Affinage

PRDM14

PR domain zinc finger protein 14 · UniProt Q9GZV8

Length
571 aa
Mass
64.1 kDa
Annotated
2026-06-10
65 papers in source corpus 27 papers cited in narrative 27 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PRDM14 is a sequence-specific PR-domain/zinc-finger transcription factor that establishes and maintains naive pluripotency and directs primordial germ cell (PGC) specification through largely repressive chromatin programs (PMID:18622394, PMID:21183938, PMID:23333148). It binds a unique DNA motif at loci shared with the core pluripotency network (overlapping Nanog and Oct4), repressing extraembryonic and somatic differentiation genes while supporting self-renewal gene expression (PMID:21183938). Repression is executed by recruiting Polycomb Repressive Complex 2 (PRC2) and depositing H3K27me3 at targets including the de novo DNA methyltransferases Dnmt3a/b and FGF-signaling effectors, thereby safeguarding the hypomethylated naive state (PMID:23333148, PMID:23280602). This PRC2-coupled repression operates through an ETO-family co-repressor scaffold: PRDM14 binds CBFA2T2/Mtgr1 tightly via its pre-SET/SET domains (a structurally defined interaction whose disruption abrogates ESC and PGC function), and CBFA2T2 in turn bridges the CtBP1/2 co-repressors required for full repression and PRC2 enrichment (PMID:26523391, PMID:32661086). In parallel, PRDM14 promotes active DNA demethylation by physically engaging TET1/TET2 and accelerating the TET–base-excision-repair cycle at pluripotency, germline, and imprinted loci (PMID:24335252, PMID:27866876). PRDM14 additionally enables X-chromosome reactivation by recruiting PRC2 to repress Rnf12/Xist (PMID:24268575) and reinforces self-renewal signaling by repressing Socs3 to potentiate LIF/JAK/STAT3 activity (PMID:36300005). In human PGC-like cells it cooperates with TFAP2C and BLIMP1 to drive germ-cell fate, though its target repertoire diverges from mouse (PMID:32152282). When aberrantly expressed in somatic cells, PRDM14 becomes oncogenic: it co-opts the hematopoietic ETO paralog CBFA2T3 to drive T-ALL, and creates permissive chromatin (H3K4me3) at a Notch1 intron that licenses RAG-dependent oncogenic deletions (PMID:31015254, PMID:27106930). Its activity supports cancer stem-like properties across multiple tumor types through interactions and transcriptional outputs including HSP90/GRP78, the miR-125a-3p/Fyn axis, and CALM2/SLC2A1 (PMID:29178343, PMID:28498896, PMID:34990589).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2008 High

    Established PRDM14 as a genetically required, BLIMP1-independent factor for the dual program of pluripotency reacquisition and epigenetic reprogramming in PGC specification, defining its core developmental role.

    Evidence Genetic knockout in mice with transcriptional/epigenetic readouts; parallel siRNA/overexpression in human ESCs

    PMID:18194669 PMID:18622394

    Open questions at the time
    • Molecular mechanism of repression not yet defined
    • No direct DNA-binding targets identified at this stage
  2. 2010 High

    Defined PRDM14 as a sequence-specific transcription factor binding a unique motif and acting at the core pluripotency network, distinguishing repressed differentiation targets from activated self-renewal targets.

    Evidence ChIP-seq, in vitro DNA-binding assay, and loss/gain-of-function in mouse ESCs

    PMID:21183938

    Open questions at the time
    • Co-repressor machinery not yet identified
    • Mechanism of dual activation/repression unresolved
  3. 2013 High

    Resolved the repressive mechanism by showing PRDM14 recruits PRC2 to silence de novo DNMTs and FGF signaling, linking it to the hypomethylated naive ground state.

    Evidence ChIP-seq, methylation/FGF signaling assays, reporter dependency, and Co-IP in mouse and human ESCs (multiple labs)

    PMID:23280602 PMID:23333148 PMID:23670199

    Open questions at the time
    • How PRDM14 physically bridges PRC2 not defined
    • Direct vs indirect PRC2 contact unresolved at this stage
  4. 2013 High

    Showed PRDM14 also acts positively on demethylation by recruiting TET1/TET2 and engaging the BER pathway, establishing a two-pronged DNA-methylation control (blocking writers, promoting erasers).

    Evidence Reciprocal Co-IP, ChIP for TET recruitment, pharmacological/genetic BER inhibition, 5hmC/5mC quantification in mouse ESCs

    PMID:24335252

    Open questions at the time
    • Direct vs scaffolded TET contact not structurally defined
    • Locus-selectivity determinants unknown
  5. 2013 High

    Extended PRDM14 function to X-chromosome reactivation, showing PRC2-mediated repression of Rnf12/Xist and a Tsix-dependent recruitment route.

    Evidence Prdm14/Tsix genetic KO in blastocysts and iPSC reprogramming, ChIP, allele-specific expression

    PMID:24268575

    Open questions at the time
    • Context-dependent Tsix requirement (blastocyst vs iPSC) mechanism unclear
  6. 2015 High

    Identified the structural basis of PRDM14 repression: the ETO-family co-repressor Mtgr1/CBFA2T2 binds the pre-SET/SET domains, and disrupting this interface abolishes ESC and PGC function.

    Evidence Crystal structure of the Prdm14–Mtgr1 complex, structure-guided mutagenesis, monobody inhibitor, ChIP-seq co-occupancy, PGC formation assay

    PMID:26523391

    Open questions at the time
    • How the Mtgr1 scaffold connects to PRC2 not resolved here
    • Role of the PR/SET domain catalytic potential unaddressed
  7. 2016 High

    Demonstrated oncogenic co-option: aberrant PRDM14 creates a permissive H3K4me3 chromatin state at a Notch1 intron that licenses RAG-dependent deletions to initiate T-ALL.

    Evidence PRDM14-FLAG knock-in ChIP, H3K4me3 ChIP, RAG-KO genetic epistasis, Notch1 deletion characterization

    PMID:27106930

    Open questions at the time
    • How PRDM14 switches from repressive to permissive chromatin in somatic cells unknown
  8. 2019 High

    Identified a tumor-type-specific co-repressor partner switch, showing PRDM14-driven T-ALL requires CBFA2T3 rather than the pluripotency partner CBFA2T2.

    Evidence Interactome mass spectrometry, Co-IP, Cbfa2t3-KO mouse leukemia models

    PMID:31015254

    Open questions at the time
    • Determinants of paralog selectivity between CBFA2T2 and CBFA2T3 unknown
  9. 2019 High

    Established the human-specific germline program, showing PRDM14 cooperates with TFAP2C and BLIMP1 in hPGCLC specification with targets that diverge from mouse.

    Evidence Inducible degron depletion, ChIP, RNA-seq in hESC-derived hPGCLCs

    PMID:32152282

    Open questions at the time
    • Basis of mouse–human target divergence unresolved
    • Direct TFAP2C/BLIMP1 contacts not mapped
  10. 2020 Medium

    Completed the naive-pluripotency repressive complex architecture, placing CtBP1/2 downstream of CBFA2T2 as effectors needed for PRC2/H3K27me3 enrichment and the primed-to-naive transition.

    Evidence Co-IP, Ctbp1/2 KO, ChIP for PRC2/H3K27me3, expression analysis in mESCs

    PMID:32661086

    Open questions at the time
    • Single lab
    • Stoichiometry of the PRDM14–CBFA2T2–CtBP–PRC2 assembly undefined
  11. 2022 Medium

    Broadened the somatic-cancer mechanism, showing PRDM14 sustains cancer stem-like states through transcriptional outputs (CALM2/SLC2A1; miR-125a-3p/Fyn) and chaperone interactions.

    Evidence Genome-scale rescue screen, xenograft/organoid models, shRNA, and biophysical binding assays across colon, pancreatic, and breast cancer

    PMID:28498896 PMID:29178343 PMID:34990589

    Open questions at the time
    • Whether these outputs are direct PRDM14 targets in all contexts unclear
    • Connection to the core repressive complex not established
  12. 2025 Medium

    Defined autoregulatory control of PRDM14 itself, with rodent-specific enhancers driving naive-state induction and a PRDM14-binding negative feedback loop timing exit from pluripotency and global demethylation.

    Evidence CRISPR enhancer deletion, ChIP, methylation and expression assays in mESCs

    PMID:41267649

    Open questions at the time
    • Species-specificity of feedback wiring not generalized to human
    • Link to UHRF1 degradation mechanistically incomplete

Open questions

Synthesis pass · forward-looking unresolved questions
  • How PRDM14 toggles between PRC2-mediated repression and the permissive/activating chromatin states seen at germline, signaling, and oncogenic loci, and what determines its locus and co-repressor selectivity, remains unresolved.
  • No unified model for repression-vs-activation switching
  • PR/SET domain catalytic function undefined
  • Determinants of mouse–human and pluripotent-vs-cancer target divergence unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 3 GO:0003677 DNA binding 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 2
Pathway
R-HSA-4839726 Chromatin organization 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1474165 Reproduction 2 R-HSA-1643685 Disease 2 R-HSA-74160 Gene expression (Transcription) 2
Partners
CBFA2T2CBFA2T3CTBP1CTBP2HOXA1HSP90AA1TET1TET2
Complex memberships
PRC2PRDM14-CBFA2T2/Mtgr1 co-repressor complex

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 Prdm14 is required for reacquisition of potential pluripotency and genome-wide epigenetic reprogramming during primordial germ cell (PGC) specification in mice, operating in a genetic pathway independent of Prdm1/Blimp1. Genetic knockout in mice with transcriptional and epigenetic phenotypic readouts Nature genetics High 18622394
2008 PRDM14 knockdown in human ES cells induces expression of early differentiation marker genes, while forced expression suppresses differentiation marker expression, indicating PRDM14 maintains self-renewal by transcriptional repression. siRNA knockdown and forced expression in human ESCs with gene expression readouts Biochemical and biophysical research communications Medium 18194669
2010 Prdm14 occupies and represses genomic loci encoding extraembryonic endoderm (ExEn) differentiation factors while binding to and promoting expression of ESC self-renewal genes; Prdm14-associated regions contain a unique DNA-sequence motif recognized by Prdm14 in vitro, and its binding overlaps substantially with Nanog and Oct4. ChIP-seq, in vitro DNA binding assay, loss-of-function and gain-of-function in mouse ESCs Nature structural & molecular biology High 21183938
2013 PRDM14 ensures naive pluripotency by (1) antagonizing FGFR signaling activation and (2) repressing expression of de novo DNA methyltransferases (Dnmt3a/b), and exerts these effects by recruiting Polycomb Repressive Complex 2 (PRC2) specifically to key target loci. ChIP-seq, gene expression profiling, FGFR signaling assays, and functional rescue in mouse ESCs cultured in serum vs. 2i conditions Cell stem cell High 23333148
2013 Prdm14 contributes to naive pluripotency in ESCs by repressing the DNA methylation machinery and FGF signalling, consistent with its role in PGC specification. Loss-of-function and gain-of-function in mouse ESCs with methylation and FGF signaling readouts EMBO reports Medium 23670199
2013 PRDM14 physically interacts with TET1 and TET2 proteins and enhances their recruitment to target loci, accelerating the TET-mediated oxidation and base excision repair (BER) cycle to promote active DNA demethylation at pluripotency-associated, germline-specific, and imprinted loci in ESCs. Knockdown of TET1/TET2 or inhibition of BER pathway components (APE1, PARP1, TDG) impairs PRDM14-induced demethylation. Co-immunoprecipitation, ChIP, pharmacological BER inhibition, siRNA knockdown, 5hmC/5mC quantification in mouse ESCs Development (Cambridge, England) High 24335252
2013 PRDM14 directly interacts with PRC2 in human ESCs; PRDM14 binding is enriched for H3K27me3, depletion of PRDM14 reduces PRC2 binding and H3K27me3 at target loci, and PRDM14-mediated repression requires both PRDM14 and PRC2 as shown by reporter assays. In iPSC reprogramming, PRDM14 recruits PRC2 to repress the mesenchymal gene ZEB1, enhancing mesenchymal-to-epithelial transition. Co-immunoprecipitation, ChIP-seq, reporter assays, shRNA knockdown in human ESCs and fibroblasts Stem cells (Dayton, Ohio) High 23280602
2013 PRDM14 is heterogeneously expressed in 4-cell-stage mouse embryos; forced expression at the 2-cell stage leads to increased H3R26me2 and can induce a pluripotent ICM fate. Quantitative microfluidics single-cell profiling, mRNA microinjection into 2-cell embryos, immunofluorescence for H3R26me2 Cell reports Medium 24183668
2013 PRDM14 represses Rnf12 by recruiting PRC2, thereby enabling X chromosome reactivation (XCR); Tsix enables PRDM14 to bind Xist. Both Tsix and PRDM14 are required for XCR in blastocysts, while in iPSC reprogramming XCR requires PRDM14 but not Tsix. Genetic knockout of Prdm14 and Tsix in mouse blastocysts and iPSC reprogramming; ChIP for PRDM14/PRC2 at Rnf12 and Xist loci; allele-specific expression analysis Molecular cell High 24268575
2015 PRDM14's repressive function in ESCs and PGC formation is mediated through the ETO-family co-repressor Mtgr1, which binds tightly to the pre-SET/SET domains of Prdm14 and co-occupies its genomic targets. Crystal structure of the Prdm14-Mtgr1 complex was determined; structure-guided point mutants and a synthetic monobody inhibitor of the Prdm14-Mtgr1 interaction disrupted Prdm14 function in mESC gene expression and PGC formation. Protein crystallography (crystal structure determination), Co-IP, ChIP-seq co-occupancy, monobody inhibitor, structure-guided mutagenesis, functional PGC formation assay eLife High 26523391
2016 PRDM14 recruits OCT3/4 to enhancer regions of naive pluripotency genes via TET-BER-mediated active DNA demethylation during conversion from epiblast-like cells to ESC-like cells; this requires KLF2 and TET proteins. ChIP, bisulfite sequencing, genetic loss-of-function (Klf2 KO, TET KD), overexpression in EpiLCs Stem cell reports Medium 27866876
2017 PRDM14 directly interacts with HSP90α and GRP78 through its C-terminal zinc finger-containing region; these interactions were confirmed by pulldown/mass spectrometry, immunoprecipitation in two TNBC cell lines, surface plasmon resonance with GST-PRDM14, and NanoBRET in living cells. HSP90 inhibitors decreased breast cancer stem-like cells in a PRDM14-dependent manner. Pulldown/mass spectrometry, Co-IP, surface plasmon resonance, NanoBRET assay, pharmacological inhibition with PRDM14 KD Cancer science High 29178343
2018 PRDM14 interacts with HOXA1 via the homeodomain of HOXA1 and the PR domain/zinc fingers of PRDM14; PRDM14 reduces the stability and transcriptional activity of HOXA1. Co-immunoprecipitation, domain deletion mapping, protein stability assays, transcriptional reporter assays Biochimica et biophysica acta. Gene regulatory mechanisms Medium 29471045
2019 PRDM14 cooperates with TFAP2C and BLIMP1 to upregulate germ cell and pluripotency genes while repressing WNT signalling and somatic markers in human PGC-like cells; PRDM14 depletion using inducible degrons significantly reduces specification efficiency and causes aberrant transcriptome. PRDM14 targets are not conserved between mouse and human. Inducible degron-mediated rapid protein depletion, ChIP, RNA-seq in hESC-derived hPGCLCs Nature communications High 32152282
2019 PRDM14-induced T-ALL requires the hematopoietic regulator CBFA2T3; PRDM14 and CBFA2T3 associate in leukemic cells independently of CBFA2T2 (the primary pluripotent cell partner). Prdm14-induced T-ALL does not develop in Cbfa2t3-deficient mice, demonstrating CBFA2T3 is essential for PRDM14-driven leukemogenesis. Mass spectrometry interactome, Co-IP, genetic mouse models (Cbfa2t3 KO), in vivo leukemia development assay Molecular cancer research : MCR High 31015254
2019 PRDM14 is the first known factor instrumental for both global H3K27me3 upregulation and X-chromosomal H3K27me3 removal during PGC migration in vivo; global and X-chromosomal reprogramming of H3K27me3 are PRDM14 dosage-dependent but functionally separable. In vivo analysis of Prdm14 heterozygous and knockout migrating PGCs; immunofluorescence for H3K27me3 on X chromosome and globally Epigenetics & chromatin Medium 31221220
2019 Amphioxus and zebrafish PRDM14 orthologs can compensate for mouse Prdm14 function in ESC pluripotency maintenance, demonstrating functional conservation. Sea urchin PRDM14 requires co-expression of sea urchin CBFA2T to complement mouse Prdm14 KO ESCs, implicating the PRDM14-CBFA2T complex as the functional unit co-opted from motor neurons to pluripotent cells during vertebrate evolution. Complementation assay in Prdm14 KO mouse ESCs using orthologous proteins; cross-species expression analysis Development (Cambridge, England) Medium 30630825
2020 The PRDM14 repressive complex includes CtBP1/2, which binds PRDM14 via CBFA2T2 (a core complex component); loss of Ctbp1/2 impairs PRDM14-mediated transcriptional repression and the transition from primed to naive pluripotency, and reduces PRC2/H3K27me3 enrichment at target genes after Prdm14 induction. Co-immunoprecipitation, genetic KO of Ctbp1/2, ChIP for PRC2/H3K27me3, gene expression analysis in mESCs Journal of cell science Medium 32661086
2012 In zebrafish, Prdm14 binds to the promoter region of islet2 (a transcription factor required for CaP motoneuron development) and activates its expression; overexpression of islet2 in prdm14 mutant embryos rescues shortened CaP axon phenotypes, placing Prdm14 upstream of islet2 in a motor neuron axon growth pathway. Gene-trap mutant, morpholino knockdown, ChIP of Prdm14 at islet2 promoter, islet2 overexpression rescue in zebrafish Development (Cambridge, England) Medium 23136389
2014 Full-length PRDM14 transactivates NOXA and PUMA promoters in HPV-positive cancer cells; transactivation is abolished upon deletion of the PRDM14 DNA binding domain, and a consensus PRDM14 binding motif in the NOXA promoter was identified. Ectopic PRDM14 expression induces apoptosis in HPV-positive cancer cells. Luciferase reporter/transactivation assays, domain deletion mutants, annexin V apoptosis assay, mRNA profiling Carcinogenesis Medium 25233927
2017 PRDM14 knockdown in pancreatic cancer cells upregulates miR-125a-3p, which reduces expression of the Src-family kinase Fyn and decreases activation of downstream signaling, suppressing cancer stem-like properties including sphere formation and liver metastasis. lentiviral shRNA knockdown, sphere formation assay, side population analysis, xenograft and liver metastasis in mice, miRNA and Fyn expression analysis Carcinogenesis Medium 28498896
2022 PRDM14 can substitute for YAP1 in YAP1-dependent colon cancer cells; PRDM14 transcriptionally activates calmodulin 2 (CALM2) and the glucose transporter SLC2A1, and expression of either is required for the rescue of YAP1 suppression. Genome-scale genetic rescue screen, inducible YAP1 shRNA, xenograft and organoid models, transcriptional target validation Developmental cell Medium 34990589
2016 PRDM14 binds within an intron of Notch1 prior to leukemia development and promotes a permissive chromatin state (increased H3K4me3) that allows access of the RAG recombinase to cryptic signal sequences, leading to RAG-dependent Notch1 promoter deletions and T-ALL. T-ALL is abrogated in a RAG-deficient background. ChIP with PRDM14-FLAG knock-in mouse, H3K4me3 ChIP, genetic epistasis with RAG KO, PCR characterization of Notch1 deletions Biology open High 27106930
2022 Prdm14 directly binds the promoter of Socs3 and represses its transcription, thereby increasing phosphorylation of Stat3 and enhancing LIF/JAK/Stat3 signaling, which promotes mESC self-renewal and PGC-like cell generation. ChIP, luciferase reporter assay, Socs3 overexpression epistasis, Stat3 KD, JAK inhibitor treatment in mESCs iScience Medium 36300005
2024 PKC inhibition (via Go6983 or PKCδ inhibition specifically) increases Prdm14 expression; Suv39h1/2-mediated H3K9 dimethylation and trimethylation at the Prdm14 promoter epigenetically represses Prdm14, and PKC inhibition reduces this mark and increases RNA Pol II binding, thereby elevating Prdm14 levels. Prdm14 upregulation mediates Go6983-induced repression of Dnmt3a/b/l. ChIP for H3K9me2/me3 and RNA Pol II at Prdm14 promoter, Suv39h RNAi, chaetocin inhibitor, RNA-seq, Prdm14 KD epistasis The Journal of biological chemistry Medium 38309502
2024 Wnt/β-catenin signaling activation during trophoblast stem cell (TSC) formation reduces PRDM14 expression; PRDM14 extinction leads to erasure of H3K27me3 marks and chromatin opening at TSC transcription factor loci (GATA3 and TFAP2C), enabling their expression and initiating TSC formation. ATAC-seq, ChIP for H3K27me3, Wnt pathway manipulation, PRDM14 KO/KD in ESCs undergoing TSC conversion Cellular and molecular life sciences : CMLS Medium 38710919
2025 Rodent-specific cis-regulatory enhancer elements downstream of Prdm14 (containing POU5F1 and TFCP2L1 recognition sequences) are essential for Prdm14 transcriptional upregulation in naive ESCs; PRDM14-binding motifs within these enhancers form a negative feedback loop required for timely exit from naive pluripotency. Loss of these enhancers impairs UHRF1 degradation and global DNA demethylation under 2iL conditions. CRISPR/Cas9 deletion of enhancer elements, ChIP, gene expression analysis, DNA methylation assays in mESCs Development (Cambridge, England) Medium 41267649

Source papers

Stage 0 corpus · 65 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Critical function of Prdm14 for the establishment of the germ cell lineage in mice. Nature genetics 438 18622394
2013 PRDM14 ensures naive pluripotency through dual regulation of signaling and epigenetic pathways in mouse embryonic stem cells. Cell stem cell 249 23333148
2010 Sequence-specific regulator Prdm14 safeguards mouse ESCs from entering extraembryonic endoderm fates. Nature structural & molecular biology 171 21183938
2013 Identification of nine new susceptibility loci for testicular cancer, including variants near DAZL and PRDM14. Nature genetics 132 23666240
2013 Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation. EMBO reports 131 23670199
2013 Single-cell profiling of epigenetic modifiers identifies PRDM14 as an inducer of cell fate in the mammalian embryo. Cell reports 122 24183668
2013 PRDM14 promotes active DNA demethylation through the ten-eleven translocation (TET)-mediated base excision repair pathway in embryonic stem cells. Development (Cambridge, England) 105 24335252
2007 Gene amplification and overexpression of PRDM14 in breast cancers. Cancer research 99 17942894
2020 A critical role of PRDM14 in human primordial germ cell fate revealed by inducible degrons. Nature communications 90 32152282
2013 Tsix RNA and the germline factor, PRDM14, link X reactivation and stem cell reprogramming. Molecular cell 87 24268575
2008 PRDM14 suppresses expression of differentiation marker genes in human embryonic stem cells. Biochemical and biophysical research communications 87 18194669
2008 Specification of the germ cell lineage in mice: a process orchestrated by the PR-domain proteins, Blimp1 and Prdm14. Cell cycle (Georgetown, Tex.) 73 19001867
2014 PRDM14: a unique regulator for pluripotency and epigenetic reprogramming. Trends in biochemical sciences 64 24811060
2013 A PRC2-dependent repressive role of PRDM14 in human embryonic stem cells and induced pluripotent stem cell reprogramming. Stem cells (Dayton, Ohio) 59 23280602
2015 ETO family protein Mtgr1 mediates Prdm14 functions in stem cell maintenance and primordial germ cell formation. eLife 48 26523391
2011 Prdm14 initiates lymphoblastic leukemia after expanding a population of cells resembling common lymphoid progenitors. Oncogene 48 21339739
2021 Blastocyst complementation using Prdm14-deficient rats enables efficient germline transmission and generation of functional mouse spermatids in rats. Nature communications 41 33637711
2017 Inhibition of PRDM14 expression in pancreatic cancer suppresses cancer stem-like properties and liver metastasis in mice. Carcinogenesis 38 28498896
2018 PRDM14 Is a Unique Epigenetic Regulator Stabilizing Transcriptional Networks for Pluripotency. Frontiers in cell and developmental biology 34 29487849
2014 Methylation-mediated repression of PRDM14 contributes to apoptosis evasion in HPV-positive cancers. Carcinogenesis 33 25233927
2016 PRDM14 Drives OCT3/4 Recruitment via Active Demethylation in the Transition from Primed to Naive Pluripotency. Stem cell reports 32 27866876
2008 The zinc finger SET domain gene Prdm14 is overexpressed in lymphoblastic lymphomas with retroviral insertions at Evi32. PloS one 30 19043588
2017 Glucose insult elicits hyperactivation of cancer stem cells through miR-424-cdc42-prdm14 signalling axis. British journal of cancer 28 29024936
2019 PRDM14 controls X-chromosomal and global epigenetic reprogramming of H3K27me3 in migrating mouse primordial germ cells. Epigenetics & chromatin 27 31221220
2018 PRDM14 is expressed in germ cell tumors with constitutive overexpression altering human germline differentiation and proliferation. Stem cell research 27 29324254
2017 Silencing PRDM14 expression by an innovative RNAi therapy inhibits stemness, tumorigenicity, and metastasis of breast cancer. Oncotarget 26 28423353
2012 Prdm14 acts upstream of islet2 transcription to regulate axon growth of primary motoneurons in zebrafish. Development (Cambridge, England) 24 23136389
2013 A mouse model for inducible overexpression of Prdm14 results in rapid-onset and highly penetrant T-cell acute lymphoblastic leukemia (T-ALL). Disease models & mechanisms 23 24046360
2020 Germline development in rat revealed by visualization and deletion of Prdm14. Development (Cambridge, England) 22 32001439
2015 PRDM14 promotes the migration of human non-small cell lung cancer through extracellular matrix degradation in vitro. Chinese medical journal 22 25635434
2015 PRDM14 maintains pluripotency of embryonic stem cells through TET-mediated active DNA demethylation. Biochemical and biophysical research communications 20 26325469
2015 Combined Overexpression of JARID2, PRDM14, ESRRB, and SALL4A Dramatically Improves Efficiency and Kinetics of Reprogramming to Induced Pluripotent Stem Cells. Stem cells (Dayton, Ohio) 20 26523946
2017 PRDM14 directly interacts with heat shock proteins HSP90α and glucose-regulated protein 78. Cancer science 19 29178343
2019 PRDM14 and BLIMP1 control the development of chicken primordial germ cells. Developmental biology 18 31271752
2022 YAP1 and PRDM14 converge to promote cell survival and tumorigenesis. Developmental cell 17 34990589
2025 Maternal Exposure to Polystyrene Nanoplastics Disrupts Spermatogenesis in Mouse Offspring by Inducing Prdm14 Overexpression in Undifferentiated Spermatogonia. ACS nano 14 39791560
2020 The PRDM14-CtBP1/2-PRC2 complex regulates transcriptional repression during the transition from primed to naïve pluripotency. Journal of cell science 14 32661086
2021 Treatment of primary and metastatic breast and pancreatic tumors upon intravenous delivery of a PRDM14-specific chimeric siRNA/nanocarrier complex. International journal of cancer 12 33783816
2015 Histone demethylation maintains Prdm14 and Tsix expression and represses xIst in embryonic stem cells. PloS one 12 25993097
2021 LncRNA DNAJC3-AS1 functions as oncogene in renal cell carcinoma via regulation of the miR-27a-3p/PRDM14 axis. European review for medical and pharmacological sciences 10 33629299
2020 PRDM14 mediates chemosensitivity and glycolysis in drug‑resistant A549/cisplatin cells and their progenitor A549 human lung adenocarcinoma cells. Molecular medicine reports 9 33355367
2019 Co-option of the PRDM14-CBFA2T complex from motor neurons to pluripotent cells during vertebrate evolution. Development (Cambridge, England) 9 30630825
2019 Off to a Bad Start: Cancer Initiation by Pluripotency Regulator PRDM14. Trends in genetics : TIG 9 31130394
2018 PRDM14 is overexpressed in chronic pancreatitis prior to pancreatic cancer. FEBS open bio 9 30338223
2012 Mouse Lymphoblastic Leukemias Induced by Aberrant Prdm14 Expression Demonstrate Widespread Copy Number Alterations Also Found in Human ALL. Cancers 9 23487523
2019 The Pluripotency Regulator PRDM14 Requires Hematopoietic Regulator CBFA2T3 to Initiate Leukemia in Mice. Molecular cancer research : MCR 8 31015254
2018 PRDM14, a Zinc Finger Protein, Regulates Cancer Stemness. Methods in molecular biology (Clifton, N.J.) 8 30155811
2016 PRDM14 promotes RAG-dependent Notch1 driver mutations in mouse T-ALL. Biology open 8 27106930
2016 PRDM14 inhibits 293T cell proliferation by influencing the G1/S phase transition. Gene 8 27693212
2010 [Relationship between the expression of PRDM14 in non-small cell lung cancer and the clinicopathologic characteristics]. Zhongguo fei ai za zhi = Chinese journal of lung cancer 8 20840815
2018 PRDM14, a putative histone methyl-transferase, interacts with and decreases the stability and activity of the HOXA1 transcription factor. Biochimica et biophysica acta. Gene regulatory mechanisms 7 29471045
2018 PRDM14: A Potential Target for Cancer Therapy. Current cancer drug targets 6 29714146
2024 PRDM14 extinction enables the initiation of trophoblast stem cell formation. Cellular and molecular life sciences : CMLS 4 38710919
2019 Silencing PRDM14 via Oligonucleotide Therapeutics Suppresses Tumorigenicity and Metastasis of Breast Cancer. Methods in molecular biology (Clifton, N.J.) 4 31099008
2015 Identification and Characterization of a PRDM14 Homolog in Japanese Flounder (Paralichthys olivaceus). International journal of molecular sciences 4 25915026
2025 PRDM14 is essential for vertebrate gastrulation and safeguards avian germ cell identity. Developmental biology 3 39938772
2022 Prdm14 promotes mouse ESC self-renewal and PGCLC specification through enhancement of Stat3 activity. iScience 3 36300005
2018 Effects of PRDM14 Silencing on Parthenogenetically Activated Porcine Embryos. Cellular reprogramming 2 30325654
2016 A Pluripotency Platform for Prdm14. Developmental cell 2 27404351
2012 Epigenetic reprogramming: Prdm14 hits the accelerator. The EMBO journal 2 22522701
2025 Lineage-specific enhancer insertions regulate Prdm14 to drive the rapid transition from naïve to formative pluripotency in rodents. Development (Cambridge, England) 1 41267649
2024 Inhibition of protein kinase C increases Prdm14 level to promote self-renewal of embryonic stem cells through reducing Suv39h-induced H3K9 methylation. The Journal of biological chemistry 1 38309502
2025 Functional and molecular single-cell analyses implicate PRDM14 in the initiation of B cell leukemia in mice. Scientific reports 0 40087379
2025 PRDM14 promoted NSCLC cell proliferation, migration and invasion via modulating H3K27me3-mediated PEBP1/Raf-1/MEK/ERK MAPK signaling. Genes & genomics 0 40856954
2025 PRDM14 promotes the bovine somatic stem cell reprogramming through enhancing oxidative phosphorylation at the initial stage. Gene 0 41448293

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