Affinage

ZBTB17

Zinc finger and BTB domain-containing protein 17 · UniProt Q13105

Length
803 aa
Mass
87.9 kDa
Annotated
2026-04-28
100 papers in source corpus 62 papers cited in narrative 62 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ZBTB17 (MIZ1) is a BTB/POZ zinc finger transcription factor that functions as a central transcriptional switch at initiator/core promoter elements, activating cell cycle inhibitors (p15INK4b, p21Cip1, p57Kip2), anti-apoptotic genes (BCL2, TMBIM4), and diverse targets including Dph1, Rpl22, and SOCS1, but converting to a transcriptional repressor when its coactivators (nucleophosmin, p300) are displaced by binding partners such as c-MYC, BCL6, Gfi-1, or MYCN, which recruit HDAC1 to silence target loci (PMID:11283613, PMID:16142238, PMID:19164764, PMID:21123453). MIZ1 also performs transcription-independent functions: it sequesters MTDH to suppress NF-κB signaling in hepatocytes, retains PRDX6 in the cytosol to permit Parkin-mediated mitophagy, and inhibits TRAF2 K63-linked polyubiquitination to restrain TNF-α-induced JNK1 activation (PMID:34038747, PMID:37040844, PMID:19815509). Post-translational regulation of MIZ1 includes Akt-mediated phosphorylation enabling 14-3-3η binding to block DNA binding, Ser178 phosphorylation enabling HDAC1 recruitment for inflammatory gene repression, and K48-linked polyubiquitination by Mule/HUWE1 targeting MIZ1 for proteasomal degradation downstream of TNF-α or viral infection (PMID:15580267, PMID:23525087, PMID:20624960, PMID:38593156). Homozygous Miz1 knockout in mice is embryonic lethal at E7.5 due to ectodermal apoptosis, and tissue-specific loss causes lineage-specific defects including loss of B and T cell progenitors via impaired IL-7R/STAT5 signaling, cerebellar neurodegeneration from defective autophagy, peripheral neuropathy, and COPD-like lung inflammation (PMID:14560010, PMID:21167753, PMID:24088869, PMID:29217679, PMID:32851183).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1997 Medium

    Identification of MIZ1 as a zinc finger transcriptional activator that physically interacts with Myc established the foundational concept that Myc can repress transcription through a partner distinct from Max.

    Evidence Yeast two-hybrid, co-IP, and reporter assays in two independent studies

    PMID:9256341 PMID:9308237

    Open questions at the time
    • No endogenous target genes identified yet
    • Mechanism of Myc-mediated repression through MIZ1 undefined
  2. 2001 High

    Discovery that MIZ1 binds initiator elements of p15INK4b and activates its transcription — with Myc/Max displacing coactivators to repress it — and that TGFβ/Smad signaling relieves this repression, established MIZ1 as a signal-integrating transcriptional platform at CDK inhibitor promoters.

    Evidence ChIP, reporter assays, Myc point mutants, primary MEF phenotypes, Smad epistasis across companion papers

    PMID:11283613 PMID:11283614

    Open questions at the time
    • MIZ1 DNA-binding specificity/consensus not yet defined
    • Whether this mechanism extends to other CKI promoters unknown
  3. 2002 High

    Extension to p21Cip1 and identification of p300 and TopBP1 as coactivator and negative regulator, respectively, revealed a general mechanism: MIZ1 activates CKI transcription at core promoters, with Myc and other repressors competing for coactivator binding sites.

    Evidence ChIP in c-myc−/− cells, MycV394D mutant, UV irradiation, Nramp1 promoter competition assays

    PMID:12110671 PMID:12408820

    Open questions at the time
    • Whether p300 displacement is sufficient or HDAC recruitment is also required
    • Full set of MIZ1 coactivators not determined
  4. 2003 High

    Miz1 knockout lethality at E7.5 with ectodermal apoptosis and loss of p57Kip2 demonstrated that MIZ1 is essential for embryonic survival and has gene-specific, non-redundant transcriptional functions in vivo.

    Evidence Homologous recombination knockout, in situ hybridization, immunostaining in mouse embryos

    PMID:14560010

    Open questions at the time
    • Which of many possible target genes mediate the apoptosis phenotype
    • Tissue-specific functions beyond ectoderm undefined
  5. 2004 High

    Discovery that Akt phosphorylates MIZ1 to enable 14-3-3η binding and inhibit DNA binding revealed the first post-translational regulatory mechanism controlling MIZ1 activity, linking growth factor signaling to DNA damage checkpoint recovery.

    Evidence Kinase assays, co-IP, domain mapping, cell-cycle analysis

    PMID:15580267

    Open questions at the time
    • Specific phosphorylation sites on MIZ1 not fully mapped
    • Whether other kinases regulate MIZ1 unknown
  6. 2005 High

    Demonstration that BCL6 binds MIZ1 to repress p21 in germinal center B cells, and that Myc inactivation of MIZ1 is specifically required for Myc-induced apoptosis (via BCL2 repression) but dispensable for proliferation, functionally separated MIZ1-dependent transcriptional programs.

    Evidence Reciprocal co-IP, ChIP, MycV394D separation-of-function mutant, shRNA, BCL2 inhibitor rescue

    PMID:16142238 PMID:16352593 PMID:17082179

    Open questions at the time
    • How BCL6 versus Myc are differentially recruited to MIZ1 at overlapping promoters
    • Role of MIZ1 in lymphomagenesis not yet tested in vivo
  7. 2007 High

    Crystal structure of the MIZ1 POZ domain revealing a tetrameric architecture with a novel β-sheet dimerization interface provided the structural basis for understanding MIZ1 oligomerization and heteromeric interactions with BCL6 and NAC1.

    Evidence X-ray crystallography at 2.1 Å with solution validation; later structures of heterodimers at 2.6 Å

    PMID:17880999 PMID:20493880 PMID:25484205

    Open questions at the time
    • No structure of full-length MIZ1 or MIZ1-DNA complex
    • How POZ tetramerization affects promoter binding in vivo unclear
  8. 2009 High

    Identification of a transcription-independent function — MIZ1 suppresses TNFα-induced JNK1 by inhibiting TRAF2 K63-linked ubiquitination, with TNFα triggering MIZ1 proteasomal degradation to relieve this suppression — established MIZ1 as a dual-function protein operating beyond transcription.

    Evidence Miz1−/− MEFs reconstituted with transcription-deficient mutant, TRAF2 ubiquitination assays, JNK assays

    PMID:19815509

    Open questions at the time
    • How MIZ1 inhibits TRAF2 ubiquitination mechanistically
    • Whether other non-transcriptional functions exist (later confirmed)
  9. 2010 High

    Mule/HUWE1 was identified as the E3 ligase catalyzing K48-linked polyubiquitination of MIZ1 at Lys388/Lys472 upon TNFα, providing the degradation mechanism that connects TNFα signaling to JNK1 de-repression; in vivo, Mule suppresses Ras-driven tumorigenesis by preventing accumulation of Myc/MIZ1 repressor complexes.

    Evidence In vitro ubiquitination with defined E3, mutagenesis of K388/K472, Mule siRNA, conditional KO mouse with genetic epistasis

    PMID:20624960 PMID:22184250 PMID:23699408

    Open questions at the time
    • Whether additional E3 ligases target MIZ1 in other contexts
    • Site-specific ubiquitination in non-TNFα settings not mapped
  10. 2010 High

    Conditional MIZ1 POZ-domain deletion in immune cells showed MIZ1 is essential for B and T cell development by repressing SOCS1 to enable IL-7R/STAT5 signaling and BCL2 expression, establishing MIZ1 as a master regulator of lymphocyte survival.

    Evidence Conditional Zbtb17ΔPOZ/ΔPOZ knockout, ChIP, STAT5 phosphorylation, genetic rescue with Bcl2 and SOCS1 siRNA

    PMID:21167753 PMID:21258009

    Open questions at the time
    • Whether MIZ1 regulates additional cytokine receptor pathways beyond IL-7R
    • MIZ1 role in mature lymphocyte function not yet explored
  11. 2013 High

    Genome-wide ChIP-seq defined the MIZ1 binding consensus and revealed targets in autophagy and vesicular transport; CNS-specific POZ deletion caused defective autophagic flux and cerebellar neurodegeneration, while Ser178 phosphorylation was shown to recruit HDAC1 for inflammatory gene repression.

    Evidence ChIP-seq, conditional Nestin-Cre KO with autophagy flux assays, phospho-site mutagenesis, ChIP for HDAC1

    PMID:23525087 PMID:24088869

    Open questions at the time
    • Identity of kinase phosphorylating Ser178 not determined
    • Whether autophagy regulation is direct or indirect through target genes
  12. 2016 High

    NMR structure of MIZ1 zinc fingers 3–4 revealed an autoinhibitory compact fold restricting DNA binding, explaining how MIZ1 achieves sequence specificity during promoter scanning; concurrently, the Myc/MIZ1 interaction was shown to distinguish medulloblastoma subgroups and repress circadian clock genes.

    Evidence NMR, A86K mutagenesis, MycV394D mouse tumor models, ChIP, gene expression profiling

    PMID:26766587 PMID:27339797 PMID:28035002

    Open questions at the time
    • Full-length ZF domain–DNA co-structure not available
    • Whether autoinhibition is relieved by partner binding
  13. 2020 High

    MIZ1 was shown to suppress NF-κB in lung epithelium (loss causing COPD-like disease rescued by RelA heterozygosity), to maintain AML stem cells through Myc/MIZ1-mediated Cebpα/δ repression, and to activate Dph1 transcription for diphthamide biosynthesis — expanding MIZ1 functions to innate immunity, leukemia maintenance, and translational fidelity.

    Evidence Conditional KO with RelA compound KO, MycV394D AML model, genome-wide CRISPR screen with ChIP

    PMID:32040550 PMID:32851183 PMID:33057331

    Open questions at the time
    • Mechanism by which MIZ1 suppresses NF-κB in lung (direct or MTDH-mediated)
    • Whether Dph1 regulation is conserved across tissues
  14. 2021 High

    Two additional transcription-independent functions were established: MIZ1 sequesters MTDH to suppress NF-κB in hepatocytes (preventing HCC), and the MYC/MIZ1 complex suppresses TLR3-mediated dsRNA recognition and MHC-I expression to enable PDAC immune evasion.

    Evidence Hepatocyte-specific KO with MTDH co-IP, PDAC mouse model with TBK1 epistasis

    PMID:34038747 PMID:34145038

    Open questions at the time
    • Whether MTDH sequestration operates in non-hepatic tissues
    • Structural basis of MIZ1-MTDH interaction unknown
  15. 2023 High

    MIZ1 was found to retain PRDX6 in the cytosol, preventing its interaction with mitochondrial Parkin and thereby permitting mitophagy; in NASH, TNFα-induced MIZ1 degradation releases PRDX6 to inhibit mitophagy, creating a pathological feed-forward loop.

    Evidence Co-IP/mass spectrometry, hepatocyte-specific KO, human NASH liver organoids, mitophagy assays

    PMID:37040844

    Open questions at the time
    • Whether PRDX6 sequestration occurs in non-hepatic tissues
    • How MIZ1-PRDX6 binding is regulated beyond MIZ1 degradation
  16. 2024 High

    MIZ1 was shown to induce TMBIM4 to control Ca²⁺ homeostasis in IgG1+ GC B cells during positive selection, and to epigenetically repress IFNα/β via HDAC1 recruitment — with viral CUL4B-mediated Mule degradation stabilizing MIZ1 to limit antiviral type I IFN responses.

    Evidence CRISPR screen in GC B cells with conditional genetics and Ca²⁺ assays; ChIP for HDAC1 at Ifn loci, Mule/CUL4B degradation pathway in IAV infection

    PMID:38579014 PMID:38593156

    Open questions at the time
    • Whether TMBIM4 induction is POZ-dependent
    • How CUL4B-Mule-MIZ1 axis is engaged by other viruses

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the full-length structure of MIZ1 bound to DNA, how POZ-domain tetramerization influences promoter selectivity in vivo, the complete catalog of non-transcriptional sequestration targets, and how tissue-specific cofactor availability determines whether MIZ1 activates or represses a given locus.
  • No full-length MIZ1–DNA co-crystal structure
  • Mechanism selecting activation versus repression at individual promoters in different tissues
  • Whether additional non-transcriptional binding partners remain to be discovered

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 8 GO:0003677 DNA binding 5 GO:0098772 molecular function regulator activity 3
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 3 GO:0005856 cytoskeleton 1 GO:0005929 cilium 1
Pathway
R-HSA-74160 Gene expression (Transcription) 7 R-HSA-162582 Signal Transduction 6 R-HSA-168256 Immune System 6 R-HSA-1640170 Cell Cycle 5 R-HSA-1266738 Developmental Biology 4 R-HSA-4839726 Chromatin organization 4 R-HSA-5357801 Programmed Cell Death 4 R-HSA-9612973 Autophagy 2
Partners
BCL6GFI1HDAC1HUWE1MTDHMYCNPM1TOPBP1
Complex memberships
BCL6/MIZ1 repressor complexGfi-1/MIZ1/MYC complexMYC/MIZ1 repressor complexSP1/MIZ1/MYCN/HDAC1 complex

Evidence

Reading pass · 62 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 Miz-1 (ZBTB17) was identified as a novel zinc finger protein that physically interacts with Msx2, enhancing its DNA-binding affinity for the osteocalcin promoter; Miz-1 itself functions as a sequence-specific DNA-binding transcriptional activator. Yeast two-hybrid screen, in vitro binding assay, gel shift/DNA binding assays, transcriptional reporter assays Mechanisms of development Medium 9256341
1997 Miz-1 associates with the carboxy-terminus of Myc and this interaction defines a pathway for transcriptional repression by Myc that is distinct from the Myc/Max complex. Yeast two-hybrid cloning, co-immunoprecipitation Current topics in microbiology and immunology Medium 9308237
2001 Miz-1 binds to the initiator element of the p15INK4b promoter and activates its transcription; Myc and Max form a complex with Miz-1 at this site to repress p15INK4b expression, thereby inhibiting G1 arrest. Myc alleles unable to bind Miz-1 fail to suppress p15INK4b accumulation and are deficient in cell immortalization. Chromatin immunoprecipitation, reporter assays, Myc point mutants, primary MEF cell-cycle analysis Nature cell biology High 11283613
2001 TGFβ signaling prevents recruitment of Myc to the p15INK4b initiator by Miz-1, relieving repression and allowing a Smad protein complex to contact Miz-1 and transactivate p15INK4b. Thus Miz-1 is a platform that integrates Myc-mediated repression and Smad-mediated activation at the p15INK4b promoter. Chromatin immunoprecipitation, reporter assays, dominant-negative Smad experiments, gel shift assays Nature cell biology High 11283614
2001 Miz-1 is regulated by association with microtubules; it is largely cytoplasmic but accumulates in the nucleus upon microtubule depolymerization. Miz-1 binds directly to the LDLR promoter and activates its transcription. Indirect immunofluorescence, soft X-ray microscopy, GFP time-lapse imaging, chromatin/promoter binding assays Molecular cell Medium 11545736
2002 Miz-1 binds to the p21Cip1 core promoter in vivo and is required for upregulation of p21Cip1 upon UV irradiation. Topoisomerase II binding protein (TopBP1) negatively regulates Miz-1 transactivation; UV downregulates TopBP1, releasing Miz-1 to activate p21Cip1. Myc binds Miz-1 at the p21Cip1 promoter to negatively regulate p21Cip1 expression after UV irradiation. ChIP, c-myc-/- cells, Myc Miz-1-binding point mutant (MycV394D), reporter assays, gene expression analysis Molecular cell High 12408820
2002 Miz-1 activates the Nramp1 promoter through initiator elements; c-Myc competes with p300/CBP for binding to Miz-1 to repress Nramp1 transcription. Reporter assays, co-transfection, promoter deletion analysis, RNAi The Journal of biological chemistry Medium 12110671
2002 Host cell factor-1 (HCF-1) directly binds to Miz-1, targeting its transactivation domain; HCF-1 represses Miz-1-mediated p15INK4b promoter activation by interfering with recruitment of the coactivator p300 to Miz-1. Co-immunoprecipitation, GST pulldown, reporter assays, protein-protein interaction domain mapping The Journal of biological chemistry Medium 12244100
2003 Miz1 homologous knockout in mice causes lethality at E7.5 due to massive apoptosis of ectodermal cells and failure to undergo normal gastrulation; p57Kip2 (a Miz1 target gene) is absent in Miz1-/- embryos, while p21Cip1 expression is unaltered, indicating gene-specific transcriptional requirements. Homologous recombination/gene targeting, in situ hybridization, immunostaining Molecular and cellular biology High 14560010
2003 IRF-8 interacts with Miz-1 in immune cells; together with PU.1, this complex binds the Nramp1 promoter and mediates its macrophage-specific expression. Yeast two-hybrid, co-immunoprecipitation, ChIP The Journal of biological chemistry Medium 12904288
2003 Miz-1 and c-Myc form a repressor complex at the Mad4 initiator element to suppress Mad4 expression in proliferating cells; loss of this complex during differentiation allows Mad4 activation. Reporter assays, EMSA/gel shift, cell differentiation model The Biochemical journal Medium 12418961
2004 Akt phosphorylates Miz1, enabling 14-3-3η to bind Miz1's DNA-binding domain and inhibit its transcriptional activating function; this regulates recovery from DNA-damage-induced cell-cycle arrest. Miz1 has two distinct functions in DNA damage: c-Myc-regulated gene upregulation, and 14-3-3η/Akt-regulated gene repression. Co-immunoprecipitation, kinase assays, domain mapping, cell-cycle analysis Nature cell biology High 15580267
2004 MAGE-A4 C-terminal fragment (cleaved by caspase-induced processing) binds Miz-1 and is recruited to the p21Cip1 promoter via Miz-1, downregulating p21Cip1 transcription and inducing apoptosis. Yeast two-hybrid, co-immunoprecipitation, ChIP, reporter assays The Journal of biological chemistry Medium 14739298
2005 BCL6 interacts with Miz-1 and, via Miz-1, binds the CDKN1A (p21) promoter to suppress transcription and prevent p53-independent cell cycle arrest in germinal center B cells. Co-immunoprecipitation, ChIP, reporter assays, germinal center B cell functional analysis Nature immunology High 16142238
2005 Miz-1 inactivation by c-Myc is required for apoptosis induction by Myc in primary diploid human fibroblasts under growth factor withdrawal, but Miz-1 inactivation is dispensable for Myc-induced cell cycle progression and transformation. shRNA knockdown, MycV394D mutant defective in Miz-1 binding, apoptosis and cell-cycle assays The Journal of biological chemistry High 16352593
2005 Pontin (Tip49) and Reptin (Tip48) interact with c-Myc and function as co-repressors in the c-Myc/Miz-1 pathway to repress p21 expression and control cell proliferation in Xenopus embryos. Xenopus embryo overexpression/knockdown, rescue with c-Myc RNA and dominant-negative Miz-1, reporter assays Mechanisms of development Medium 15804567
2006 MIZ-1 activates BCL2 transcription; c-MYC binding and inactivation of MIZ-1 represses BCL2, and this repression is the essential consequence of MIZ-1 targeting during Myc-induced apoptosis. shRNA knockdown of Miz-1, Myc mutant defective in Miz-1 binding, BCL2 inhibitor rescue, reporter assays The Journal of biological chemistry High 17082179
2006 Myc-Miz1 complex regulates keratinocyte adhesion and TGFβ responsiveness; Miz1 is required for Myc to decrease keratinocyte adhesion and spreading. Target genes include α6 and β1 integrins, directly bound by both Myc and Miz1 in vivo. Miz1-dependent regulation is required for Myc-induced premature differentiation in reconstituted epidermis. MycV394D mutant, ChIP, reconstituted epidermis, keratinocyte adhesion assays, integrin overexpression rescue The Journal of cell biology High 16391002
2007 Crystal structure of the Miz-1 POZ domain at 2.1 Å resolution reveals a tetrameric organization with two types of subunit interfaces: an α-helical dimerization interface and a novel β-sheet interface that directs tetramerization of two POZ domain dimers in solution. X-ray crystallography, solution studies confirming β-sheet interface mediates tetramerization Journal of molecular biology High 17880999
2008 Miz1 is required for recruitment of TopBP1 to chromatin and for protection of TopBP1 from proteasomal degradation by the HectH9 ubiquitin ligase; Myc antagonizes TopBP1 binding to Miz1, causing TopBP1 dissociation from chromatin and attenuation of ATR-dependent checkpoint signaling. Co-immunoprecipitation, chromatin fractionation, proteasome inhibition, Myc overexpression The EMBO journal High 18923429
2008 Myc promotes neural progenitor cell self-renewal through Miz-1; a Myc mutant (MycV394D) deficient in Miz-1 binding does not increase self-renewing cells though it still stimulates proliferation, demonstrating the Miz-1 interaction specifically mediates the self-renewal effect. Retroviral transduction, MycV394D mutant, neurosphere self-renewal assays Journal of cell science Medium 19001505
2009 BCL6 interacts with Miz-1 to bind the BCL2 promoter and suppresses Miz1-induced BCL2 expression in germinal center B cells; this BCL6-Miz1-mediated BCL2 suppression is lost in follicular lymphoma and DLBCL. Co-immunoprecipitation, ChIP, reporter assays, B cell functional studies Proceedings of the National Academy of Sciences of the United States of America High 19549844
2009 Gfi-1 represses CDKN2B (p15INK4B) by interacting with Miz-1 and being recruited to the CDKN2B core promoter via Miz-1, not via direct DNA binding. Gfi-1 and c-Myc collaborate through Miz-1 on the CDKN2B promoter. Co-immunoprecipitation, ChIP, reporter assays, Gfi-1 knockdown Proceedings of the National Academy of Sciences of the United States of America High 19164764
2009 Miz1 selectively suppresses TNF-α-induced JNK1 activation (but not IL-1β- or UV-induced JNK activation) independently of its transcriptional activity; Miz1 inhibits TRAF2 K63-linked polyubiquitination. Upon TNF-α stimulation, Miz1 undergoes proteasomal degradation to relieve JNK1 suppression. Miz1-/- MEFs, reconstitution with transcription-deficient Miz1 mutant, JNK activity assays, TRAF2 ubiquitination assays Proceedings of the National Academy of Sciences of the United States of America High 19815509
2009 ARF interacts with Miz-1 (via Miz-1's zinc finger domain) and counteracts Miz-1-mediated inhibition of p53 transcriptional activity. Miz-1 binds p53 through its DNA-binding domain and reduces p53 promoter occupancy; ARF and p53 competitively bind Miz-1. Yeast two-hybrid, in vitro binding assay, competitive ChIP, reporter assays Oncogene Medium 19901969
2010 The Myc-Miz1 interaction is continuously required in established T-cell lymphomas to repress CKI expression and prevent accumulation of trimethylated H3K9, a senescence marker. TGFβ autocrine signaling induces CKI expression and senescence when Myc is suppressed; Myc/Miz1 interaction antagonizes this TGFβ-induced senescence program. MycV394D mutant lymphoma model, Myc suppression, ChIP for H3K9me3, TGFβ pathway analysis Genes & development High 20551174
2010 Arf interacts with Miz1, disrupts Miz1-nucleophosmin co-activator interaction, induces sumoylation of Miz1, and promotes assembly of a heterochromatic complex containing Myc and H3K9me3 at Miz1 target loci, leading to repression of cell adhesion genes and induction of apoptosis. Co-immunoprecipitation, sumoylation assay, ChIP for H3K9me3, gene expression analysis, apoptosis assays The Journal of cell biology High 20308430
2010 Mule (HectH9) is the E3 ubiquitin ligase that catalyzes K48-linked polyubiquitination of Miz1 upon TNF-α stimulation, targeting Miz1 for proteasomal degradation and thereby relieving Miz1-mediated suppression of JNK activation. Co-immunoprecipitation, in vitro ubiquitination assays, Mule siRNA, Miz1 degradation assays Proceedings of the National Academy of Sciences of the United States of America High 20624960
2010 Gfi-1 interacts with Miz-1 and forms a ternary complex with c-Myc on the CDKN1A core promoter to repress p21Cip1 expression, independent of Gfi-1's direct DNA binding activity. Co-immunoprecipitation, ChIP, reporter assays, Gfi-1 knockdown Oncogene Medium 20190815
2010 The Miz-1 BTB/POZ domain crystal structure was solved at 2.6 Å, revealing a strand-swapped dimer with a shorter N-terminus unable to form the interchain sheet characteristic of classical BTB dimers. X-ray crystallography, cysteine cross-linking in solution Journal of molecular biology High 20493880
2010 Miz1 (Zbtb17) lacking its POZ domain causes nearly complete absence of follicular B cells due to failure to activate the JAK-STAT5 pathway upon IL-7 stimulation. Miz-1 directly represses SOCS1 and activates Bcl2; combined re-expression of Bcl2 and Ebf1 rescues B cell development. Conditional knockout (Zbtb17ΔPOZ/ΔPOZ), Jak-Stat5 signaling assays, ChIP, genetic rescue experiments Immunity High 21167753
2010 A SP1/MIZ1/MYCN repression complex recruits HDAC1 to the TRKA and p75NTR promoters to repress their transcription in neuroblastoma cells. ChIP, co-immunoprecipitation, reporter assays, HDAC inhibitor TSA Cancer research High 21123453
2011 Miz-1 (Zbtb17ΔPOZ) is required for IL-7R-dependent survival and differentiation of early T-lineage progenitors; Miz-1 binds the SOCS1 promoter to repress it, enabling STAT5 activation and Bcl2 upregulation. Overexpression of Bcl-2 or SOCS1 inhibition restores pro-T cell numbers. Conditional knockout, ChIP, STAT5 phosphorylation assays, genetic rescue with Bcl2 transgene and SOCS1 siRNA Blood High 21258009
2011 Site-specific K48-linked polyubiquitination of Miz1 at Lys388 and Lys472 (promoted by TRAF2 upon TNF-α stimulation) is required for Miz1 degradation and de-repression of JNK activation; a non-degradable Miz1 mutant (K388R/K472R) significantly suppresses TNF-α-induced JNK1 activation. Mutagenesis of ubiquitination sites, in vivo ubiquitination assays, JNK activity assays Proceedings of the National Academy of Sciences of the United States of America High 22184250
2011 Myc and Miz-1 co-occupy Hox gene promoters in human ES cells and together suppress differentiation-promoting genes to maintain pluripotency; Myc and Miz-1 proteins interact and associate with corepressor factors in ES cells. ChIP-chip, Myc/Miz-1 knockdown, co-immunoprecipitation Epigenetics & chromatin Medium 22053792
2011 Miz-1 is required at the pre-TCR β-selection checkpoint; Miz-1-deficient DN3 cells fail to express pre-TCR at the surface and show elevated expression of p53 target genes. Only combined re-expression of rearranged TCRαβ and Bcl2 rescues the block. Conditional knockout, gene expression analysis, genetic rescue Journal of immunology High 21841135
2013 Miz-1 activates transcription upon binding a non-palindromic sequence in core promoters; Miz1 target genes include regulators of autophagy and vesicular transport. Deletion of Miz1 POZ domain in CNS causes defective autophagic flux and cerebellar neurodegeneration. ChIP-Seq, biochemical analysis, Nestin-Cre conditional knockout, autophagy flux assays (p62/ubiquitin accumulation) Nature communications High 24088869
2013 Miz1 suppresses LPS-induced inflammation by being phosphorylated at Ser178 after stimulation, enabling recruitment of HDAC1 to the C/EBP-δ gene promoter to repress its transcription and terminate the inflammatory response. Conditional POZ-domain knockout mouse, phosphorylation site mutagenesis, ChIP for HDAC1, inflammatory cytokine assays Nature immunology High 23525087
2013 In vivo, Mule/Huwe1 suppresses Ras-driven tumorigenesis by preventing accumulation of c-Myc/Miz1 transcriptional complexes that repress p21 and p15; Mule-deficient keratinocyte tumorigenesis could be reversed by concomitant c-Myc knockout or Miz1 knockdown. Conditional knockout mouse (K14Cre;Mule flox/flox), Miz1 knockdown, genetic epistasis with c-Myc KO Genes & development High 23699408
2013 Miz1 regulates Hedgehog signaling by binding Smo and Gli2; Miz1 overexpression increases Gli reporter activity, and Smo activation induces Miz1 translocation to primary cilia with Smo and Gli2. Miz1 translocates to the nucleus in a Smo-dependent manner and is required for Gli2 nuclear translocation. Co-immunoprecipitation, Gli reporter assays, confocal imaging of primary cilia, Miz1 knockdown, allograft tumor model PloS one Medium 23671675
2014 Miz-1 directly activates the ribosomal protein L22 (Rpl22) gene; Rpl22 protein binds p53 mRNA and negatively regulates its translation, thereby limiting p53-dependent apoptosis in pro-B and DN3a pre-T cells undergoing V(D)J recombination. ChIP, gene expression analysis, conditional KO, Rpl22 rescue experiments, translational assays Proceedings of the National Academy of Sciences of the United States of America High 25468973
2014 Crystal structures of heterodimeric POZ domains of Miz1/BCL6 and Miz1/NAC1 were solved, revealing the structural basis for POZ domain heteromeric interactions relevant to B-cell lymphoma and ovarian carcinoma. X-ray crystallography of forced heterodimers, tethered POZ domain purification strategy Acta crystallographica Section F High 25484205
2014 Nac1 interacts with Miz1 through a heterodimeric POZ domain interaction, relocalizes Miz1 to nuclear bodies, and suppresses p21Cip1 expression; Nac1 knockdown increases Miz1 target gene p21Cip1 in ovarian cancer cells. Chemical crosslinking, co-immunoprecipitation, confocal imaging, siRNA knockdown with p21 expression analysis Bioscience reports Medium 24702277
2014 EBNA3A interacts with Miz-1 in EBV-infected cells, causes a fraction of Miz-1 to translocate from cytoplasm to nucleus, forms a trimeric complex with Miz-1 on its recognition DNA element, prevents Miz-1-nucleophosmin interaction, and represses CDKN2B transcription with H3K27 repressive marks. Co-immunoprecipitation at endogenous levels, EMSA, ChIP for H3K27me3, gene expression analysis Nucleic acids research High 25092922
2015 ZBTB17 (Miz1) interacts with cysteine and glycine-rich protein 3 (CSRP3/MLP) by yeast 2-hybrid; cardiac myocyte-specific Zbtb17 deletion in mice causes cardiomyopathy and fibrosis after biomechanical stress. ZBTB17 protects cardiomyocytes from apoptosis and regulates hypertrophy in a calcineurin-dependent manner. Yeast two-hybrid, conditional cardiac-specific knockout, biomechanical stress model, apoptosis and hypertrophy assays Circulation. Cardiovascular genetics Medium 26175529
2016 MYC/MIZ1 complex represses core circadian clock genes BMAL1 (ARNTL), CLOCK, and NPAS2, thereby attenuating the circadian clock and promoting cell proliferation; this requires formation of repressive MYC-MIZ1 complexes. MYC overexpression/knockdown, MycV394D mutant, reporter assays, gene expression in lymphoma samples Nature communications High 27339797
2016 Myc/Miz1 interaction distinguishes medulloblastoma subgroup identity; Myc binds Miz1 strongly (unlike MycN) and suppresses ciliogenesis and reprograms GNP transcriptome through Miz1-dependent repression. Genetic disruption of Myc/Miz1 interaction inhibited Group 3 medulloblastoma development. MycV394D mutant mouse models, ChIP, gene expression profiling, tumor development assays Cancer cell High 26766587
2016 NMR structural analysis revealed that Miz-1 zinc fingers 3 and 4 form an unusual compact structure that restricts DNA binding of the first four ZF modules; an A86K mutation disrupts this compact structure and increases DNA-binding affinity 30-fold, suggesting ZFs 3–4 function to prevent nonspecific DNA binding during sequence scanning. NMR (2D 1H-1H), mutagenesis (A86K), DNA binding affinity measurements The Journal of biological chemistry High 28035002
2017 Miz1 controls Schwann cell proliferation by directly repressing the H3K36me2 demethylase Kdm8; loss of Miz1 POZ domain releases Kdm8 repression, causing decreased H3K36me2 at cell-cycle genes and re-entry of adult Schwann cells into the cell cycle, leading to peripheral neuropathy. Conditional POZ-domain knockout in Schwann cells, RNA-seq, ChIP, Kdm8 expression analysis The Journal of neuroscience High 29217679
2020 Miz1 acts as a negative regulator of NF-κB signaling in lung epithelial cells; loss of Miz1 causes sustained NF-κB activation and a COPD-like phenotype. Concomitant partial loss of NF-κB/RelA prevents COPD-like phenotype in Miz1-deficient mice. Miz1 also represses ACE2 expression in lung epithelium. Lung epithelial conditional knockout, NF-κB/RelA compound knockout, gene expression analysis Science advances High 32851183
2020 Myc-Miz1-mediated transcriptional repression of Cebpα and Cebpδ is required for maintaining undifferentiated state and self-renewal capacity of leukemia stem cells in AML; MycV394D (Miz1-binding deficient) AML cells are partially differentiated with reduced LSC frequency. MycV394D mutant, MLL-AF9 AML mouse model, colony-forming assay, serial transplantation, gene expression Blood High 32040550
2020 Miz1 was identified as an essential regulator of diphthamide biosynthesis via genome-wide CRISPR screen; Miz1 binds directly to the Dph1 proximal promoter via an evolutionarily conserved consensus site to activate Dph1 transcription. Genome-wide CRISPR KO screen, ChIP, reporter assays, promoter binding analysis PLoS genetics High 33057331
2021 Miz1 sequestrates oncoprotein metadherin (MTDH) in hepatocytes independently of its transcriptional activity, preventing MTDH from promoting NF-κB activation; hepatocyte-specific Miz1 deletion promotes pro-inflammatory cytokine production, macrophage polarization toward pro-inflammatory phenotypes, and HCC. Hepatocyte-specific Miz1 knockout, co-immunoprecipitation with MTDH, NF-κB activation assays Immunity High 34038747
2021 MYC suppresses loading of nuclear-derived dsRNA onto TLR3 and its subsequent lysosomal degradation via association with MIZ1; MYC/MIZ1 complex suppresses TBK1 activation and downstream MHC class I expression in PDAC, enabling immune evasion. MYC deletion in PDAC mouse model, TBK1 KO rescue, dsRNA vesicular trafficking analysis, MIZ1 co-association Cancer research High 34145038
2021 Miz1 directly binds to and represses the ACE2 promoter in mouse and human lung epithelial cells. ChIP, reporter assays in lung epithelial cells Frontiers in immunology Medium 34305888
2021 MXD proteins activate transcription of Miz1 target genes p15 and p21 by interacting with MIZ1; MXD mutants deficient in MIZ1 binding cannot activate MYC-repressed genes even while retaining MAX interaction. Reporter assays, MXD/MIZ1 binding mutants, DNA binding assays FEBS letters Medium 33914337
2022 Miz1 promotes KRAS-driven lung tumorigenesis by directly binding the Pcdh10 promoter to repress its expression; silencing Pcdh10 rescues the anti-proliferative and anti-tumorigenic effects of Miz1 loss in mutant KRAS tumor cells. Conditional KO in KRAS mouse model, ChIP, RNA-seq, Pcdh10 rescue experiments Cancer letters High 36538983
2022 Miz1 directly represses IL-12 in lung epithelial cells and dendritic cells by binding the Il12 promoter and recruiting HDAC1, thereby preventing Th1 skewing and promoting allergic asthma pathogenesis. Cell-specific conditional KO, ChIP-seq, ChIP-qPCR, HDAC1 recruitment assays, cytokine measurement American journal of respiratory cell and molecular biology High 35833903
2023 ZBTB17 interacts with nuclear receptor RXRA; ZBTB17 knockdown activates RXRA-dependent ITPR2-mediated intracellular calcium signaling, causing mitochondrial dysfunction, ROS accumulation, DNA damage, and cellular senescence. Co-immunoprecipitation, ZBTB17 knockdown, calcium imaging, ITPR2 knockdown epistasis FASEB journal Medium 37698375
2023 Miz1 binds peroxiredoxin 6 (PRDX6) in hepatocyte cytosol, retaining it there and blocking its interaction with mitochondrial Parkin at Cys431, thereby enabling Parkin-mediated mitophagy. In NASH, TNFα-induced E3-ubiquitination of Miz1 causes its degradation, releasing PRDX6 to inhibit mitophagy and propagate a TNFα/Miz1 positive feedback loop. Co-immunoprecipitation, mass spectrometry, hepatocyte-specific Miz1 KO, human NASH liver organoids, mitophagy assays Journal of hepatology High 37040844
2024 MIZ1 induces TMBIM4 (an anti-apoptotic protein that regulates IP3R-mediated Ca2+ mobilization downstream of BCR signaling) specifically in IgG1+ GC B cells; MIZ1-TMBIM4 axis prevents excessive Ca2+ accumulation and mitochondrial dysfunction specifically in IgG1+ B cells during positive selection. CRISPR-Cas9 screen in GC B cells, conditional mouse genetics, Ca2+ mobilization assays, mitochondrial function assays Science immunology High 38579014
2024 Miz1 epigenetically represses Ifna and Ifnb gene promoters by recruiting HDAC1; during influenza A virus infection, CUL4B-mediated ubiquitination and degradation of Mule (HUWE1) leads to Miz1 accumulation, which limits type I IFN production and favors viral replication. Miz1 loss-of-function in mouse lung epithelial cells, ChIP for HDAC1, in vitro and in vivo IAV infection, Mule/CUL4B degradation assays Science signaling High 38593156

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Repression of p15INK4b expression by Myc through association with Miz-1. Nature cell biology 477 11283613
2001 TGFbeta influences Myc, Miz-1 and Smad to control the CDK inhibitor p15INK4b. Nature cell biology 410 11283614
2005 BCL6 interacts with the transcription factor Miz-1 to suppress the cyclin-dependent kinase inhibitor p21 and cell cycle arrest in germinal center B cells. Nature immunology 280 16142238
2002 Negative regulation of the mammalian UV response by Myc through association with Miz-1. Molecular cell 263 12408820
2009 BCL6 suppression of BCL2 via Miz1 and its disruption in diffuse large B cell lymphoma. Proceedings of the National Academy of Sciences of the United States of America 155 19549844
2013 Mule/Huwe1/Arf-BP1 suppresses Ras-driven tumorigenesis by preventing c-Myc/Miz1-mediated down-regulation of p21 and p15. Genes & development 110 23699408
2006 Myc regulates keratinocyte adhesion and differentiation via complex formation with Miz1. The Journal of cell biology 103 16391002
2010 The interaction between Myc and Miz1 is required to antagonize TGFbeta-dependent autocrine signaling during lymphoma formation and maintenance. Genes & development 99 20551174
2016 MYC/MIZ1-dependent gene repression inversely coordinates the circadian clock with cell cycle and proliferation. Nature communications 97 27339797
2013 The role of MIZ-1 in MYC-dependent tumorigenesis. Cold Spring Harbor perspectives in medicine 88 24296348
2018 MIZ1 regulates ECA1 to generate a slow, long-distance phloem-transmitted Ca2+ signal essential for root water tracking in Arabidopsis. Proceedings of the National Academy of Sciences of the United States of America 87 30012618
1997 Miz1, a novel zinc finger transcription factor that interacts with Msx2 and enhances its affinity for DNA. Mechanisms of development 87 9256341
2010 A SP1/MIZ1/MYCN repression complex recruits HDAC1 at the TRKA and p75NTR promoters and affects neuroblastoma malignancy by inhibiting the cell response to NGF. Cancer research 84 21123453
2001 Transcription factor MIZ-1 is regulated via microtubule association. Molecular cell 78 11545736
2004 Akt and 14-3-3eta regulate Miz1 to control cell-cycle arrest after DNA damage. Nature cell biology 76 15580267
2010 Transcription factor miz-1 is required to regulate interleukin-7 receptor signaling at early commitment stages of B cell differentiation. Immunity 72 21167753
2013 Suppression of inflammation and acute lung injury by Miz1 via repression of C/EBP-δ. Nature immunology 71 23525087
2008 Miz1 and HectH9 regulate the stability of the checkpoint protein, TopBP1. The EMBO journal 70 18923429
2021 The zinc finger protein Miz1 suppresses liver tumorigenesis by restricting hepatocyte-driven macrophage activation and inflammation. Immunity 68 34038747
2003 Miz1 is required for early embryonic development during gastrulation. Molecular and cellular biology 68 14560010
2016 The Interaction of Myc with Miz1 Defines Medulloblastoma Subgroup Identity. Cancer cell 65 26766587
2005 Pontin and Reptin regulate cell proliferation in early Xenopus embryos in collaboration with c-Myc and Miz-1. Mechanisms of development 60 15804567
2011 Hormonal regulation of lateral root development in Arabidopsis modulated by MIZ1 and requirement of GNOM activity for MIZ1 function. Plant physiology 57 21940997
2023 A TNFα/Miz1-positive feedback loop inhibits mitophagy in hepatocytes and propagates non-alcoholic steatohepatitis. Journal of hepatology 53 37040844
2006 BCL2 is a downstream effector of MIZ-1 essential for blocking c-MYC-induced apoptosis. The Journal of biological chemistry 53 17082179
2004 A cleaved form of MAGE-A4 binds to Miz-1 and induces apoptosis in human cells. The Journal of biological chemistry 52 14739298
2009 Gfi-1 represses CDKN2B encoding p15INK4B through interaction with Miz-1. Proceedings of the National Academy of Sciences of the United States of America 48 19164764
2008 Myc increases self-renewal in neural progenitor cells through Miz-1. Journal of cell science 47 19001505
2013 Miz1 is required to maintain autophagic flux. Nature communications 46 24088869
1999 Zimp encodes a homologue of mouse Miz1 and PIAS3 and is an essential gene in Drosophila melanogaster. Gene 46 10095110
1997 Association of Myc with the zinc-finger protein Miz-1 defines a novel pathway for gene regulation by Myc. Current topics in microbiology and immunology 46 9308237
2010 E3 ubiquitin ligase Mule ubiquitinates Miz1 and is required for TNFalpha-induced JNK activation. Proceedings of the National Academy of Sciences of the United States of America 43 20624960
2012 MIZ1, an essential protein for root hydrotropism, is associated with the cytoplasmic face of the endoplasmic reticulum membrane in Arabidopsis root cells. FEBS letters 42 22285304
2006 Sleeping Beauty transposase modulates cell-cycle progression through interaction with Miz-1. Proceedings of the National Academy of Sciences of the United States of America 42 16537485
2003 Mad4 is regulated by a transcriptional repressor complex that contains Miz-1 and c-Myc. The Biochemical journal 42 12418961
2011 The role of the transcription factor Miz-1 in lymphocyte development and lymphomagenesis-Binding Myc makes the difference. Seminars in immunology 39 22000024
2011 IL-7R-dependent survival and differentiation of early T-lineage progenitors is regulated by the BTB/POZ domain transcription factor Miz-1. Blood 38 21258009
2005 Targeting of Miz-1 is essential for Myc-mediated apoptosis. The Journal of biological chemistry 38 16352593
2013 MIZ1-regulated hydrotropism functions in the growth and survival of Arabidopsis thaliana under natural conditions. Annals of botany 35 23658369
2010 The Arf tumor suppressor protein inhibits Miz1 to suppress cell adhesion and induce apoptosis. The Journal of cell biology 35 20308430
2014 Miz-1 regulates translation of Trp53 via ribosomal protein L22 in cells undergoing V(D)J recombination. Proceedings of the National Academy of Sciences of the United States of America 30 25468973
2007 A beta-sheet interaction interface directs the tetramerisation of the Miz-1 POZ domain. Journal of molecular biology 30 17880999
2003 Nramp1-mediated innate resistance to intraphagosomal pathogens is regulated by IRF-8, PU.1, and Miz-1. The Journal of biological chemistry 30 12904288
2021 MYC- and MIZ1-Dependent Vesicular Transport of Double-Strand RNA Controls Immune Evasion in Pancreatic Ductal Adenocarcinoma. Cancer research 29 34145038
2007 Miz1 is required for hair follicle structure and hair morphogenesis. Journal of cell science 29 17635993
2002 The SUMO ubiquitin-protein isopeptide ligase family member Miz1/PIASxbeta /Siz2 is a transcriptional cofactor for TFII-I. The Journal of biological chemistry 28 12193603
2014 Epstein-Barr virus nuclear antigen 3A protein regulates CDKN2B transcription via interaction with MIZ-1. Nucleic acids research 26 25092922
2011 Myc and Miz-1 have coordinate genomic functions including targeting Hox genes in human embryonic stem cells. Epigenetics & chromatin 26 22053792
2011 Site-specific ubiquitination is required for relieving the transcription factor Miz1-mediated suppression on TNF-α-induced JNK activation and inflammation. Proceedings of the National Academy of Sciences of the United States of America 26 22184250
2002 Host cell factor-1 interacts with and antagonizes transactivation by the cell cycle regulatory factor Miz-1. The Journal of biological chemistry 25 12244100
2020 Myc-Miz1 signaling promotes self-renewal of leukemia stem cells by repressing Cebpα and Cebpδ. Blood 24 32040550
2014 Structures of heterodimeric POZ domains of Miz1/BCL6 and Miz1/NAC1. Acta crystallographica. Section F, Structural biology communications 24 25484205
2002 c-Myc represses and Miz-1 activates the murine natural resistance-associated protein 1 promoter. The Journal of biological chemistry 24 12110671
2010 A role of Miz-1 in Gfi-1-mediated transcriptional repression of CDKN1A. Oncogene 23 20190815
2009 ARF antagonizes the ability of Miz-1 to inhibit p53-mediated transactivation. Oncogene 22 19901969
2019 Cloning and characterization of a gene encoding MIZ1, a domain of unknown function protein and its role in salt and drought stress in rice. Protoplasma 21 31786672
2011 Miz-1 is required to coordinate the expression of TCRbeta and p53 effector genes at the pre-TCR "beta-selection" checkpoint. Journal of immunology (Baltimore, Md. : 1950) 21 21841135
2010 Insights into strand exchange in BTB domain dimers from the crystal structures of FAZF and Miz1. Journal of molecular biology 21 20493880
2020 Epithelial cell-specific loss of function of Miz1 causes a spontaneous COPD-like phenotype and up-regulates Ace2 expression in mice. Science advances 20 32851183
2004 Induction of G1 cell cycle arrest and P15INK4b expression by ECRG1 through interaction with Miz-1. Journal of cellular biochemistry 20 15095404
2017 Miz1 Controls Schwann Cell Proliferation via H3K36me2 Demethylase Kdm8 to Prevent Peripheral Nerve Demyelination. The Journal of neuroscience : the official journal of the Society for Neuroscience 18 29217679
2009 Miz1 is a signal- and pathway-specific modulator or regulator (SMOR) that suppresses TNF-alpha-induced JNK1 activation. Proceedings of the National Academy of Sciences of the United States of America 18 19815509
2019 Deletion of the Miz-1 POZ Domain Increases Efficacy of Cytarabine Treatment in T- and B-ALL/Lymphoma Mouse Models. Cancer research 17 31273062
2011 Expression of NLRR3 orphan receptor gene is negatively regulated by MYCN and Miz-1, and its downregulation is associated with unfavorable outcome in neuroblastoma. Clinical cancer research : an official journal of the American Association for Cancer Research 16 21908575
2007 De novo identification of MIZ-1 (ZBTB17) encoding a MYC-interacting zinc-finger protein as a new favorable neuroblastoma gene. Clinical cancer research : an official journal of the American Association for Cancer Research 16 17947461
2000 Interaction of insulin-like growth factor binding protein-4, Miz-1, leptin, lipocalin-type prostaglandin D synthase, and granulin precursor with the N-terminal half of type III hexokinase. Archives of biochemistry and biophysics 16 11068878
2014 Nac1 interacts with the POZ-domain transcription factor, Miz1. Bioscience reports 15 24702277
2011 The proto-oncoprotein KR-POK represses transcriptional activation of CDKN1A by MIZ-1 through competitive binding. Oncogene 15 21804610
2012 Miz1 is a critical repressor of cdkn1a during skin tumorigenesis. PloS one 14 22509363
2015 ZBTB17 (MIZ1) Is Important for the Cardiac Stress Response and a Novel Candidate Gene for Cardiomyopathy and Heart Failure. Circulation. Cardiovascular genetics 13 26175529
2013 Polymorphism of ZBTB17 gene is associated with idiopathic dilated cardiomyopathy: a case control study in a Han Chinese population. European journal of medical research 13 23570452
2016 Structural Insights into c-Myc-interacting Zinc Finger Protein-1 (Miz-1) Delineate Domains Required for DNA Scanning and Sequence-specific Binding. The Journal of biological chemistry 12 28035002
2017 A missense mutation in zbtb17 blocks the earliest steps of T cell differentiation in zebrafish. Scientific reports 10 28266617
2013 Regulation of hedgehog signaling by Myc-interacting zinc finger protein 1, Miz1. PloS one 10 23671675
2013 Structural and dynamical characterization of the Miz-1 zinc fingers 5-8 by solution-state NMR. Journal of biomolecular NMR 10 23975355
2022 Myc-Interacting Zinc Finger Protein 1 (Miz-1) Is Essential to Maintain Homeostasis and Immunocompetence of the B Cell Lineage. Biology 9 35453704
2013 Biphasic influence of Miz1 on neural crest development by regulating cell survival and apical adhesion complex formation in the developing neural tube. Molecular biology of the cell 9 24307680
2003 Characterization of the murine Nramp1 promoter: requirements for transactivation by Miz-1. The Journal of biological chemistry 9 12840021
2016 Solution structure of the 13th C2H2 Zinc Finger of Miz-1. Biochemical and biophysical research communications 8 26972249
2016 Miz-1 promotes the proliferation of esophageal cancer cells via suppression of p21 and release of p21-arrested cyclin D1. Oncology reports 8 27109891
2022 Suppression of Allergic Asthma by Loss of Function of Miz1-mediated Th1 Skewing. American journal of respiratory cell and molecular biology 7 35833903
2014 Miz1 deficiency in the mammary gland causes a lactation defect by attenuated Stat5 expression and phosphorylation. PloS one 7 24586582
2024 Miz1 represses type I interferon production and limits viral clearance during influenza A virus infection. Science signaling 6 38593156
2023 MIZU-KUSSEI1 (MIZ1) and GNOM/MIZ2 control not only positive hydrotropism but also phototropism in Arabidopsis roots. Journal of experimental botany 6 37220914
2023 Zinc finger protein ZBTB17 controls cellular senescence via interacting with nuclear receptor RXRA and its downstream calcium signaling. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 6 37698375
2022 Miz1 promotes KRAS-driven lung tumorigenesis by repressing the protocadherin Pcdh10. Cancer letters 6 36538983
2018 ZBTB17 loss-of-function mutation contributes to familial dilated cardiomyopathy. Heart and vessels 6 29445930
2025 Foraging for water by MIZ1-mediated antagonism between root gravitropism and hydrotropism. Proceedings of the National Academy of Sciences of the United States of America 5 40372432
2024 Modulation of Root Hydrotropism and Recovery From Drought by MIZ1-like Genes in Tomato. Plant, cell & environment 5 39526383
2021 Identification of the SARS-CoV-2 Entry Receptor ACE2 as a Direct Target for Transcriptional Repression by Miz1. Frontiers in immunology 5 34305888
2014 Late onset neuropathy with spontaneous clinical remission in mice lacking the POZ domain of the transcription factor Myc-interacting zinc finger protein 1 (Miz1) in Schwann cells. The Journal of biological chemistry 5 25416780
2024 Meta-analysis and transcriptomic analysis reveal that NKRF and ZBTB17 regulate the NF-κB signaling pathway, contributing to the shared molecular mechanisms of Alzheimer's disease and atherosclerosis. CNS neuroscience & therapeutics 4 38738952
2020 Identification of the transcription factor Miz1 as an essential regulator of diphthamide biosynthesis using a CRISPR-mediated genome-wide screen. PLoS genetics 4 33057331
2016 Miz1, a Novel Target of ING4, Can Drive Prostate Luminal Epithelial Cell Differentiation. The Prostate 4 27527891
2024 Amyloplast is involved in the MIZ1-modulated root hydrotropism. Journal of plant physiology 3 38507925
2024 Regulation of BCR-mediated Ca2+ mobilization by MIZ1-TMBIM4 safeguards IgG1+ GC B cell-positive selection. Science immunology 3 38579014
2024 Chromosome 8q24 amplification associated with human hepatocellular carcinoma predicts MYC/ZEB1/MIZ1 transcriptional regulation. Scientific reports 3 39424877
2021 MXD/MIZ1 transcription regulatory complexes activate the expression of MYC-repressed genes. FEBS letters 3 33914337
2015 Decreased MIZ1 Expression in Severe Experimental Acute Pancreatitis: A Rat Study. Digestive diseases and sciences 3 26581215
2014 The transcription factor Miz-1 is required for embryonic and stress-induced erythropoiesis but dispensable for adult erythropoiesis. American journal of blood research 3 25232500