Affinage

ING5

Inhibitor of growth protein 5 · UniProt Q8WYH8

Length
240 aa
Mass
27.8 kDa
Annotated
2026-06-10
55 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ING5 is a chromatin-associated reader/adaptor that targets histone acetyltransferase complexes to genes regulating proliferation, self-renewal, and differentiation, and functions broadly as a tumor suppressor (PMID:38446206, PMID:39787145). It is the targeting subunit of HBO1, MOZ/MORF, and KAT6A/KAT6B/KAT7 acetyltransferase complexes, engaging chromatin through a C-terminal PHD domain that binds the H3K4me3 mark and thereby directing H3K14 and H3K23 acetylation in vivo (PMID:28925404, PMID:38446206). Loss of ING4/ING5 abolishes global H3K14ac and reduces H3K23ac, causing embryonic arrest, while Ing5 nulls show isolated developmental defects and a 6-fold elevated lymphoma incidence with accumulation of γH2AX-positive cells, linking ING5 to genomic integrity (PMID:38446206, PMID:39787145). Structurally, ING5 forms homodimers and ING4 heterodimers via an N-terminal coiled-coil, with a disordered central region that binds dsDNA and a PHD domain that reads H3K4me3 in the dimeric state; cancer-associated N-terminal mutations destabilize the coiled-coil and perturb cell cycle progression (PMID:31026448). Beyond its HAT-targeting role, ING5 functions as a cofactor that enhances p300 autoacetylation to activate its HAT activity and promotes Tip60-mediated acetylation of p53 at K120, driving p53-dependent transcription of p21, BAX, and GADD45 and consequent apoptosis and cell cycle arrest (PMID:12750254, PMID:23576563, PMID:29416718). ING5 restrains oncogenic signaling—suppressing EGFR/PI3K/Akt and IL-6/STAT3-driven EMT and metastasis—and reprograms metabolism away from aerobic glycolysis through a TIE1→PDK1-Y163→PDHA1 axis (PMID:39269568, PMID:28903339). Its antiproliferative output requires the partner INCA1 (PMID:21750715), it is phosphorylated at T152 by cyclin/CDK2 within a bipartite nuclear localization sequence (PMID:25860957), and its own transcription is activated by an SRF–YY1–p53 complex at the ING5 promoter (PMID:35747809).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2003 High

    Established ING5 as a p53 co-activator, answering whether ING5 functions in the p53 tumor-suppressor axis by linking it to histone acetyltransferase activity.

    Evidence Reciprocal Co-IP, luciferase reporter, cell cycle and apoptosis assays in human cells

    PMID:12750254

    Open questions at the time
    • Did not define which HAT complexes ING5 targets to chromatin
    • Mechanism of p300 activation by ING5 not resolved
  2. 2010 Low

    Implicated specific ING5 structural domains in tumor suppression by finding cancer-restricted missense mutations and reduced mRNA, framing ING5 as a candidate tumor suppressor.

    Evidence RT-PCR, sequencing and qRT-PCR of matched oral squamous cell carcinoma tumor/normal pairs

    PMID:20131318

    Open questions at the time
    • Mutations not functionally reconstituted
    • No biochemical validation of mutant effects on HAT targeting
  3. 2011 High

    Identified INCA1 as the partner required for ING5's growth-suppressive output, showing the antiproliferative function is not cell-autonomous to ING5 alone.

    Evidence Yeast two-hybrid plus genetic epistasis in Inca1-/- MEFs and bone marrow with phenotypic readouts

    PMID:21750715

    Open questions at the time
    • Molecular mechanism by which INCA1 enables ING5 function unknown
    • No structural basis for the interaction
  4. 2013 High

    Defined a DNA-damage-specific role by showing ING5 is a Tip60 cofactor for p53-K120 acetylation, distinguishing it from the earlier p300/K382 pathway and routing p53 toward apoptotic targets.

    Evidence Co-IP, ChIP, K120R mutagenesis and siRNA in human cells

    PMID:23576563

    Open questions at the time
    • How DNA damage triggers trimeric complex assembly not established
    • Site selectivity vs hMOF mechanistically unexplained
  5. 2015 High

    Connected ING5 to cell-cycle control by showing CDK2 phosphorylates T152 within its NLS, while also demonstrating p53-independent proliferation effects.

    Evidence In vitro kinase assay, phospho-specific antibody, mutagenesis and siRNA cell-cycle analysis

    PMID:25860957

    Open questions at the time
    • T152 phosphorylation alone does not alter localization—functional consequence unclear
    • Identity of the p53-independent effector pathway unknown
  6. 2017 Medium

    Established ING5 as the targeting subunit of HBO1/MOZ/MORF HAT complexes and its PHD-H3K4me3 reading as required for glioblastoma stem cell self-renewal, defining the chromatin-recruitment mechanism.

    Evidence PHD-domain mutant analysis, sphere formation assays and western blot in BTICs

    PMID:28925404

    Open questions at the time
    • Pathway activation measured by western blot without complex reconstitution
    • Direct chromatin targets in stem cells not mapped
  7. 2017 High

    Showed ING5 promotes p300 autoacetylation at specific HAT-domain lysines to stimulate its enzymatic activity, providing a biochemical basis for ING5-driven p53/histone acetylation.

    Evidence SILAC acetylome mass spectrometry with site mapping and C646 inhibitor rescue

    PMID:29416718

    Open questions at the time
    • Whether ING5 directly contacts the p300 HAT domain not shown
    • Stoichiometry of activation unresolved
  8. 2017 Medium

    Demonstrated ING5 loss activates EGFR/PI3K/Akt and IL-6/STAT3 signaling to drive EMT and metastasis, establishing ING5 as a restraint on oncogenic signaling.

    Evidence Phospho-kinase array, shRNA, pharmacological rescue and xenograft metastasis model

    PMID:28903339

    Open questions at the time
    • Pathway activation inferred from phosphorylation changes only
    • Link between chromatin function and signaling suppression unclear
  9. 2019 High

    Resolved ING5 quaternary structure, showing N-terminal coiled-coil-mediated homo/heterodimerization, central dsDNA binding, and PHD reading of H3K4me3, and linking cancer mutations to coiled-coil destabilization.

    Evidence NMR, X-ray crystallography, SEC, DNA-binding assays and mutagenesis with cell cycle analysis

    PMID:31026448

    Open questions at the time
    • Functional role of ING4 heterodimerization vs homodimerization undefined
    • How dimerization couples to HAT complex assembly unknown
  10. 2022 Medium

    Placed ING5 genetically as a co-regulator of self-renewal with Set1A/COMPASS, identifying it as a dependency of catalytically dead COMPASS in ESCs.

    Evidence Genome-wide CRISPR dropout screen in Set1A-ΔSET knock-in ESCs with gene expression

    PMID:35500115

    Open questions at the time
    • No biochemical link between ING5 and COMPASS shown
    • Mechanism of synthetic lethality unresolved
  11. 2022 High

    Identified the upstream transcriptional control of ING5 itself, showing SRF and YY1 directly activate its promoter as an SRF-YY1-ING5-p53 complex.

    Evidence EMSA, ChIP, luciferase reporter and Co-IP in gastric cancer cells

    PMID:35747809

    Open questions at the time
    • Upstream signals controlling SRF/YY1 occupancy not defined
    • Functional role of p53 within the promoter complex unclear
  12. 2023 High

    Used the Drosophila ortholog to show TCTP gates Ing5 nuclear translocation and MOZ/MORF chromatin binding, identifying a regulatory switch on H3K23 acetylation and EGFR/Yorkie signaling.

    Evidence Yeast two-hybrid, in vivo genetics, H3K23ac ChIP and epistasis in Drosophila

    PMID:37014852

    Open questions at the time
    • Conservation of TCTP regulation in mammals not tested
    • Mechanism of TCTP-mediated nuclear exclusion unknown
  13. 2023 Medium

    Defined an ING5→miR-34c-5p→Snail1 axis suppressing TGF-β/Smad3-driven EMT, providing a transcriptional/post-transcriptional route for metastasis suppression.

    Evidence Overexpression, dual-luciferase 3'UTR validation, TGF-β inhibitor and xenograft model

    PMID:37249332

    Open questions at the time
    • ING5→miR-34c-5p linkage shown by overexpression only
    • Direct chromatin mechanism for miR-34c-5p induction not shown
  14. 2023 Medium

    Showed ING5 supports fetal liver hematopoiesis cell-extrinsically, refining its tissue-level role apart from intrinsic stem-cell function.

    Evidence Ing5-null mice, flow cytometry and competitive bone-marrow transplantation

    PMID:37275850

    Open questions at the time
    • Cell-extrinsic mediator not identified
    • Niche cell type responsible undefined
  15. 2024 High

    Established ING4/ING5 as essential, non-redundant components of KAT6A/KAT6B/KAT7 complexes required for H3K14ac and H3K23ac in vivo, tying epigenetic marks to specific developmental phenotypes.

    Evidence Knockout mouse genetics, histone-mark western blot, transcriptomics and developmental phenotyping

    PMID:38446206

    Open questions at the time
    • Gene-specific targeting rules of ING5 within these complexes unclear
    • Basis of tissue-specific phenotypes (heart) not fully resolved
  16. 2024 High

    Identified a metabolic tumor-suppressive mechanism: ING5 induces TIE1 to phosphorylate PDK1-Y163, activating PDHA1 and shifting cells from glycolysis to oxidative phosphorylation to suppress invasion.

    Evidence SILAC phosphoproteomics, PDK1-Y163F mutagenesis, metabolic assays and xenografts

    PMID:39269568

    Open questions at the time
    • How ING5 chromatin function induces TIE1 not shown
    • Generality beyond lung cancer untested
  17. 2025 High

    Provided in vivo proof of ING5 tumor suppression and genome maintenance, showing knockout mice develop lymphoma and KO MEFs accumulate in G2 with elevated DNA damage.

    Evidence CRISPR knockout mice, tumor pathology and flow cytometry for cell cycle/γH2AX

    PMID:39787145

    Open questions at the time
    • Molecular cause of γH2AX accumulation not defined
    • Link between HAT-complex function and genome stability unresolved
  18. 2025 Medium

    Linked ING5 (via MORF/Kat6b/Brpf1) to chromatin topology, showing it antagonizes CTCF/cohesin-mediated transcriptional insulation at developmental genes.

    Evidence Genome-wide CRISPR screen, acute depletion, Hi-C and Kat6b inhibition in ESCs (preprint)

    PMID:bio_10.1101_2025.02.21.639596

    Open questions at the time
    • ING5-specific role inferred from complex membership
    • Preprint, single lab; direct ING5 contribution to insulation not isolated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ING5's PHD/H3K4me3 reading and HAT-complex targeting mechanistically connect to its downstream signaling, metabolic, and genome-stability outputs remains unresolved.
  • No unified model linking chromatin function to EGFR/STAT3/Wnt and TIE1-PDK1 axes
  • Mammalian regulators of ING5 nuclear localization beyond CDK2 unknown
  • Genomic targets directing ING5/HAT acetylation in each tissue not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0042393 histone binding 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2 GO:0003677 DNA binding 1
Localization
GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 2
Pathway
R-HSA-4839726 Chromatin organization 3 R-HSA-5357801 Programmed Cell Death 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-1266738 Developmental Biology 2 R-HSA-162582 Signal Transduction 2 R-HSA-1640170 Cell Cycle 2
Partners
CDK2INCA1ING4KAT5P300TCTPTP53
Complex memberships
HBO1 HAT complexKAT7 HAT complexMOZ/MORF (KAT6) HAT complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 ING5 (p28ING5) physically interacts with p300 (a histone acetyltransferase) and p53 in vivo, enhances p53 acetylation at Lys-382, activates the p21/WAF1 promoter, and induces p53-dependent apoptosis and cell cycle arrest. Co-immunoprecipitation (in vivo), colony formation assay, cell cycle analysis, luciferase reporter assay, western blot Cancer research High 12750254
2013 ING5 acts as a cofactor of Tip60 (KAT5) acetyltransferase to promote acetylation of p53 at K120 in response to DNA damage; ING5 forms a trimeric complex with p53 and Tip60, and K120-acetylated p53 binds the BAX and GADD45 promoters to drive apoptosis. ING5 had no effect on p53 acetylation at K373/382 and did not assist hMOF in acetylating p53-K120. Co-immunoprecipitation, western blot, chromatin immunoprecipitation (ChIP), site-directed mutagenesis (K120R), siRNA knockdown, gene expression analysis Cancer research High 23576563
2011 ING5 interacts with INCA1 (inhibitor of cyclin A1), and this interaction is required for ING5's antiproliferative and pro-apoptotic functions; ING5 overexpression suppresses cell proliferation, delays S-phase progression, and enhances Fas-induced apoptosis only in INCA1-sufficient cells (Inca1-/- cells are refractory). Yeast two-hybrid, retroviral overexpression in Inca1+/+ and Inca1-/- MEFs and bone marrow, colony formation assay, cell cycle analysis, apoptosis assay PloS one High 21750715
2015 ING5 is phosphorylated at threonine 152 by cyclin E/CDK2 and cyclin A/CDK2 in vitro; this phosphorylation is cell-cycle-regulated in cells and is located in a bipartite nuclear localization sequence, but phosphorylation at T152 alone is not sufficient to alter ING5 subcellular localization. ING5 knockdown reduces tumor cell proliferation and induces apoptosis independently of p53 status. In vitro kinase assay, phospho-specific antibody, cyclin E/CDK2 overexpression, CDK2 inhibitor (p27KIP1), site-directed mutagenesis, siRNA knockdown, cell cycle analysis PloS one High 25860957
2017 ING5 differentially regulates protein lysine acetylation: overexpression of ING5 promotes autoacetylation of p300 at K1555, K1558, K1560, K1647 and K1794 within/near its HAT domain, activating p300 HAT activity and leading to increased acetylation of p53-K382 and histone H3-K18 and downstream expression of p21 and Bax. A p300 HAT inhibitor (C646) blocked these effects. SILAC-based quantitative mass spectrometry acetylome profiling, western blot, pharmacological inhibition (C646), gene expression analysis Oncotarget High 29416718
2019 ING5 forms homodimers through an N-terminal coiled-coil domain, and can also form heterodimers with ING4. The central region is disordered but binds dsDNA with micromolar affinity. The C-terminal PHD domain binds the H3K4me3 mark equivalently in the dimer. Three cancer-associated N-terminal mutations destabilize the coiled-coil structure and affect cell proliferation and cell cycle distribution. NMR spectroscopy, X-ray crystallography (coiled-coil domain), size-exclusion chromatography, DNA-binding assay, site-directed mutagenesis, cell cycle analysis Journal of molecular biology High 31026448
2017 ING5 is the targeting subunit of HBO1, MOZ, and MORF histone acetyltransferase (HAT) complexes and promotes self-renewal of glioblastoma stem-like cells (BTICs) by increasing Oct4, Olig2, and Nestin expression, preventing differentiation, and enhancing PI3K/AKT and MEK/ERK signaling. These effects require the PHD domain of ING5 that binds H3K4me3. Ectopic expression, PHD-domain mutant analysis, sphere formation assay, immunofluorescence, western blot, in silico TCGA analysis Oncogene Medium 28925404
2022 In a CRISPR/Cas9 synthetic-lethality dropout screen in mouse ESCs, ING5 was identified as a genetic dependency of catalytically dead Set1A/COMPASS; loss of ING5 in Set1A-ΔSET ESCs decreases cell fitness and upregulates differentiation-associated genes, placing ING5 and Set1A/COMPASS as co-regulators of self-renewal vs. differentiation. CRISPR/Cas9 genome-wide dropout screen, Set1A catalytic-dead knock-in ESCs, gene expression analysis Proceedings of the National Academy of Sciences of the United States of America Medium 35500115
2023 In Drosophila, ING5 ortholog Ing5 is a unique binding partner of TCTP; TCTP inhibits nuclear translocation of Ing5 and chromatin binding of the MOZ/MORF (Enok) complex, thereby suppressing H3K23 acetylation. Loss of TCTP rescues Ing5 mutant phenotypes by increasing nuclear Ing5 and Enok chromatin association. Ing5 also controls EGF receptor signaling and organ size via the Yorkie pathway. Yeast two-hybrid, in vivo Drosophila genetics (loss-of-function mutants), chromatin immunoprecipitation (H3K23ac), immunofluorescence, epistasis analysis Proceedings of the National Academy of Sciences of the United States of America High 37014852
2024 ING5 and ING4 are essential components of KAT6A, KAT6B, and KAT7 HAT complexes required for histone H3K14 acetylation and H3K23 acetylation in vivo; Ing4-/-Ing5-/- mouse embryos arrest at E8.5 with global loss of H3K14ac and reduction of H3K23ac, while Ing5-/- mice develop isolated ventricular septal defects and Ing4+/-Ing5-/- hearts show loss of epicardial cells due to defective cell adhesion gene expression. Knockout mouse generation, western blot (histone marks), immunofluorescence, transcriptome analysis, developmental phenotyping Development (Cambridge, England) High 38446206
2024 ING5 overexpression upregulates TIE1 (a tyrosine kinase), which phosphorylates pyruvate dehydrogenase kinase 1 (PDK1) at Y163; pY163-PDK1 causes PDHA1 dephosphorylation and activation, switching metabolism from aerobic glycolysis to oxidative phosphorylation, and suppressing lung cancer cell invasion. PDK1-Y163F mutation abrogates these effects. Quantitative phosphoproteomics (SILAC), siRNA screening, site-directed mutagenesis (PDK1-Y163F), oxygen consumption/lactate production assays, xenograft mouse model, immunohistochemistry Frontiers of medicine High 39269568
2022 ING5 transcription is positively regulated by the transcription factors SRF and YY1 through direct binding to the ING5 promoter (SRF at -717 to -678 bp and YY1 at -48 to +25 bp), forming a SRF-YY1-ING5-p53 complex that activates ING5 expression in gastric cancer cells. Electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP), luciferase reporter assay, co-immunoprecipitation Frontiers in oncology High 35747809
2025 ING5 (as part of the MORF acetyltransferase complex with Kat6b and Brpf1) antagonizes transcriptional insulation mediated by the CTCF/cohesin loop-extrusion machinery at developmental genes in mouse ESCs; inhibition of Kat6b partially rescues insulator defects caused by loss of the cohesin loader Nipbl. Genome-wide CRISPR screen, acute protein depletion (cohesin/CTCF), Hi-C/chromatin topology, transcriptomics, pharmacological inhibition of Kat6b bioRxivpreprint Medium bio_10.1101_2025.02.21.639596
2025 ING5 knockout mice develop diffuse large B-cell lymphomas at a 6-fold higher rate than wild-type controls, and ING5 KO mouse embryo fibroblasts accumulate in G2, exhibit elevated γH2AX (DNA damage marker), and have abnormal nuclei, establishing an in vivo tumor-suppressor role for ING5 in hematopoietic cells and a function in maintaining genomic integrity. CRISPR/Cas9 knockout mice, flow cytometry (cell cycle, γH2AX), pathological tumor analysis, wound healing assay PloS one High 39787145
2017 ING5 knockdown in lung cancer A549 cells activates EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways to promote EMT and metastasis; pharmacological inhibition of PI3K (ZSTK474) or STAT3 (Niclosamide) abolishes ING5-knockdown-promoted migration, invasion, and metastasis in mouse xenograft models. Phospho-kinase array, western blot, shRNA knockdown, pharmacological inhibition, xenograft tail-vein injection metastasis model, EMT marker analysis Oncotarget Medium 28903339
2023 ING5 overexpression in lung cancer cells induces upregulation of miR-34c-5p, which directly targets the 3'UTR of Snail1 (confirmed by dual-luciferase reporter), reducing Snail1 expression and inactivating the TGF-β/Smad3 pathway to inhibit EMT and invasion. Overexpression, dual-luciferase reporter assay, miRNA overexpression/inhibition, TGF-β inhibitor (LY2157299), xenograft metastasis model (tail vein injection), TCGA data analysis Acta biochimica et biophysica Sinica Medium 37249332
2010 Three missense mutations in ING5 located within the leucine zipper-like (LZL) and novel conserved region (NCR) domains were detected specifically in oral squamous cell carcinoma tumors; five alternative splicing variants of ING5 were also identified. ING5 mRNA was decreased in 61% of primary tumors, implicating these structural domains in tumor-suppressor function. RT-PCR, sequencing, quantitative real-time RT-PCR (qRT-PCR), analysis of matched normal/tumor pairs International journal of cancer Low 20131318
2023 ING5 is required for normal hematopoietic cell numbers in the fetal liver in a cell-extrinsic manner; Ing5-null mice showed decreased fetal liver cellularity, fewer hematopoietic stem cells, and perturbed erythropoiesis, but competitive transplantation showed no cell-intrinsic long-term repopulation defect. Knockout mouse model (null allele), cell counting, flow cytometry, competitive bone-marrow transplantation Frontiers in immunology Medium 37275850

Source papers

Stage 0 corpus · 55 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 Exosomal miR-196a derived from cancer-associated fibroblasts confers cisplatin resistance in head and neck cancer through targeting CDKN1B and ING5. Genome biology 359 30642385
2003 p29ING4 and p28ING5 bind to p53 and p300, and enhance p53 activity. Cancer research 240 12750254
2013 ING5 is a Tip60 cofactor that acetylates p53 in response to DNA damage. Cancer research 57 23576563
2017 ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways. Oncotarget 55 28903339
2015 The miR-193a-3p-regulated ING5 gene activates the DNA damage response pathway and inhibits multi-chemoresistance in bladder cancer. Oncotarget 53 25991669
2015 Upregulated in Hepatitis B virus-associated hepatocellular carcinoma cells, miR-331-3p promotes proliferation of hepatocellular carcinoma cells by targeting ING5. Oncotarget 53 26497554
2017 MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression. Journal of ovarian research 49 28086946
2015 ING5 suppresses proliferation, apoptosis, migration and invasion, and induces autophagy and differentiation of gastric cancer cells: a good marker for carcinogenesis and subsequent progression. Oncotarget 48 25980581
2010 Tumor-specific mutation and downregulation of ING5 detected in oral squamous cell carcinoma. International journal of cancer 47 20131318
2010 The altered expression of ING5 protein is involved in gastric carcinogenesis and subsequent progression. Human pathology 45 21062663
2010 Decreased nuclear expression and increased cytoplasmic expression of ING5 may be linked to tumorigenesis and progression in human head and neck squamous cell carcinoma. Journal of cancer research and clinical oncology 43 20182888
2010 The nuclear to cytoplasmic shift of ING5 protein during colorectal carcinogenesis with their distinct links to pathologic behaviors of carcinomas. Human pathology 39 21193223
2020 LncRNA CASC2 inhibits hypoxia-induced pulmonary artery smooth muscle cell proliferation and migration by regulating the miR-222/ING5 axis. Cellular & molecular biology letters 35 32206065
2015 ING5 inhibits epithelial-mesenchymal transition in breast cancer by suppressing PI3K/Akt pathway. International journal of clinical and experimental medicine 34 26629040
2017 ING5 activity in self-renewal of glioblastoma stem cells via calcium and follicle stimulating hormone pathways. Oncogene 33 28925404
2017 ING5 suppresses breast cancer progression and is regulated by miR-24. Molecular cancer 31 28490335
2020 MicroRNA-196b-5p promotes malignant progression of colorectal cancer by targeting ING5. Cancer cell international 30 32308564
2019 ING5 inhibits lung cancer invasion and epithelial-mesenchymal transition by inhibiting the WNT/β-catenin pathway. Thoracic cancer 30 30810286
2011 The inhibitor of growth protein 5 (ING5) depends on INCA1 as a co-factor for its antiproliferative effects. PloS one 30 21750715
2017 Overexpression of ING5 inhibits HGF-induced proliferation, invasion and EMT in thyroid cancer cells via regulation of the c-Met/PI3K/Akt signaling pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 27 29272787
2019 The Tumor Suppressor ING5 Is a Dimeric, Bivalent Recognition Molecule of the Histone H3K4me3 Mark. Journal of molecular biology 26 31026448
2015 ING5 is phosphorylated by CDK2 and controls cell proliferation independently of p53. PloS one 23 25860957
2020 miR-200b/200a/429 Cluster Stimulates Ovarian Cancer Development by Targeting ING5. Journal of oncology 21 32377191
2020 MiR-193 promotes cell proliferation and invasion by ING5/PI3K/AKT pathway of triple-negative breast cancer. European review for medical and pharmacological sciences 20 32271430
2018 ING5 inhibits cell proliferation and invasion in esophageal squamous cell carcinoma through regulation of the Akt/NF-κB/MMP-9 signaling pathway. Biochemical and biophysical research communications 20 29326045
2017 The nucleocytoplasmic translocation and up-regulation of ING5 protein in breast cancer: a potential target for gene therapy. Oncotarget 19 29137236
2022 The roles of ING5 in cancer: A tumor suppressor. Frontiers in cell and developmental biology 17 36425530
2017 ING5 differentially regulates protein lysine acetylation and promotes p300 autoacetylation. Oncotarget 17 29416718
2016 The down-regulated ING5 expression in lung cancer: a potential target of gene therapy. Oncotarget 17 27409347
2023 ING5 overexpression upregulates miR-34c-5p/Snail1 to inhibit EMT and invasion of lung cancer cells. Acta biochimica et biophysica Sinica 14 37249332
2019 Upregulation of miR-376c-3p alleviates oxygen-glucose deprivation-induced cell injury by targeting ING5. Cellular & molecular biology letters 14 31844418
2019 ING5 inhibits cancer aggressiveness by inhibiting Akt and activating p53 in prostate cancer. Cell biology international 13 31475765
2017 The roles of ING5 in gliomas: a good marker for tumorigenesis and a potential target for gene therapy. Oncotarget 13 28915612
2022 A synthetic lethality screen reveals ING5 as a genetic dependency of catalytically dead Set1A/COMPASS in mouse embryonic stem cells. Proceedings of the National Academy of Sciences of the United States of America 12 35500115
2018 ING5-mediated antineuroblastoma effects of suberoylanilide hydroxamic acid. Cancer medicine 12 30091530
2017 The roles of ING5 expression in ovarian carcinogenesis and subsequent progression: a target of gene therapy. Oncotarget 11 29262575
2018 Hepatitis B virus X protein promotes proliferation of hepatocellular carcinoma cells by upregulating miR-181b by targeting ING5. Biological chemistry 10 29604207
2024 Mechanism of non-small cell lung cancer cell-derived exosome miR-196b-5p promoting pyroptosis of tumor T cells and tumor cell proliferation by downregulating ING5. Journal of biochemical and molecular toxicology 9 38229318
2024 The Antitumor and Sorafenib-resistant Reversal Effects of Ursolic Acid on Hepatocellular Carcinoma via Targeting ING5. International journal of biological sciences 8 39247819
2022 Hsa_circ_0010729 is Involved in Oxygen-Glucose Deprivation/Reoxygenation-Induced Human Microvascular Endothelial Cell Deprivation by Targeting miR-665/ING5. Biochemical genetics 8 35482130
2021 ING5 Inhibits Migration and Invasion of Esophageal Cancer Cells by Downregulating the IL-6/CXCL12 Signaling Pathway. Technology in cancer research & treatment 8 34520285
2024 ING4 and ING5 are essential for histone H3 lysine 14 acetylation and epicardial cell lineage development. Development (Cambridge, England) 7 38446206
2018 Expression pattern and level of ING5 protein in normal and cancer tissues. Oncology letters 7 30655738
2024 ING5 inhibits aerobic glycolysis of lung cancer cells by promoting TIE1-mediated phosphorylation of pyruvate dehydrogenase kinase 1 at Y163. Frontiers of medicine 6 39269568
2022 Transcriptional Regulation of ING5 and its Suppressive Effects on Gastric Cancer. Frontiers in oncology 6 35747809
2018 ING5 is a Potential Target for Osteosarcoma Therapy. Technology in cancer research & treatment 6 29528777
2023 The chromatin reader protein ING5 is required for normal hematopoietic cell numbers in the fetal liver. Frontiers in immunology 5 37275850
2025 Knockout of the ING5 epigenetic regulator confirms roles in stem cell maintenance and tumor suppression in vivo. PloS one 3 39787145
2024 Hepatitis E virus infection upregulates ING5 expression in vitro and in vivo. Acta biochimica et biophysica Sinica 2 38877781
2023 Tctp, a unique Ing5-binding partner, inhibits the chromatin binding of Enok in Drosophila. Proceedings of the National Academy of Sciences of the United States of America 2 37014852
2018 [Nucleocytoplasmic translocation of ING5 protein in breast cancer and its correlation with poor clinicopathological characteristics of breast cancer]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 1 29595458
2026 Resveratrol inhibits pancreatic cancer progression via the ING5 signaling pathway. Scientific reports 0 41826634
2025 RETRACTION: ING5-Mediated Antineuroblastoma Effects of Suberoylanilide Hydroxamic Acid. Cancer medicine 0 40183226
2025 ING5: multifaceted roles beyond tumor suppression in cellular physiology and disease. Epigenetics & chromatin 0 41063239
2025 ING5-mediated regulation of lung cancer progression via the OIP5-AS1/miR-381-3p/SEC24A axis. Translational cancer research 0 41378010

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