyme competing with TRIM28. Co-immunoprecipitation, site-specific SUMOylation assay (K532 mutagenesis), ubiquitination assay, autophagic degradation assay, Trim28 conditional KO mouse, SENP3 competition assay Cell death and differentiation High 39875520
2023 TIAM1 interacts with TRIM28 in the nucleus of non-small cell lung cancer cells; the TIAM1-TRIM28 complex promotes H3K9me3-mediated silencing of protocadherins and decreases E-cadherin expression, driving epithelial-to-mesenchymal transition and cell migration/invasion. Co-immunoprecipitation, ChIP (H3K9me3), siRNA depletion, invasion and migration assays, clinical specimen correlation Proceedings of the National Academy of Sciences of the United States of America Medium 37748077
2023 TRIM28 modulates uterine function by complexing with estrogen receptor α (ERα) and progesterone receptor (PR); TRIM28 impairment suppresses PR and ERα chromatin binding and impairs early pregnancy support in the uterus. RIME (rapid immunoprecipitation mass spectrometry), co-immunoprecipitation, ChIP, conditional Trim28 KO in PR-expressing uterine cells Nature communications High 37528140
2011 MAGE-A3 binds KAP1 and differentially regulates KRAB zinc finger proteins (KZNFs): MAGE-A3 relieves KAP1-mediated repression and induces polyubiquitination and degradation of KZNFs with A+B box KRAB domains, whereas it enhances KAP1-mediated repression for A or A+b box KZNFs. MAGE-A3 expression decreases KAP1 and H3K9me3 binding at the ID1 gene (a ZNF382 target), de-repressing ID1 expression. Co-immunoprecipitation, ChIP (KAP1, H3K9me3), reporter gene assay, ubiquitination assay, siRNA knockdown PloS one Medium 21876767
2015 CCAR2/DBC1 is required for Chk2-dependent phosphorylation of KAP1; loss of CCAR2 impairs Chk2 activation, reduces KAP1 phosphorylation needed for heterochromatin relaxation, and consequently impairs repair of heterochromatic (but not euchromatic) DNA lesions. CCAR2 knockout cells, Chk2 kinase assay, γH2AX foci resolution assay, HP1β depletion epistasis Oncotarget Medium 26158765
2006 KAP1 functions as a transcriptional co-repressor for PAX3 by augmenting PAX3 repressional activity; HP1γ competes with KAP1 for binding to the N-terminal paired domain of PAX3, and the C-terminal domain of PAX3 governs its subcellular localization. Co-immunoprecipitation, competition binding assay, transcriptional reporter assay, subcellular localization analysis Biochemical and biophysical research communications Medium 16945326

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 In embryonic stem cells, ZFP57/KAP1 recognize a methylated hexanucleotide to affect chromatin and DNA methylation of imprinting control regions. Molecular cell 464 22055183
2011 KAP1 protein: an enigmatic master regulator of the genome. The Journal of biological chemistry 295 21652716
2010 KRAB-zinc finger proteins and KAP1 can mediate long-range transcriptional repression through heterochromatin spreading. PLoS genetics 295 20221260
2005 MDM2 interaction with nuclear corepressor KAP1 contributes to p53 inactivation. The EMBO journal 210 16107876
2017 The complexity of TRIM28 contribution to cancer. Journal of biomedical science 188 28851455
2013 Acetylated hsp70 and KAP1-mediated Vps34 SUMOylation is required for autophagosome creation in autophagy. Proceedings of the National Academy of Sciences of the United States of America 171 23569248
2014 Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements. Genome research 168 24879559
2007 Genome-wide analysis of KAP1 binding suggests autoregulation of KRAB-ZNFs. PLoS genetics 155 17542650
2007 Role for KAP1 serine 824 phosphorylation and sumoylation/desumoylation switch in regulating KAP1-mediated transcriptional repression. The Journal of biological chemistry 148 17942393
2013 Distinct roles of KAP1, HP1 and G9a/GLP in silencing of the two-cell-specific retrotransposon MERVL in mouse ES cells. Epigenetics & chromatin 146 23735015
2013 De novo DNA methylation of endogenous retroviruses is shaped by KRAB-ZFPs/KAP1 and ESET. Development (Cambridge, England) 143 23293284
2021 TRIM28 SUMOylates and stabilizes NLRP3 to facilitate inflammasome activation. Nature communications 129 34373456
2014 TRIM28 regulates RNA polymerase II promoter-proximal pausing and pause release. Nature structural & molecular biology 122 25173174
2011 The ATM substrate KAP1 controls DNA repair in heterochromatin: regulation by HP1 proteins and serine 473/824 phosphorylation. Molecular cancer research : MCR 119 22205726
2008 Structural insights into human KAP1 PHD finger-bromodomain and its role in gene silencing. Nature structural & molecular biology 111 18488044
2021 RIPK3 activation induces TRIM28 derepression in cancer cells and enhances the anti-tumor microenvironment. Molecular cancer 105 34419074
2011 The TRIM family protein KAP1 inhibits HIV-1 integration. Cell host & microbe 102 21669397
2018 TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression. Nature communications 99 30479348
2016 TRIM28 regulates the nuclear accumulation and toxicity of both alpha-synuclein and tau. eLife 96 27779468
2012 TRIM28 prevents autoinflammatory T cell development in vivo. Nature immunology 94 22544392
2011 Functional analysis of KAP1 genomic recruitment. Molecular and cellular biology 94 21343339
2019 TRIM28 promotes HIV-1 latency by SUMOylating CDK9 and inhibiting P-TEFb. eLife 92 30652970
2014 KAP1 promotes proliferation and metastatic progression of breast cancer cells. Cancer research 92 25421577
2013 A KRAB/KAP1-miRNA cascade regulates erythropoiesis through stage-specific control of mitophagy. Science (New York, N.Y.) 91 23493425
2018 KAP1 regulates endogenous retroviruses in adult human cells and contributes to innate immune control. EMBO reports 87 30061100
2017 TRIM28 Controls a Gene Regulatory Network Based on Endogenous Retroviruses in Human Neural Progenitor Cells. Cell reports 84 28052240
2014 KAPtain in charge of multiple missions: Emerging roles of KAP1. World journal of biological chemistry 83 25225599
2015 The nuclear oncogene SET controls DNA repair by KAP1 and HP1 retention to chromatin. Cell reports 79 25818296
2007 Regulation of E2F1 function by the nuclear corepressor KAP1. The Journal of biological chemistry 78 17704056
2023 TRIM28 promotes the escape of gastric cancer cells from immune surveillance by increasing PD-L1 abundance. Signal transduction and targeted therapy 74 37357254
2017 TRIM28 interacts with EZH2 and SWI/SNF to activate genes that promote mammosphere formation. Oncogene 66 28068325
2019 Structure of KAP1 tripartite motif identifies molecular interfaces required for retroelement silencing. Proceedings of the National Academy of Sciences of the United States of America 65 31289231
2007 Physical and functional interactions between STAT3 and KAP1. Oncogene 65 18037959
2021 The SETDB1-TRIM28 Complex Suppresses Antitumor Immunity. Cancer immunology research 61 34848497
2016 Metabolic Stress-Induced Phosphorylation of KAP1 Ser473 Blocks Mitochondrial Fusion in Breast Cancer Cells. Cancer research 60 27364555
2020 Sequential ubiquitination of p53 by TRIM28, RLIM, and MDM2 in lung tumorigenesis. Cell death and differentiation 54 33328571
2008 Phosphorylation at Ser473 regulates heterochromatin protein 1 binding and corepressor function of TIF1beta/KAP1. BMC molecular biology 53 18590578
2022 KAP1/TRIM28: Transcriptional Activator and/or Repressor of Viral and Cellular Programs? Frontiers in cellular and infection microbiology 52 35281453
2017 TRIM28 multi-domain protein regulates cancer stem cell population in breast tumor development. Oncotarget 51 27845900
2014 Inhibition of KAP1 enhances hypoxia-induced Kaposi's sarcoma-associated herpesvirus reactivation through RBP-Jκ. Journal of virology 51 24696491
2023 N6-methyladenosine hypomethylation of circGPATCH2L regulates DNA damage and apoptosis through TRIM28 in intervertebral disc degeneration. Cell death and differentiation 50 37438603
2018 TRIM17 and TRIM28 antagonistically regulate the ubiquitination and anti-apoptotic activity of BCL2A1. Cell death and differentiation 49 30042493
2014 High levels of KAP1 expression are associated with aggressive clinical features in ovarian cancer. International journal of molecular sciences 48 25548895
2018 The long non-coding RNA Paupar promotes KAP1-dependent chromatin changes and regulates olfactory bulb neurogenesis. The EMBO journal 47 29661885
2015 LMP1-Induced Sumoylation Influences the Maintenance of Epstein-Barr Virus Latency through KAP1. Journal of virology 47 25948750
2020 KAP1 Is a Chromatin Reader that Couples Steps of RNA Polymerase II Transcription to Sustain Oncogenic Programs. Molecular cell 43 32402252
2016 KAP1 is overexpressed in hepatocellular carcinoma and its clinical significance. International journal of clinical oncology 43 27095111
2014 KAP1 represses differentiation-inducible genes in embryonic stem cells through cooperative binding with PRC1 and derepresses pluripotency-associated genes. Molecular and cellular biology 43 24687849
2019 Hdac3, Setdb1, and Kap1 mark H3K9me3/H3K14ac bivalent regions in young and aged liver. Aging cell 41 31858687
2013 Zfp819, a novel KRAB-zinc finger protein, interacts with KAP1 and functions in genomic integrity maintenance of mouse embryonic stem cells. Stem cell research 41 23954693
2018 Germline mutations and somatic inactivation of TRIM28 in Wilms tumour. PLoS genetics 40 29912901
2024 TRIM28-mediated nucleocapsid protein SUMOylation enhances SARS-CoV-2 virulence. Nature communications 38 38172120
2011 MAGE I transcription factors regulate KAP1 and KRAB domain zinc finger transcription factor mediated gene repression. PloS one 38 21876767
2019 TRIM28 activates autophagy and promotes cell proliferation in glioblastoma. OncoTargets and therapy 37 30655676
2022 Structure and functional mapping of the KRAB-KAP1 repressor complex. The EMBO journal 36 36341546
2018 KAP1 facilitates reinstatement of heterochromatin after DNA replication. Nucleic acids research 36 29955894
2002 Polymorphisms in the human high sulfur hair keratin-associated protein 1, KAP1, gene family. The Journal of biological chemistry 36 12228244
2023 E3 ligase TRIM28 promotes anti-PD-1 resistance in non-small cell lung cancer by enhancing the recruitment of myeloid-derived suppressor cells. Journal of experimental & clinical cancer research : CR 35 37865804
2018 A unique subset of low-risk Wilms tumors is characterized by loss of function of TRIM28 (KAP1), a gene critical in early renal development: A Children's Oncology Group study. PloS one 35 30543698
2022 TRIM28-dependent SUMOylation protects the adult ovary from activation of the testicular pathway. Nature communications 33 35906245
2013 Cutting Edge: a novel, human-specific interacting protein couples FOXP3 to a chromatin-remodeling complex that contains KAP1/TRIM28. Journal of immunology (Baltimore, Md. : 1950) 31 23543754
2001 Disruption of the Crithidia fasciculata KAP1 gene results in structural rearrangement of the kinetoplast disc. Molecular and biochemical parasitology 31 11606228
2018 Individual retrotransposon integrants are differentially controlled by KZFP/KAP1-dependent histone methylation, DNA methylation and TET-mediated hydroxymethylation in naïve embryonic stem cells. Epigenetics & chromatin 30 29482634
2013 Relationship between epithelial and stromal TRIM28 expression predicts survival in colorectal cancer patients. Journal of gastroenterology and hepatology 30 23425061
2021 Inhibition of HIV-1 gene transcription by KAP1 in myeloid lineage. Scientific reports 29 33514850
2017 TRIM28 epigenetic corepressor is indispensable for stable induced pluripotent stem cell formation. Stem cell research 27 28759843
2022 IFI16 Partners with KAP1 to Maintain Epstein-Barr Virus Latency. Journal of virology 26 35969079
2021 TRIM28 Selective Nanobody Reduces Glioblastoma Stem Cell Invasion. Molecules (Basel, Switzerland) 26 34500575
2016 URI Regulates KAP1 Phosphorylation and Transcriptional Repression via PP2A Phosphatase in Prostate Cancer Cells. The Journal of biological chemistry 26 27780869
2025 Redox regulation of TRIM28 facilitates neuronal ferroptosis by promoting SUMOylation and inhibiting OPTN-selective autophagic degradation of ACSL4. Cell death and differentiation 25 39875520
2019 ZFP30 promotes adipogenesis through the KAP1-mediated activation of a retrotransposon-derived Pparg2 enhancer. Nature communications 24 31000713
2018 TRIM28 promotes cervical cancer growth through the mTOR signaling pathway. Oncology reports 24 29393469
2023 TRIM28 represses renal cell carcinoma cell proliferation by inhibiting TFE3/KDM6A-regulated autophagy. The Journal of biological chemistry 23 36935008
2021 TRIM28 Expression on Dendritic Cells Prevents Excessive T Cell Priming by Silencing Endogenous Retrovirus. Journal of immunology (Baltimore, Md. : 1950) 23 33619215
2015 CCAR2/DBC1 is required for Chk2-dependent KAP1 phosphorylation and repair of DNA damage. Oncotarget 23 26158765
2007 Polymorphism of the KAP1.1, KAP1.3 and K33 genes in Merino sheep. Molecular and cellular probes 23 17532184
2022 LncRNA PVT-1 promotes osteosarcoma cancer stem-like properties through direct interaction with TRIM28 and TSC2 ubiquitination. Oncogene 22 36348010
2021 Deletion of Trim28 in committed adipocytes promotes obesity but preserves glucose tolerance. Nature communications 22 33397965
2021 TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2. Cellular signalling 21 34146659
2021 TRIM28 variants and Wilms' tumour predisposition. The Journal of pathology 20 33565090
2020 MAGEA3 promotes proliferation and suppresses apoptosis in cervical cancer cells by inhibiting the KAP1/p53 signaling pathway. American journal of translational research 20 32774721
2011 Identification of the ovine keratin-associated protein KAP1-2 gene (KRTAP1-2). Experimental dermatology 20 21771088
2024 TRIM28 in cancer and cancer therapy. Frontiers in genetics 19 39100077
2015 Expression of KAP1 in epithelial ovarian cancer and its correlation with drug-resistance. International journal of clinical and experimental medicine 19 26770323
2014 MAGE proteins regulate KRAB zinc finger transcription factors and KAP1 E3 ligase activity. Archives of biochemistry and biophysics 18 25107531
2023 TRIM28 negatively regulates the RLR signaling pathway by targeting MAVS for degradation via K48-linked polyubiquitination. The Journal of biological chemistry 17 37119745
2023 TRIM28 modulates nuclear receptor signaling to regulate uterine function. Nature communications 17 37528140
2020 Infertility-Causing Haploinsufficiency Reveals TRIM28/KAP1 Requirement in Spermatogonia. Stem cell reports 17 32302554
2014 TRIM28/KAP1 regulates senescence. Immunology letters 17 25160591
2006 Transcriptional repression activity of PAX3 is modulated by competition between corepressor KAP1 and heterochromatin protein 1. Biochemical and biophysical research communications 17 16945326
2023 A TIAM1-TRIM28 complex mediates epigenetic silencing of protocadherins to promote migration of lung cancer cells. Proceedings of the National Academy of Sciences of the United States of America 16 37748077
2021 Phosphorylation of the HP1β hinge region sequesters KAP1 in heterochromatin and promotes the exit from naïve pluripotency. Nucleic acids research 16 34214177
2020 TRIM28 Regulates Dlk1 Expression in Adipogenesis. International journal of molecular sciences 16 33008113
2018 Characterization of interaction between Trim28 and YY1 in silencing proviral DNA of Moloney murine leukemia virus. Virology 16 29407374
2023 The Host E3-Ubiquitin Ligase TRIM28 Impedes Viral Protein GP4 Ubiquitination and Promotes PRRSV Replication. International journal of molecular sciences 15 37446143
2018 KAP1 inhibits the Raf-MEK-ERK pathway to promote tumorigenesis in A549 lung cancer cells. Molecular carcinogenesis 15 29917268
2021 Acute myeloid leukemia cell-derived extracellular vesicles carrying microRNA-548ac regulate hematopoietic function via the TRIM28/STAT3 pathway. Cancer gene therapy 14 34453123
2020 KAP1-associated transcriptional inhibitory complex regulates C2C12 myoblasts differentiation and mitochondrial biogenesis via miR-133a repression. Cell death & disease 14 32908124
2018 TRIM28 is overexpressed in glioma and associated with tumor progression. OncoTargets and therapy 14 30349292
2023 Co-option of endogenous retroviruses through genetic escape from TRIM28 repression. Cell reports 13 37294634