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ZBTB38

Zinc finger and BTB domain-containing protein 38 · UniProt Q8NAP3

Length
1195 aa
Mass
134.3 kDa
Annotated
2026-06-11
33 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ZBTB38 (CIBZ) is a methyl-CpG-binding transcriptional regulator that reads DNA methylation through two independent sets of zinc fingers and controls developmental gene expression, cell proliferation, and apoptosis (PMID:21625269, PMID:30355731, PMID:35297517). Its N-terminal and C-terminal zinc-finger arrays each recognize a distinct methylated CpG consensus, with the C-terminal fingers (ZF6–9) binding methylated DNA at high affinity via base-specific contacts from ZF7 and ZF8 while ZF6 and ZF9 provide structural stabilization, a methyl-CpG recognition mode distinct from other zinc-finger methyl readers (PMID:29287967, PMID:30355731). Genome-wide, ZBTB38 occupies methylated sites in largely closed chromatin and upstream of active CpG islands (PMID:36000449). It functions principally as a methylation-dependent repressor, associating with the CtBP corepressor through a PLDLR motif and acting through both HDAC-dependent and HDAC-independent repression domains (PMID:16115196), and represses methylated promoters of myogenic and mesendodermal regulators including Myogenin, Brachyury (T), and Mesp1 to restrain differentiation (PMID:21625269, PMID:27659197). ZBTB38 supports proliferation and pluripotency by sustaining Nanog and Sox2, and its heterozygous loss in mice causes peri-implantation lethality from reduced epiblast proliferation and increased apoptosis (PMID:22315219, PMID:35297517). The protein is a node controlling apoptosis and stress responses: it is a direct caspase-3 substrate whose depletion triggers mitochondrial p53-independent apoptosis (PMID:18375381), it transcriptionally activates the anti-apoptotic factor XIAP via E-box binding (PMID:41842907), and its abundance is governed post-translationally by RBBP6-mediated ubiquitination/destabilization and USP9X-mediated deubiquitination/stabilization, the latter linking it to oxidative-stress control (PMID:24726359, PMID:29490077). Through these axes ZBTB38 also influences DNA replication by limiting MCM10 (PMID:24726359), autophagy initiation via RB1CC1/FIP200 (PMID:30075197), and responses to DNA methyltransferase inhibitors (PMID:30310057).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2005 High

    Established how ZBTB38 represses transcription by defining its corepressor partner and the motif required for that interaction, framing it as a recruiter of CtBP-based repression machinery.

    Evidence Co-IP, PLDLR motif mutagenesis, heterologous DNA-targeting repression assay and immunofluorescence

    PMID:16115196

    Open questions at the time
    • Did not link CtBP recruitment to specific endogenous target genes
    • HDAC-independent BTB repression mechanism not resolved at the molecular level
  2. 2008 High

    Showed ZBTB38 is a direct caspase-3 substrate and that its loss triggers mitochondrial apoptosis, placing it as a pro-survival factor cleaved during cell death.

    Evidence In vitro caspase-3 cleavage with cleavage-site mutagenesis, siRNA knockdown, apoptosis and caspase assays in p53-/- cells

    PMID:18375381

    Open questions at the time
    • Transcriptional targets mediating the anti-apoptotic effect not identified at this stage
    • Functional consequence of caspase cleavage products unknown
  3. 2011 High

    Demonstrated methylation-dependent target repression in a developmental context, showing ZBTB38 binds the methylated Myog promoter to restrain myogenic differentiation without demethylation.

    Evidence ChIP, luciferase reporter, loss/gain-of-function and differentiation assays in C2C12 cells

    PMID:21625269

    Open questions at the time
    • Did not define the consensus motif recognized at the Myog promoter
    • Corepressor requirement at this locus not tested
  4. 2012 Medium

    Connected ZBTB38 to proliferation control in pluripotent cells via post-transcriptional maintenance of Nanog, advancing it from a repressor to a regulator of stem-cell cycle progression.

    Evidence siRNA knockdown, deletion, overexpression, cell-cycle analysis and Nanog rescue in ESCs

    PMID:22315219

    Open questions at the time
    • Mechanism by which ZBTB38 maintains Nanog protein not defined
    • Only partial rescue, implying additional effectors
  5. 2014 High

    Identified post-translational control of ZBTB38 abundance and a downstream replication target, linking RBBP6-driven degradation to MCM10 levels and fork stability.

    Evidence Ubiquitination assays, RBBP6/ZBTB38 knockdown, ChIP, DNA fiber and common fragile site FISH

    PMID:24726359

    Open questions at the time
    • Whether MCM10 regulation is direct or methylation-dependent not fully resolved
    • Cell-type generality of the RBBP6 axis untested
  6. 2016 High

    Extended ZBTB38's developmental repression to germ-layer specification, showing it directly silences Brachyury and Mesp1 to suppress mesoderm and cardiomyocyte differentiation.

    Evidence ChIP, luciferase, ESC knockout/overexpression and cardiomyocyte differentiation assays

    PMID:27659197

    Open questions at the time
    • Methylation status of these promoters during differentiation not detailed
    • Corepressor dependence not addressed
  7. 2017 Medium

    Defined the biochemical basis of ZBTB38's C-terminal zinc-finger methyl-CpG selectivity and showed these fingers occupy cognate promoters in a methylation-dependent manner.

    Evidence Fluorescence polarization binding, SAXS modeling, ChIP and expression analysis

    PMID:29287967

    Open questions at the time
    • Atomic basis of recognition not yet resolved
    • Relative in vivo contribution of N- vs C-terminal fingers unquantified
  8. 2017 Medium

    Placed ZBTB38 downstream of ER-stress signaling by showing ATF4 directly activates its transcription, with reduced binding after spinal cord injury exacerbating apoptosis.

    Evidence ChIP-qPCR and lentiviral ZBTB38 rescue in an SCI mouse model with apoptosis and motor readouts

    PMID:28514761

    Open questions at the time
    • Direct ZBTB38 targets mediating the SCI phenotype not defined
    • Generality beyond the injury model untested
  9. 2018 High

    Provided atomic-resolution insight into methyl-CpG readout, defining how ZF7/ZF8 make base-specific contacts at the methylated CpG while ZF6/ZF9 stabilize binding.

    Evidence 1.75 A crystal structure with bound methylated DNA, NMR and EMSA

    PMID:30355731

    Open questions at the time
    • Structure of the N-terminal ZF array bound to its consensus not solved
    • Allosteric coordination between the two ZF arrays unknown
  10. 2018 High

    Revealed stabilizing post-translational control opposing RBBP6, with USP9X deubiquitinating ZBTB38 and the axis buffering oxidative stress.

    Evidence Co-IP, MS interactor identification, deubiquitination and ubiquitination assays, ROS measurements with knockdowns

    PMID:29490077

    Open questions at the time
    • Transcriptional targets linking ZBTB38 to ROS control not identified
    • Crosstalk timing between RBBP6 and USP9X not resolved
  11. 2018 Medium

    Linked ZBTB38 to inflammation by showing it represses the methylated IL1r2 promoter, bridging an arthritis-associated epimutation to anti-inflammatory gene silencing.

    Evidence ChIP and expression/methylation correlation in a murine RA model

    PMID:30343694

    Open questions at the time
    • Single-lab study with limited mechanistic follow-up
    • Causality between the epimutation and phenotype not established in vivo
  12. 2018 Medium

    Connected ZBTB38 to DNA methyltransferase inhibitor sensitivity, showing its depletion enhances DNMTi toxicity partly via CDKN1C upregulation.

    Evidence siRNA knockdown, viability assays and CDKN1C RT-PCR across multiple cancer lines

    PMID:30310057

    Open questions at the time
    • Whether CDKN1C is a direct ZBTB38 target not established
    • Mechanism of DNMTi-induced ZBTB38 downregulation unknown
  13. 2021 Medium

    Showed ZBTB38 can act as a positive regulator, promoting DKK1 expression to suppress prostate cancer cell migration, and identified PRKDC as an interactor repressing its function.

    Evidence ChIP, DKK1 rescue, Co-IP for PRKDC, migration/proliferation assays

    PMID:34697293

    Open questions at the time
    • Mechanism of activation versus repression at different loci unresolved
    • How PRKDC represses ZBTB38 function not defined
  14. 2022 Medium

    Mapped ZBTB38 genome-wide, validating both ZF consensus motifs in vivo and showing predominant binding in closed chromatin with partial CTCF overlap.

    Evidence ChIP-seq in a human cell line with ENCODE chromatin/TF intersection

    PMID:36000449

    Open questions at the time
    • Functional consequence of binding in closed chromatin unclear
    • Single cell-line dataset
  15. 2022 High

    Established ZBTB38's essential developmental role in vivo, with heterozygous loss causing peri-implantation lethality through reduced epiblast proliferation and Nanog/Sox2 loss.

    Evidence Cre-loxP knockout, proliferation/apoptosis IF, Nanog/Sox2 qRT-PCR/WB, ESC derivation

    PMID:35297517

    Open questions at the time
    • Direct versus indirect regulation of Nanog/Sox2 in embryo not resolved
    • Reason for haploinsufficiency not explained
  16. 2024 Medium

    Linked ZBTB38 to autophagy initiation by identifying RB1CC1/FIP200 as a transcriptional target whose restoration rescues the autophagy block and proliferation upon ZBTB38 loss.

    Evidence siRNA knockdown, LC3B/p62 WB, transcriptome sequencing and RB1CC1 rescue

    PMID:30075197

    Open questions at the time
    • Directness of RB1CC1 promoter regulation not shown by ChIP
    • Whether autophagy effect is methylation-dependent unknown
  17. 2026 Medium

    Defined the anti-apoptotic transcriptional effector of ZBTB38, showing it activates XIAP via E-box binding to rescue apoptosis from its loss, independent of p53.

    Evidence Knockdown/overexpression, ChIP at XIAP regulatory regions, XIAP rescue and apoptosis assays in ESC and cancer cells

    PMID:41842907

    Open questions at the time
    • Relationship between E-box (XIAP) activation and methyl-CpG repression modes unresolved
    • Single study
  18. 2026 Medium

    Characterized the N-terminal ZF domain's methyl-discriminating recognition, showing it requires the methyl group and an additional finger for stable engagement, distinguishing ZBTB38 from ZBTB33 and ZBTB4.

    Evidence Fluorescence polarization binding and systematic ZF mutagenesis with mCpG versus TpG oligonucleotides (preprint)

    PMID:42146383

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Structure of N-terminal ZF-DNA complex not determined
    • In vivo significance of the two distinct consensus motifs not functionally separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ZBTB38 switches between methylation-dependent repression and target activation (e.g. DKK1, XIAP), and how its two distinct ZF consensus motifs and post-translational regulators are coordinated across developmental, stress, and disease contexts, remains unresolved.
  • No unified model reconciling repressor and activator functions
  • Locus-specific corepressor versus coactivator recruitment not mapped
  • Integration of RBBP6/USP9X/PRKDC inputs into target selection unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 4 GO:0140110 transcription regulator activity 4
Localization
GO:0000228 nuclear chromosome 1 GO:0005634 nucleus 1
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-69306 DNA Replication 1 R-HSA-9612973 Autophagy 1
Partners
CTBPPRKDCRBBP6USP9X

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 ZBTB38 (CIBZ) physically associates with the transcriptional corepressor CtBP via a conserved PLDLR motif. CIBZ represses transcription through two independent repression domains: an N-terminal BTB domain (HDAC-independent) and a PLDLR-containing RD2 region (HDAC-dependent). CIBZ redistributes CtBP from diffuse nuclear localization to pericentromeric foci; mutation of the PLDLR motif abolishes CtBP interaction, RD2 repression activity, and pericentromeric targeting of CtBP, but not CIBZ's own localization to pericentromeric foci. Co-immunoprecipitation, site-directed mutagenesis of PLDLR motif, heterologous DNA-targeting transcriptional repression assay, immunofluorescence localization Genes to cells : devoted to molecular & cellular mechanisms High 16115196
2008 ZBTB38 (CIBZ) is a direct substrate of caspase-3: in vitro caspase cleavage assays with mutagenesis identified two caspase-3 recognition sites in CIBZ. Knockdown of CIBZ induces apoptosis through the mitochondrial pathway (activating caspases-3, -7, and -9 and PARP cleavage) in a p53-independent manner. In vitro caspase-3 cleavage assay, site-directed mutagenesis of caspase recognition sites, siRNA knockdown, annexin V/PI flow cytometry, caspase activation assays in p53-/- cells The Journal of biological chemistry High 18375381
2011 ZBTB38 (CIBZ) binds to a methylated CpG-containing proximal region of the Myogenin (Myog) promoter and represses Myog transcription in a DNA methylation-dependent manner, thereby suppressing myogenic differentiation. Loss of CIBZ promotes myogenic differentiation; ectopic CIBZ expression impairs it. Importantly, CIBZ-mediated repression does not require demethylation of the Myog promoter CpGs. siRNA knockdown and ectopic overexpression in C2C12 cells, chromatin immunoprecipitation (ChIP), luciferase reporter assay, myogenic differentiation assays in vitro and in vivo Cell research High 21625269
2012 ZBTB38 (CIBZ) promotes ESC proliferation and G1/S transition at least in part by post-transcriptionally maintaining Nanog protein levels. CIBZ deletion or siRNA knockdown inhibits ESC proliferation and delays G1/S transition; ectopic CIBZ expression accelerates it. Constitutive overexpression of Nanog partially rescues the proliferation defect caused by CIBZ knockdown. siRNA knockdown, CIBZ deletion, ectopic overexpression in ESCs, cell cycle analysis, Nanog rescue experiment, western blotting The Journal of biological chemistry Medium 22315219
2014 RBBP6 (an E3 ubiquitin ligase) ubiquitinates ZBTB38, destabilizing it. ZBTB38 in turn negatively regulates transcription and chromatin-associated levels of the MCM10 replication factor. Cells lacking RBBP6 accumulate ZBTB38, which causes MCM10 downregulation, reduced replication fork progression, and increased DNA damage at common fragile sites. Ubiquitination assays, siRNA knockdown of RBBP6 and ZBTB38, ChIP, DNA fiber assay for replication fork speed, FISH for common fragile site stability Cell reports High 24726359
2016 ZBTB38 (CIBZ) binds directly to the promoters of Brachyury (T) and Mesp1 in undifferentiated ESCs, repressing their transcription and thereby suppressing mesodermal and cardiac differentiation. Loss of CIBZ induces mesoderm specification and cardiomyocyte differentiation; overexpression delays these processes. ChIP assay, luciferase reporter assay, CIBZ knockout and overexpression in ESCs, differentiation assays toward cardiomyocytes Scientific reports High 27659197
2017 ZBTB38's C-terminal zinc fingers (ZFs 6–9) exhibit high-affinity, methyl-CpG-selective DNA binding to a consensus sequence distinct from the N-terminal ZF consensus. These C-terminal ZFs can directly occupy promoters containing this motif in cells in a DNA methylation-dependent manner and modulate transcriptional responses at those loci. Fluorescence polarization DNA binding assays, small-angle X-ray scattering (SAXS) structural modeling, ChIP in cell lines, gene expression analysis Journal of molecular biology Medium 29287967
2017 ATF4 (an ER-stress-inducible transcription factor) directly activates ZBTB38 transcription by binding to the ZBTB38 promoter under normal conditions; this binding is significantly reduced following spinal cord injury, causing decreased ZBTB38 expression and increased ER stress-associated apoptosis. ChIP-qPCR, lentiviral overexpression of ZBTB38 in SCI mouse model, apoptosis assays, motor function assessment Oncotarget Medium 28514761
2018 Crystal structure of ZBTB38 C-terminal zinc fingers 6–9 in complex with a methylated consensus DNA sequence (1.75 Å resolution) reveals that methyl-selective binding is mediated by base-specific interactions from residues in the α-helices of ZF7 and ZF8 at the 5' mCpG site, while ZF6 and ZF9 serve structural stabilization roles. This represents a mode of mCpG recognition distinct from other ZF methyl-CpG binding proteins. X-ray crystallography (1.75 Å), solution NMR spectroscopy, electrophoretic mobility shift assay (EMSA) The Journal of biological chemistry High 30355731
2018 The deubiquitinase USP9X interacts with ZBTB38, deubiquitinates it, and stabilizes it. USP9X is itself stabilized by oxidative stress. The USP9X/ZBTB38 axis limits basal ROS production and is required for the cellular response to acute oxidative stress; loss of either protein increases ROS toxicity. Co-immunoprecipitation, ubiquitination assay, mass spectrometry identification of USP9X as ZBTB38 interactor, siRNA knockdown of USP9X and ZBTB38, ROS measurement assays Nucleic acids research High 29490077
2018 ZBTB38 binds methylated promoters of IL1r2 (interleukin-1 receptor 2) in B cells and represses IL1r2 transcription, forming a molecular bridge between an arthritis-associated DNA hypomethylation epimutation at the Zbtb38 locus and silencing of an anti-inflammatory gene. ChIP, gene expression studies, correlation of Zbtb38 promoter methylation with IL1r2 expression in a murine RA model Biochimica et biophysica acta. Gene regulatory mechanisms Medium 30343694
2018 ZBTB38 regulates the cellular response to DNA methyltransferase inhibitors (DNMTi; 5-azacytidine, decitabine, zebularine): DNMTi treatment causes ZBTB38 protein downregulation. ZBTB38 depletion enhances DNMTi toxicity, and this effect is mediated at least in part through upregulation of CDKN1C mRNA. siRNA knockdown of ZBTB38, western blotting, cell viability assays, RT-PCR for CDKN1C in multiple cancer cell lines Oncogenesis Medium 30310057
2021 ZBTB38 binds the DKK1 (Dickkopf WNT signaling pathway inhibitor 1) locus and promotes DKK1 expression in prostate cancer cells. Reduction of DKK1 rescues ZBTB38-mediated suppression of migration and proliferation. PRKDC (DNA-PKcs) was identified as a ZBTB38-interacting protein that represses ZBTB38 function. ChIP demonstrating ZBTB38 binding to DKK1 promoter, DKK1 knockdown rescue experiments, Co-IP identifying PRKDC as interactor, cell migration and proliferation assays Cell death & disease Medium 34697293
2022 ZBTB38 binds methylated CpG-containing sequences in vivo at two classes of consensus sites (corresponding to its N-terminal and C-terminal ZF domains). Approximately 10% of ZBTB38 binding sites overlap with CTCF binding, while 90% reside in closed chromatin not occupied by other mapped factors; ~one-third of ZBTB38 sites are found upstream of long active CpG islands. ChIP-seq in human cell line, intersection with ENCODE datasets for chromatin state and other TF binding Epigenetics Medium 36000449
2022 Heterozygous loss of Zbtb38 in mice leads to early embryonic lethality shortly after implantation due to reduced epiblast proliferation and increased apoptosis. This is associated with reduced expression of Nanog and Sox2. Zbtb38 is dispensable for ESC establishment and identity in vitro. Conditional knockout via Cre-loxP, immunofluorescence for proliferation and apoptosis markers, qRT-PCR and western blotting for Nanog/Sox2, ESC derivation from knockout embryos Cell proliferation High 35297517
2024 ZBTB38 regulates autophagy initiation: ZBTB38 knockdown blocks autophagy (decreased LC3B II/I ratio, increased p62). RB1CC1/FIP200, a key component of the autophagy initiation complex, is transcriptionally regulated by ZBTB38 and decreases ~4.2-fold upon ZBTB38 knockdown. Overexpression of RB1CC1 in ZBTB38-knockdown cells rescues the autophagy block and restores cell proliferation. ZBTB38 siRNA knockdown, LC3B/p62 western blotting, transcriptome sequencing, RB1CC1 rescue overexpression, lentiviral ZBTB38 overexpression in SCI mouse model Gene Medium 30075197
2026 Zbtb38 transcriptionally activates XIAP by binding E-box motifs within the upstream regulatory regions of the XIAP gene. XIAP overexpression rescues apoptosis induced by Zbtb38 knockdown, indicating that Zbtb38-associated anti-apoptotic function is at least partially XIAP-dependent. This operates independently of p53 status. Loss- and gain-of-function experiments (siRNA knockdown and overexpression), ChIP for ZBTB38 binding to XIAP regulatory regions, XIAP rescue overexpression, apoptosis assays in ESC differentiation and cancer cell lines Journal of molecular cell biology Medium 41842907
2026 The N-terminal zinc finger (ZF) domain of ZBTB38 defines a distinct mCpG-containing consensus DNA sequence for binding. Unlike the other two ZBTB MBP family members (ZBTB33/Kaiso and ZBTB4), the shared core ZF domain of ZBTB38 discriminates against TpG-containing DNA (i.e., requires the methyl group), and at least one additional N-terminal ZF is required to stabilize DNA engagement. Each ZF domain preferentially recognizes its own cognate methylated consensus motif. Fluorescence polarization DNA binding assays, systematic mutagenesis of ZF domains, in vitro binding with mCpG vs. TpG-containing oligonucleotides bioRxiv : the preprint server for biologypreprint Medium 42146383

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 The RBBP6/ZBTB38/MCM10 axis regulates DNA replication and common fragile site stability. Cell reports 61 24726359
2011 The methyl-CpG-binding protein CIBZ suppresses myogenic differentiation by directly inhibiting myogenin expression. Cell research 43 21625269
2005 Identification of a novel BTB-zinc finger transcriptional repressor, CIBZ, that interacts with CtBP corepressor. Genes to cells : devoted to molecular & cellular mechanisms 40 16115196
2008 Down-regulation of CIBZ, a novel substrate of caspase-3, induces apoptosis. The Journal of biological chemistry 34 18375381
2012 CtBP-interacting BTB zinc finger protein (CIBZ) promotes proliferation and G1/S transition in embryonic stem cells via Nanog. The Journal of biological chemistry 24 22315219
2018 Stabilization of the methyl-CpG binding protein ZBTB38 by the deubiquitinase USP9X limits the occurrence and toxicity of oxidative stress in human cells. Nucleic acids research 23 29490077
2017 The C-Terminal Zinc Fingers of ZBTB38 are Novel Selective Readers of DNA Methylation. Journal of molecular biology 21 29287967
2021 ZBTB38 suppresses prostate cancer cell proliferation and migration via directly promoting DKK1 expression. Cell death & disease 19 34697293
2018 Structural insights into methylated DNA recognition by the C-terminal zinc fingers of the DNA reader protein ZBTB38. The Journal of biological chemistry 18 30355731
2018 The role of ZBTB38 in promoting migration and invasive growth of bladder cancer cells. Oncology reports 18 30569128
2016 CIBZ Regulates Mesodermal and Cardiac Differentiation of by Suppressing T and Mesp1 Expression in Mouse Embryonic Stem Cells. Scientific reports 17 27659197
2010 Molecular characterization, polymorphism of bovine ZBTB38 gene and association with body measurement traits in native Chinese cattle breeds. Molecular biology reports 17 20237851
2017 Tauroursodeoxycholic acid alleviates secondary injury in the spinal cord via up-regulation of CIBZ gene. Cell stress & chaperones 16 29151236
2012 CIBZ, a novel BTB domain-containing protein, is involved in mouse spinal cord injury via mitochondrial pathway independent of p53 gene. PloS one 16 22427977
2018 Transcription factor Zbtb38 downregulates the expression of anti-inflammatory IL1r2 in mouse model of rheumatoid arthritis. Biochimica et biophysica acta. Gene regulatory mechanisms 15 30343694
2018 DNA Methylation and Chromatin: Role(s) of Methyl-CpG-Binding Protein ZBTB38. Epigenetics insights 14 30480223
2018 Depletion of ZBTB38 potentiates the effects of DNA demethylating agents in cancer cells via CDKN1C mRNA up-regulation. Oncogenesis 13 30310057
2017 Zbtb38 is a novel target for spinal cord injury. Oncotarget 13 28514761
2018 The associations of two SNPs in miRNA-146a and one SNP in ZBTB38-RASA2 with the disease susceptibility and the clinical features of the Chinese patients of sCJD and FFI. Prion 12 29216791
2013 An SNP of the ZBTB38 gene is associated with idiopathic short stature in the Chinese Han population. Clinical endocrinology 11 23302005
2022 Context-dependent CpG methylation directs cell-specific binding of transcription factor ZBTB38. Epigenetics 10 36000449
2022 Heterozygous loss of Zbtb38 leads to early embryonic lethality via the suppression of Nanog and Sox2 expression. Cell proliferation 9 35297517
2019 Transcriptome profiling reveals the role of ZBTB38 knock-down in human neuroblastoma. PeerJ 8 30697495
2018 ZBTB38, a novel regulator of autophagy initiation targeted by RB1CC1/FIP200 in spinal cord injury. Gene 6 30075197
2022 Role of ZBTB38 Genotype and Expression in Growth and Response to Recombinant Human Growth Hormone Treatment. Journal of the Endocrine Society 5 35178492
2020 ZBTB38 is dispensable for antibody responses. PloS one 5 32956421
2023 Sex-specific DNA methylation and transcription of zbtb38 and effects of gene-environment interactions on its natural antisense transcript in zebrafish. Epigenetics 3 37782752
2012 ZBTB38 gene polymorphism associated with body measurement traits in native Chinese cattle breeds. Gene 3 23137638
2025 Epigenetic regulation of sex: the role of DNA methylation and zbtb38 in zebrafish sex differentiation and heat-induced masculinization. Molecular and cellular endocrinology 1 40759373
2024 Association of ZBTB38 gene polymorphism (rs724016) with height and fetal hemoglobin in individuals with sickle cell anemia. Molecular genetics and metabolism reports 1 38800625
2026 Zbtb38 transcriptionally activates XIAP to regulate apoptosis in development and cancer. Journal of molecular cell biology 0 41842907
2026 Circ-ZBTB38 as an oncogenic circular RNA: Mechanisms in disrupting RalGAP complexes and its clinical value in melanoma. Biochemical and biophysical research communications 0 41916004
2026 ZBTB38 requires an extended N-terminal zinc finger network to read mCpG- and discriminate TpG-containing DNA sequences. bioRxiv : the preprint server for biology 0 42146383

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