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Showing ZBTB17MIZ1 is a alias.

ZBTB17

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

Length
803 aa
Mass
87.9 kDa
Annotated
2026-06-11
100 papers in source corpus 63 papers cited in narrative 61 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ZBTB17/MIZ1 is a BTB/POZ-zinc finger transcription factor that activates target genes by binding initiator and core-promoter elements through its C2H2 zinc fingers, controlling cell-cycle arrest, differentiation, apoptosis, and inflammation (PMID:9308237, PMID:11283613, PMID:12408820). Its zinc-finger array employs an unusual recognition mechanism: ZFs 3-4 form a compact rigid module that suppresses nonspecific scanning, while µs-ms conformational exchange in the ZF10-11 linker partitions the array into two cooperating segments that read a bipartite consensus at transcription start sites (PMID:28035002, PMID:34963061). Its N-terminal POZ domain self-associates into strand-swapped dimers and higher-order tetramers, providing the scaffold for protein-protein interactions (PMID:17880999, PMID:20493880). The defining feature of MIZ1 biology is its capture by transcriptional partners: oncoproteins and repressors including Myc, BCL6, Gfi-1, and NAC1 dock at MIZ1-bound promoters, displace coactivators such as p300 and nucleophosmin, and recruit corepressors, converting MIZ1 from an activator into a repressor of CDK inhibitors (p15INK4b, p21Cip1) and pro-apoptotic and differentiation genes (PMID:11283613, PMID:12110671, PMID:12840021, PMID:16142238, PMID:19164764, PMID:20308430, PMID:25484205); conversely MXD proteins use MIZ1 to antagonize Myc-repressed genes (PMID:33914337). Through these interactions MIZ1 governs senescence and TGFβ-induced growth arrest (PMID:11283614, PMID:20551174), germinal-center and developing lymphocyte survival via SOCS1/Bcl2 and Rpl22/p53 control (PMID:21167753, PMID:21258009, PMID:25468973), and tumorigenesis in skin, medulloblastoma, AML, and lung (PMID:23699408, PMID:26766587, PMID:32040550, PMID:36538983). MIZ1 also performs transcription-independent functions: it inhibits TRAF2 ubiquitin-ligase activity to suppress TNFα-induced JNK activation (PMID:19815509, PMID:22184250), sequesters MTDH to restrain NF-κB (PMID:34038747), and retains PRDX6 in the cytosol to regulate Parkin-mediated mitophagy (PMID:37040844). MIZ1 protein levels are set by K48-linked polyubiquitination catalyzed by Mule/HectH9 or TRAF2 and proteasomal degradation, while Akt-dependent phosphorylation licenses inhibitory 14-3-3η binding and Ser178 phosphorylation enables HDAC1 recruitment (PMID:15580267, PMID:20624960, PMID:22184250, PMID:23525087). Genetic loss of MIZ1 is embryonic lethal and produces tissue-specific phenotypes including neurodegeneration from impaired autophagy, demyelinating neuropathy, COPD-like lung inflammation, and cardiomyopathy (PMID:14560010, PMID:17635993, PMID:24088869, PMID:29217679, PMID:32851183).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1997 Medium

    Established MIZ1 as a zinc-finger transcription factor that binds Myc and core-promoter initiator elements, defining the molecular substrate for Myc-mediated gene repression.

    Evidence Yeast two-hybrid with Myc C-terminus, in vitro DNA binding, and reporter assays

    PMID:9308237

    Open questions at the time
    • No endogenous target genes identified at this stage
    • Activator-to-repressor switch mechanism not yet defined
  2. 2001 High

    Resolved how Myc converts MIZ1 into a repressor at a physiological target, showing a Myc/Max/MIZ1 ternary complex represses p15INK4b at its initiator and that this is required for Myc-driven immortalization.

    Evidence Co-IP, ChIP, reporter assays and a Myc Miz1-binding mutant (V394D) in primary MEFs; companion paper linking TGFβ/Smad inputs to MIZ1 at p15

    PMID:11283613 PMID:11283614

    Open questions at the time
    • Coactivator displacement mechanism not yet detailed
    • Generality across other promoters untested
  3. 2002 High

    Defined the activator-to-repressor switch as competition for coactivators and added DNA-damage and microtubule-dependent regulatory layers controlling MIZ1 at p21Cip1 and other promoters.

    Evidence ChIP, Co-IP, siRNA and p300 competition at Nramp1/p21; TopBP1 negative regulation after UV; microtubule depolymerization-driven nuclear accumulation

    PMID:11545736 PMID:12110671 PMID:12244100 PMID:12408820 PMID:12840021

    Open questions at the time
    • Stoichiometry of coactivator/corepressor exchange unresolved
    • Signal controlling cytoplasmic-nuclear partitioning incompletely defined
  4. 2003 High

    Demonstrated an essential in vivo requirement for MIZ1, with knockout embryos dying at gastrulation, and broadened its partner network to immune transcription factors.

    Evidence Mouse knockout with embryonic lethality and loss of p57Kip2; yeast two-hybrid/ChIP placing MIZ1 with IRF-8 and PU.1 at Nramp1 in macrophages

    PMID:12904288 PMID:14560010

    Open questions at the time
    • Tissue-specific functions not yet separable from embryonic lethality
    • Direct vs indirect regulation of p57Kip2 unresolved
  5. 2004 High

    Showed MIZ1 mediates DNA-damage-induced arrest and is inhibited by Akt-dependent 14-3-3η binding to its DNA-binding domain, introducing kinase-controlled regulation of its dual activator/repressor outputs.

    Evidence Co-IP, Akt inhibitors, siRNA and reporter/cell-cycle assays; MAGE-A4 recruitment to p21 promoter

    PMID:14739298 PMID:15580267

    Open questions at the time
    • Precise phospho-sites enabling 14-3-3η binding not fully mapped
    • Interplay between 14-3-3 and Myc regulation unresolved
  6. 2005 High

    Generalized the MIZ1-hijacking model to BCL6 in germinal-center B cells and identified BCL2 as a pro-apoptotic MIZ1 target, establishing MIZ1 as a node for Myc-induced apoptosis.

    Evidence Reciprocal Co-IP, ChIP and BCL6 DNA-binding mutants; shRNA and BCL2 inhibitors with Myc binding mutant in fibroblasts

    PMID:16142238 PMID:16352593 PMID:17082179

    Open questions at the time
    • How a single MIZ1 platform selects activation vs repression per target unclear
    • Cell-type determinants of partner choice not defined
  7. 2006 High

    Extended the Myc-MIZ1 axis to cell-adhesion and differentiation genes, linking the complex to integrin regulation and epidermal differentiation.

    Evidence ChIP at α6/β1 integrin loci, MycV394D mutant, integrin rescue in reconstituted epidermis

    PMID:16391002

    Open questions at the time
    • Direct adhesion-gene repression mechanism vs indirect effects not fully separated
  8. 2007 High

    Provided structural and tissue-genetic grounding by showing the POZ domain tetramerizes via a novel β-sheet interface and is required cell-autonomously for skin/hair follicle proliferation control.

    Evidence 2.1 Å crystal structure with analytical ultracentrifugation and interface mutagenesis; K14-Cre POZ-deletion mouse with hair follicle phenotype

    PMID:17635993 PMID:17880999

    Open questions at the time
    • Functional role of tetramerization vs dimerization in vivo unresolved
    • POZ-dependent target genes in skin not enumerated
  9. 2008 High

    Connected MIZ1 to genome-stability signaling and stem-cell self-renewal, showing it stabilizes TopBP1 on chromatin to sustain ATR checkpoint signaling and is required for Myc-driven neural progenitor self-renewal.

    Evidence Co-IP, chromatin fractionation, ubiquitination assays and ATR readouts; MycV394D in neurosphere/differentiation assays

    PMID:18923429 PMID:19001505

    Open questions at the time
    • Whether TopBP1 protection is transcription-independent not fully resolved
    • Direct self-renewal target genes not defined
  10. 2009 High

    Broadened the corepressor catalog to Gfi-1 and uncovered the first transcription-independent MIZ1 function, inhibition of TRAF2-dependent JNK activation, with TNFα triggering MIZ1 degradation.

    Evidence Co-IP/ChIP with Gfi-1 at p15/p21; Miz1-/- MEFs with transcription-deficient mutant rescue, TRAF2 K63-ubiquitination assays; BCL6/MIZ1 at BCL2 promoter; ARF/p53 competition at MIZ1 zinc fingers

    PMID:19164764 PMID:19549844 PMID:19815509 PMID:19901969 PMID:20190815

    Open questions at the time
    • E3 ligase and sites for TNFα-induced MIZ1 degradation not yet identified
    • Structural basis of TRAF2 inhibition unresolved
  11. 2010 High

    Identified Mule/Huwe1 and ARF-driven sumoylation/heterochromatin assembly as control points and established Mule as a tumor suppressor by limiting Myc/MIZ1 complex accumulation; solved the BTB dimer structure.

    Evidence Co-IP, in-cell ubiquitination, siRNA/overexpression for Mule; sumoylation/ChIP for ARF; inducible Myc lymphoma model with TGFβ blockade; 2.6 Å BTB crystal structure

    PMID:20308430 PMID:20493880 PMID:20551174 PMID:20624960

    Open questions at the time
    • Linkage between TNFα/Mule degradation and tumor-suppressive Myc/MIZ1 control incompletely integrated
    • How ARF directs sumoylation mechanistically unresolved
  12. 2011 High

    Resolved the site-specific ubiquitin code controlling MIZ1 turnover (TRAF2 at Lys388/Lys472) and established MIZ1 as essential for B- and T-lineage development via SOCS1 repression and Bcl2 activation downstream of IL-7R/STAT5.

    Evidence Ubiquitination-site mutagenesis with JNK/inflammation rescue; ΔPOZ knockouts, ChIP at SOCS1, Bcl2/Ebf1/TCRαβ genetic rescues

    PMID:21167753 PMID:21258009 PMID:21841135 PMID:22184250

    Open questions at the time
    • How TRAF2 acts as both partner and degrading ligase context-dependently unresolved
    • Direct vs indirect control of pre-TCR expression unclear
  13. 2013 High

    Expanded MIZ1's roles into autophagy, inflammation resolution, Hedgehog signaling and Mule-dependent tumor suppression, and defined Ser178-phospho-dependent HDAC1 recruitment as the repression mechanism.

    Evidence ChIP-seq and neuronal conditional KO for autophagy; phospho-Ser178/HDAC1 ChIP at C/EBPδ in LPS models; Smo/Gli2 Co-IP and cilia localization; Mule skin-KO tumor model with Myc/Miz1 epistasis

    PMID:23525087 PMID:23671675 PMID:23699408 PMID:24088869

    Open questions at the time
    • Hedgehog regulation rests on a single Medium-confidence study
    • How Ser178 phosphorylation is signal-coupled across contexts not unified
  14. 2014 High

    Provided crystallographic basis for MIZ1 heterodimerization with oncogenic POZ partners and added Rpl22-mediated p53 restraint and viral/NAC1 hijacking to the repression repertoire.

    Evidence Crystal structures of MIZ1/BCL6 and MIZ1/NAC1 POZ heterodimers; ChIP/RNA-IP for Rpl22-p53 mRNA; NAC1 and EBNA3A Co-IP/ChIP studies

    PMID:24702277 PMID:25092922 PMID:25468973 PMID:25484205

    Open questions at the time
    • Whether heterodimers form on or off DNA in vivo not resolved
    • Selectivity rules among competing POZ partners undefined
  15. 2016 High

    Mapped the structural logic of MIZ1 DNA recognition and extended Myc/MIZ1 repression to circadian clock genes and Group 3 medulloblastoma identity.

    Evidence NMR of ZFs 1-4 with A86K affinity mutant; MycV394D knock-in, ChIP-seq and in vivo medulloblastoma models; clock-gene reporter/qPCR with MycV394D

    PMID:26766587 PMID:27339797 PMID:28035002

    Open questions at the time
    • Full-length DNA-bound architecture not determined
    • Clock-gene repression rests on a single Medium-confidence study
  16. 2017 High

    Demonstrated MIZ1 maintains the differentiated, post-mitotic state of Schwann cells by directly repressing the histone demethylase Kdm8, with loss causing cell-cycle re-entry and demyelinating neuropathy.

    Evidence ChIP, RNA-seq, Schwann-cell conditional POZ KO and H3K36me2 profiling

    PMID:29217679

    Open questions at the time
    • Whether Kdm8 repression involves a known corepressor partner not defined
  17. 2020 High

    Established Myc/MIZ1 interaction as a driver of leukemia stem-cell self-renewal and MIZ1 as a negative regulator of NF-κB-driven lung inflammation, separating transcriptional and pathway-restraint functions.

    Evidence MycV394D MLL-AF9 AML model with serial transplantation and ChIP at Cebpα/δ; lung-epithelial POZ KO with NF-κB/RelA co-deletion epistasis

    PMID:32040550 PMID:32851183

    Open questions at the time
    • Molecular mechanism of MIZ1's NF-κB restraint not defined at this stage
  18. 2021 High

    Defined the bipartite scanning-recognition mechanism of the zinc fingers and added multiple transcription-independent and target-gene functions, including MTDH sequestration restraining NF-κB, diphthamide biosynthesis via Dph1, and ACE2/TLR3 control.

    Evidence NMR relaxation dispersion of ZFs 10-11; hepatocyte KO with Miz1-MTDH Co-IP and NF-κB assays; CRISPR screens and ChIP at Dph1/ACE2; MYC/MIZ1 Co-IP in PDAC dsRNA pathway; MXD-MIZ1 binding mutants

    PMID:33057331 PMID:33914337 PMID:34038747 PMID:34145038 PMID:34305888 PMID:34963061

    Open questions at the time
    • Structural basis of MTDH sequestration unresolved
    • Whether NF-κB and JNK restraint converge mechanistically unclear
  19. 2023 High

    Uncovered MIZ1's control of mitophagy through cytosolic PRDX6 retention and a TNFα-driven degradation feedback loop, plus an RXRA-dependent senescence-suppressing role.

    Evidence Co-IP/MS, hepatocyte KO, NASH organoids and proximity ligation for PRDX6/Parkin; Co-IP and ITPR2 epistasis for RXRA-driven senescence

    PMID:37040844 PMID:37698375

    Open questions at the time
    • RXRA-senescence axis rests on a single Medium-confidence study
    • How cytosolic vs nuclear MIZ1 pools are partitioned for these roles unclear
  20. 2026 High

    Refined MIZ1's role in immunity to isotype- and signaling-specific control, regulating TMBIM4/calcium homeostasis, type I IFN and IL-12 via HDAC1, peroxisome biogenesis via PEX13, and BCR signaling/actin gene programs.

    Evidence CRISPR screens, conditional KOs, ChIP/ChIP-seq at TMBIM4/Ifna/Ifnb/Il12/PEX13, Ca2+ flux, metabolomics and BCR crosslinking assays

    PMID:35833903 PMID:38579014 PMID:38593156 PMID:40243840 PMID:41972179

    Open questions at the time
    • Whether a unifying logic governs MIZ1 activation vs HDAC1-dependent repression across these targets is undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved what determines, at any given promoter or in any given tissue, whether MIZ1 acts as a coactivator-recruiting transcriptional activator, an HDAC1-recruiting repressor, or a transcription-independent cytosolic sequestering scaffold.
  • No structure of full-length MIZ1 on DNA with a partner
  • Signal-to-output decision logic across contexts unmapped
  • Quantitative model of partner competition lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 4 GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 4 GO:0140313 molecular sequestering activity 2
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 3 GO:0005929 cilium 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-168256 Immune System 5 R-HSA-5357801 Programmed Cell Death 5 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1640170 Cell Cycle 4 R-HSA-1643685 Disease 4 R-HSA-9612973 Autophagy 2

Evidence

Reading pass · 61 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 Miz1 (ZBTB17) was identified as a novel zinc finger protein that directly interacts with the Myc oncoprotein C-terminus via yeast two-hybrid and binds to core promoter/initiator elements to activate transcription, defining a new pathway for Myc-mediated gene repression. Yeast two-hybrid, in vitro binding, reporter assays Current topics in microbiology and immunology Medium 9308237
1997 Miz1 is a sequence-specific DNA-binding transcription factor that interacts directly with Msx2 in vitro, enhancing Msx2's DNA binding affinity for the osteocalcin promoter; the craniosynostosis-associated P148H mutation in Msx2 augments this interaction. Yeast two-hybrid, in vitro binding, EMSA, reporter assays Mechanisms of development Medium 9256341
2001 Miz1 binds the initiator element of the p15INK4b promoter and activates its transcription; Myc and Max form a ternary complex with Miz1 at this initiator to repress p15INK4b, preventing cellular senescence. Myc alleles unable to bind Miz1 fail to suppress p15INK4b and are deficient in immortalization. Co-IP, ChIP, reporter assays, Myc point mutant (V394D), primary MEFs Nature cell biology High 11283613
2001 TGFβ signaling prevents Myc from being recruited to the p15INK4b initiator via Miz1, relieving repression; a TGFβ-induced Smad complex contacts Miz1 at an upstream p15INK4b promoter element to activate transcription. Thus Miz1 integrates two TGFβ-dependent inputs at p15INK4b. ChIP, Co-IP, reporter assays, dominant-negative Smad constructs Nature cell biology High 11283614
2001 Miz1 is regulated by association with microtubules: Miz1 is largely cytoplasmic and associates with beta-tubulin/microtubules; microtubule depolymerization causes Miz1 to accumulate in the nucleus, where it binds the LDLR and alpha2-integrin promoters to activate transcription. Soft X-ray microscopy, indirect immunofluorescence, GFP time-lapse microscopy, ChIP, in vitro binding Molecular cell Medium 11545736
2002 Miz1 binds the p21Cip1 core promoter in vivo and is required for UV-induced upregulation of p21Cip1. Topoisomerase II binding protein (TopBP1) associates with Miz1 and negatively regulates its transactivation activity; UV irradiation downregulates TopBP1, releasing Miz1. Myc binds Miz1 to repress p21Cip1 after UV and facilitates recovery from UV-induced arrest. ChIP, Co-IP, c-myc-/- cells, Myc point mutant deficient in Miz1 binding, siRNA Molecular cell High 12408820
2002 Miz1 activates the Nramp1 promoter via initiator elements; c-Myc represses Nramp1 by competing with p300/CBP for binding to Miz1 at the initiator. An Sp1-binding GC box is required for Miz1-dependent transactivation; c-Myc competes with p300 for Miz1 binding. Reporter assays, Co-IP, ChIP, siRNA knockdown, deletion analysis The Journal of biological chemistry Medium 12110671 12840021
2002 Host cell factor-1 (HCF-1) directly binds Miz1 at both its POZ domain and a C-terminal transactivation domain (aa 637-803), repressing Miz1-mediated transactivation of the p15INK4b promoter by interfering with recruitment of p300 to Miz1, analogous to c-Myc. Yeast two-hybrid, Co-IP, GST pulldown, reporter assays The Journal of biological chemistry Medium 12244100
2003 Miz1 is required for early embryonic development: Miz1-/- embryos die at E7.5 with failure of gastrulation, massive apoptosis of ectodermal cells, and absence of p57Kip2 expression (a Miz1 target gene), demonstrating an essential in vivo function. Homologous recombination knockout in mouse, in situ hybridization, immunostaining Molecular and cellular biology High 14560010
2003 Miz1 interacts with IRF-8 and PU.1 on the Nramp1 promoter in macrophages, forming a complex required for Nramp1 transcription; identified by yeast two-hybrid and confirmed in immune cells at the endogenous promoter. Yeast two-hybrid, Co-IP, ChIP, reporter assays The Journal of biological chemistry Medium 12904288
2004 Miz1 is required for DNA damage-induced cell cycle arrest. 14-3-3eta binds Miz1's DNA-binding domain in an Akt-phosphorylation-dependent manner, inhibiting Miz1 function and regulating recovery from arrest. Miz1 has two DNA-damage functions: upregulation of a gene group (regulated by Myc, not 14-3-3eta) and repression of another group (regulated by Akt/14-3-3eta). Co-IP, siRNA, Akt inhibitors, reporter assays, cell cycle analysis Nature cell biology High 15580267
2004 A cleaved C-terminal fragment of MAGE-A4 binds Miz1 (identified by yeast two-hybrid), is recruited to the p21Cip1 promoter via Miz1, and downregulates p21Cip1 transcription to induce apoptosis. Yeast two-hybrid, Co-IP, ChIP, reporter assays The Journal of biological chemistry Medium 14739298
2005 BCL6 interacts directly with Miz1 and, via Miz1, binds and represses the CDKN1A (p21) promoter in germinal center B cells, preventing p53-independent cell cycle arrest; this mechanism does not require a BCL6 DNA-binding site on the target gene. Co-IP, ChIP, reporter assays, BCL6 mutants Nature immunology High 16142238
2005 Miz1 inactivation by c-MYC is essential for MYC-induced apoptosis in primary human fibroblasts upon growth factor withdrawal; MIZ1 activates BCL2 transcription, and repression of BCL2 by MYC/MIZ1 is the critical pro-apoptotic event. MIZ1 inactivation is dispensable for MYC-induced cell cycle progression and transformation in the assays used. shRNA knockdown, Myc Miz1-binding mutant, reporter assays, shRNA targeting BCL2, small-molecule BCL2 inhibitors The Journal of biological chemistry High 16352593 17082179
2006 Myc-Miz1 complex directly binds alpha6 and beta1 integrin gene loci (by ChIP) and regulates keratinocyte adhesion and TGFβ responsiveness; using MycV394D (Miz1-binding deficient), Miz1 is shown to mediate Myc-dependent regulation of cell adhesion genes and Myc-induced epidermal differentiation. ChIP, Myc V394D mutant, reconstituted epidermis, overexpression of beta1 integrin The Journal of cell biology High 16391002
2007 The Miz1 POZ domain forms a tetramer in solution via two distinct interfaces: a canonical alpha-helical dimer interface and a novel beta-sheet interface that mediates association of two POZ dimers; the beta-sheet interface directs tetramerization. X-ray crystallography (2.1 Å), analytical ultracentrifugation, mutagenesis of interface residues Journal of molecular biology High 17880999
2007 Miz1 POZ domain is required for hair follicle proliferation control and hair morphogenesis; conditional deletion of the POZ domain in keratinocytes (K14-Cre) causes altered hair follicle orientation, suprabasal proliferation, and delayed catagen, demonstrating a cell-autonomous function of Miz1 in skin. Conditional knockout (K14-Cre/Miz1lox/lox), histology, BrdU proliferation assay Journal of cell science High 17635993
2008 Miz1 is required for recruitment of TopBP1 to chromatin and for protection of TopBP1 from proteasomal degradation by the HectH9 (Mule/Huwe1) ubiquitin ligase; Myc antagonizes TopBP1-Miz1 binding, causing TopBP1 dissociation from chromatin and reduced ATR-dependent checkpoint signaling. Co-IP, chromatin fractionation, siRNA, ubiquitination assays, ATR pathway readouts The EMBO journal High 18923429
2008 Myc increases self-renewal of neural progenitor cells through Miz1: Myc requires the ability to bind Miz1 (MycV394D is deficient) to increase self-renewing fractions under differentiation conditions, while proliferation stimulation is Miz1-independent. Retroviral transduction, Myc V394D mutant, neurosphere assays, differentiation assays Journal of cell science Medium 19001505
2009 BCL6 binds the BCL2 promoter via Miz1 and suppresses Miz1-induced BCL2 transcription in germinal center B cells, facilitating GC B cell apoptosis; this mechanism is disrupted in FL/DLBCL by BCL2 translocations and Miz1 deregulation. Co-IP, ChIP, reporter assays, BCL6 mutants, shRNA Proceedings of the National Academy of Sciences of the United States of America High 19549844
2009 Miz1 acts as a signal- and pathway-specific modulator (SMOR) to suppress TNFα-induced JNK1 activation independently of its transcriptional activity; Miz1 inhibits TRAF2 K63-linked polyubiquitination. Upon TNFα stimulation, Miz1 undergoes proteasomal degradation, de-repressing JNK1 activation. Miz1-/- MEFs, reintroduction of transcription-deficient Miz1 mutant, ubiquitination assays, proteomics/yeast two-hybrid, cell death assays Proceedings of the National Academy of Sciences of the United States of America High 19815509
2009 Gfi-1 represses CDKN2B (p15INK4B) by interacting with Miz1 and being recruited to the CDKN2B core promoter via Miz1; Gfi-1 and c-Myc collaborate on the CDKN2B promoter through Miz1, both repressing Miz1-mediated transactivation. Co-IP, ChIP, reporter assays, Gfi-1 knockdown/KO Proceedings of the National Academy of Sciences of the United States of America Medium 19164764
2009 ARF binds Miz1 through the zinc finger domain of Miz1, and the zinc finger domain of Miz1 mediates interaction with p53, enabling Miz1 to inhibit p53 DNA binding and transactivation; ARF and p53 compete for Miz1 binding, and ARF antagonizes Miz1-mediated p53 suppression. Yeast two-hybrid, in vitro binding, competitive ChIP, reporter assays Oncogene Medium 19901969
2010 Mule/Huwe1 E3 ubiquitin ligase is the enzyme that catalyzes K48-linked polyubiquitination of Miz1 upon TNFα stimulation, leading to proteasomal degradation of Miz1 and de-repression of JNK activation; Mule physically associates with Miz1 in a manner promoted by TNFα. Co-IP, ubiquitination assays, siRNA knockdown, ectopic expression of Mule Proceedings of the National Academy of Sciences of the United States of America High 20624960
2010 ARF interacts with Miz1, disrupts the Miz1-nucleophosmin coactivator interaction, induces Miz1 sumoylation, and promotes assembly of a heterochromatic complex (containing Myc, Miz1, and H3K9me3) that represses cell adhesion and signal transduction genes, inducing apoptosis. Co-IP, sumoylation assay, ChIP, immunofluorescence, functional adhesion assays The Journal of cell biology High 20308430
2010 Myc must continuously bind Miz1 to repress CDK inhibitor expression (p15, p21) and suppress H3K9me3 accumulation (senescence marker) in T-cell lymphomas; TGFβ2/3 autocrine signaling induces CKI expression and senescence upon Myc inactivation, and Myc/Miz1 interaction antagonizes this TGFβ-driven senescence program. Tet-off Myc system, MycV394D mutant, ChIP for H3K9me3, TGFβ blocking antibodies, conditional lymphoma model Genes & development High 20551174
2010 Gfi-1 represses CDKN1A (p21Cip1) in a DNA-binding-independent manner by interacting with Miz1 and forming a ternary complex with c-Myc on the CDKN1A core promoter; Gfi-1 knockdown elevates p21Cip1 and reduces proliferation. Co-IP, ChIP, reporter assays, siRNA knockdown Oncogene Medium 20190815
2010 Miz1 POZ domain is required for B cell development: mice lacking the POZ domain (Zbtb17ΔPOZ/ΔPOZ) almost completely lack follicular B cells because progenitors cannot activate JAK-STAT5 or upregulate Bcl2 upon IL-7 stimulation. Miz1 directly represses Socs1 and activates Bcl2; combined Bcl2 and Ebf1 re-expression rescues B cell development. Conditional knockout, FACS, ChIP, retroviral rescue experiments (Bcl2 + Ebf1) Immunity High 21167753
2010 BTB domain crystal structure of Miz1 was solved at 2.6 Å, showing a strand-swapped dimer with a shorter N-terminus compared to other BTB proteins; cysteine cross-linking experiments confirmed the dimer form. X-ray crystallography (2.6 Å), cysteine cross-linking Journal of molecular biology High 20493880
2011 Miz1 is required for T cell development: Miz1ΔPOZ mice lack early T lineage precursors and show a DN3-DN4 differentiation block due to impaired IL-7R/STAT5/Bcl2 signaling; Miz1 binds the SOCS1 promoter to repress SOCS1, and SOCS1 overexpression in Miz1ΔPOZ cells blocks IL-7 signaling. Conditional knockout, FACS, ChIP at SOCS1 promoter, transgenic Bcl2 overexpression, SOCS1 inhibition Blood High 21258009
2011 Miz1ΔPOZ pre-T cells at the beta-selection checkpoint show enhanced p53 target gene expression (Cdkn1a, PUMA, Noxa); TCRαβ coexpression with Bcl2 (but not Bcl2 alone or p21 deletion) fully rescues differentiation, establishing that Miz1 regulates both p53 target gene control and pre-TCR expression at beta-selection. Conditional knockout, FACS, gene expression analysis, retroviral rescue (TCRαβ + Bcl2) Journal of immunology High 21841135
2011 Site-specific K48-linked ubiquitination of Miz1 at Lys388 and Lys472 by TRAF2 is required for TNFα-induced degradation of Miz1; non-degradable Miz1 (K388R/K472R) sustains JNK1 inhibition and suppresses inflammation. Miz1 inhibits TRAF2's ubiquitin ligase activity by competing with Ubc13 for TRAF2 RING domain binding. Site-directed mutagenesis of ubiquitination sites, ubiquitination assays, Co-IP, JNK activation assays, inflammation models Proceedings of the National Academy of Sciences of the United States of America High 22184250
2013 Mule/Huwe1 suppresses Ras-driven tumorigenesis by preventing c-Myc/Miz1 complex accumulation; in Mule-deficient skin, c-Myc/Miz1 complexes accumulate and p21/p15 are down-regulated, increasing tumorigenesis, which is reversed by c-Myc KO but not p53 KO; Miz1 knockdown also reverses the enhanced proliferation/tumor growth. Tissue-specific knockout (K14Cre;Muleflox/flox), concomitant c-Myc/p53/p19 knockouts, Miz1 shRNA, tumor allograft Genes & development High 23699408
2013 Miz1 POZ domain is required to terminate LPS-induced inflammation; after LPS stimulation, Miz1 is phosphorylated at Ser178 which is required for HDAC1 recruitment to the C/EBP-δ promoter to repress its transcription and terminate inflammatory cytokine expression. Conditional POZ KO mice, phospho-Ser178 mutagenesis, ChIP for HDAC1, LPS challenge model, Pseudomonas pneumonia model Nature immunology High 23525087
2013 Miz1 is required to maintain autophagic flux: Miz1 directly activates transcription of genes encoding autophagy regulators and vesicular transport components by binding non-palindromic sequences at core promoters; loss of Miz1 POZ domain in neurons causes Purkinje cell neurodegeneration with accumulation of polyubiquitinated proteins and p62. ChIP-seq, neuron-specific conditional KO (Nestin-Cre), autophagic flux assays, immunohistochemistry Nature communications High 24088869
2013 Miz1 regulates Hedgehog signaling: Miz1 binds Smoothened (Smo) and Gli2, positively regulates Gli reporter activity, and translocates to primary cilia with Smo and Gli2 upon Hh activation; Miz1 is required for Smo-dependent nuclear translocation of Gli2. Co-IP, Gli-luciferase reporter, immunofluorescence of primary cilia, Miz1 siRNA knockdown, in vivo allografts PloS one Medium 23671675
2014 Miz1 directly activates Rpl22 gene expression; Rpl22 protein binds p53 mRNA to inhibit its translation, thereby restricting p53 levels and protecting pro-B and DN3 pre-T cells undergoing V(D)J recombination from DNA damage-induced apoptosis. ChIP, RNA immunoprecipitation (p53 mRNA + Rpl22), genetic KO models, translation assays Proceedings of the National Academy of Sciences of the United States of America High 25468973
2014 Crystal structures of the heterodimeric POZ domains of Miz1/BCL6 and Miz1/NAC1 were solved, revealing the structural basis of Miz1 heterodimerization with two oncogenic POZ-domain partners; the interactions are mediated by the canonical alpha-helical POZ dimerization interface. X-ray crystallography of tethered heterodimers Acta crystallographica. Section F, Structural biology communications High 25484205
2014 Nac1 (a POZ-domain repressor overexpressed in ovarian carcinoma) interacts with Miz1 via a heterodimeric POZ domain interaction and relocalizes Miz1 to discrete nuclear bodies; Nac1 siRNA knockdown elevates the Miz1 target p21Cip1, mechanistically linking Nac1-Miz1 interaction to tumor suppression. Co-IP, chemical crosslinking, immunofluorescence, siRNA knockdown, Western blot Bioscience reports Medium 24702277
2014 EBNA3A binds Miz1 (shown by yeast two-hybrid and confirmed at endogenous levels in EBV-infected B cells), causes Miz1 nuclear translocation, forms a trimeric complex with the Miz1 recognition sequence and Miz1, blocks Miz1-nucleophosmin interaction, and represses CDKN2B with establishment of H3K27me3 marks. Yeast two-hybrid, Co-IP at endogenous levels, ChIP, reporter assays, immunofluorescence Nucleic acids research Medium 25092922
2015 ZBTB17 was identified as a binding partner of CSRP3 (cysteine and glycine-rich protein 3) by yeast two-hybrid; ZBTB17 expression protected cardiomyocytes from apoptosis in vitro; cardiac myocyte-specific Zbtb17 deletion in mice develops cardiomyopathy and fibrosis after biomechanical stress; ZBTB17 regulates cardiomyocyte hypertrophy in a calcineurin-dependent manner. Yeast two-hybrid, cardiac-specific KO mouse, biomechanical stress models, in vitro apoptosis assays, hypertrophy assays Circulation. Cardiovascular genetics Medium 26175529
2016 MYC/MIZ1 repressive complexes directly downregulate core circadian clock genes BMAL1, CLOCK, and NPAS2; overexpression of MYC attenuates the clock and promotes proliferation, while MYC knockdown strengthens the clock; the mechanism requires MYC-MIZ1 complex formation. MYC overexpression/knockdown, MycV394D mutant, reporter assays, qPCR Nature communications Medium 27339797
2016 Myc/Miz1 interaction defines Group 3 medulloblastoma identity: Myc (but not MycN) binds Miz1 strongly and suppresses ciliogenesis and reprograms the SHH GNP transcriptome via Miz1-dependent gene repression; genetic disruption of Myc/Miz1 interaction inhibits G3 MB development. MycV394D knock-in, ChIP-seq, in vivo medulloblastoma mouse models, GNP culture Cancer cell High 26766587
2016 NMR structural analysis of Miz1 ZFs 1-4 shows that ZFs 3 and 4 form an unusually compact, stable structure that restricts their motion and limits DNA scanning speed, preventing nonspecific binding; an A86K mutation destabilizes this compact structure and increases DNA affinity 30-fold. NMR (solution structure), mutagenesis (A86K), DNA binding assays 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 in Schwann cells releases Kdm8 repression, causing H3K36 hypomethylation at cell-cycle gene loci and re-entry of adult Schwann cells into the cell cycle, leading to demyelinating neuropathy. RNA-seq, ChIP (direct Miz1 binding at Kdm8 promoter), Schwann cell-specific conditional KO, H3K36me2 ChIP The Journal of neuroscience High 29217679
2020 Myc-Miz1 interaction is required for leukemia stem cell self-renewal in AML: MycV394D-expressing HSPCs generate AML with reduced penetrance; AML cells expressing MycV394D show partial differentiation, reduced colony-forming ability, and reduced leukemogenic capacity with decreased LSC frequency. Mechanistically, Myc represses Miz1-mediated activation of Cebpα and Cebpδ to maintain the undifferentiated LSC state. MycV394D mutant, MLL-AF9 AML mouse model, serial transplantation, ChIP, shRNA Blood High 32040550
2020 Lung epithelial cell-specific loss of Miz1 POZ domain in mice causes spontaneous COPD-like phenotype through sustained NF-κB-dependent inflammation; concomitant partial loss of NF-κB/RelA prevents the COPD phenotype, positioning Miz1 as a negative regulator of NF-κB signaling in lung epithelium. Miz1 loss also upregulates Ace2 expression. Lung epithelial-specific conditional KO, NF-κB/RelA genetic co-deletion, qPCR, histology Science advances High 32851183
2021 MYC suppresses loading of nuclear-derived double-stranded RNA onto TLR3 and its lysosomal degradation via association with MIZ1, thereby enabling immune evasion in PDAC; deletion of TBK1 bypasses the requirement for high MYC expression. Myc deletion in KRAS/TP53 PDAC model, TBK1 deletion, dsRNA localization, MYC/MIZ1 co-IP Cancer research Medium 34145038
2021 Miz1 suppresses hepatocellular carcinoma by sequestering the oncoprotein metadherin (MTDH) to prevent MTDH-driven NF-κB activation; this function is independent of Miz1 transcriptional activity. Hepatocyte-specific Miz1 deletion generates pro-inflammatory cytokine-producing hepatocytes that polarize tumor-associated macrophages. Hepatocyte-specific KO, Co-IP of Miz1-MTDH, NF-κB reporter, macrophage polarization assays Immunity High 34038747
2021 ACE2 is a direct transcriptional target of Miz1 repression: Miz1 binds the ACE2 promoter (by ChIP) in mouse and human lung epithelial cells and represses its expression; loss of Miz1 upregulates ACE2. ChIP, reporter assays, Miz1 conditional KO Frontiers in immunology Medium 34305888
2021 Miz1 (ZBTB17) is absolutely required for diphthamide biosynthesis by directly activating Dph1 transcription via binding to the Dph1 proximal promoter at an evolutionarily conserved Miz1 consensus site; identified by genome-wide CRISPR KO screens. CRISPR genome-wide KO screen (two independent), ChIP at Dph1 promoter, reporter assays PLoS genetics High 33057331
2021 MXDs activate transcription of p15 and p21 through interaction with MIZ1; MXD mutants deficient in MIZ1 binding retain DNA binding and MAX interaction but fail to activate MYC-repressed genes, establishing that MXD-MIZ1 interaction is required for antagonism of MYC-repressed (not MYC-activated) target genes. MXD-MIZ1 binding mutants, reporter assays, RT-PCR FEBS letters Medium 33914337
2021 NMR characterization of Miz1 ZFs 10-11 reveals conformational exchange in the linker between ZFs 10 and 11 on the μs-ms timescale; this exchange uncouples ZFs 7-10 from ZFs 11-12 and promotes a scanning-recognition mechanism where two segments cooperate to bind two sub-sites of the 24 bp consensus at transcriptional start sites. NMR (15N relaxation dispersion), DNA binding assays, NMR structure Structure High 34963061
2022 Miz1 directly represses IL-12 transcription by recruiting HDAC1 to the Il12 promoter (by ChIP) in lung epithelial cells and dendritic cells; loss of Miz1 upregulates IL-12, stimulating a Th1 response that counteracts Th2/allergic asthma. Cell-specific conditional KO (epithelial and dendritic cell Cre), ChIP-seq/ChIP-qPCR at Il12 promoter, asthma mouse models American journal of respiratory cell and molecular biology High 35833903
2022 Miz1 promotes KRAS-driven lung tumorigenesis by directly binding and repressing the Pcdh10 promoter (by ChIP); silencing Pcdh10 rescues proliferation and tumor growth in Miz1-knockout KRAS-mutant cells in vitro and in vivo, establishing the Miz1/Pcdh10 axis. Miz1 conditional KO, ChIP at Pcdh10 promoter, RNA-seq, Pcdh10 siRNA rescue, allograft model Cancer letters High 36538983
2023 Miz1 binds PRDX6 and retains it in the cytosol, blocking PRDX6 interaction with mitochondrial Parkin at Cys431 and inhibiting Parkin-mediated mitophagy; in NASH livers, Miz1 loss allows PRDX6-mediated mitophagy inhibition, accumulation of dysfunctional mitochondria, and TNFα production, which in turn causes Miz1 E3-ubiquitination and degradation, forming a positive feedback loop. Co-IP/mass spectrometry, hepatocyte-specific Miz1 KO, AAV8 overexpression, human NASH organoids, proximity ligation assay Journal of hepatology High 37040844
2023 ZBTB17 interacts with nuclear receptor RXRA; knockdown of ZBTB17 induces RXRA-dependent activation of ITPR2-mediated intracellular calcium signaling, leading to mitochondrial dysfunction, ROS accumulation, DNA damage, and cellular senescence; silencing ITPR2 abolishes the senescence induced by ZBTB17 knockdown. Co-IP, siRNA knockdown, calcium imaging, ROS assays, senescence markers FASEB journal Medium 37698375
2024 Miz1 epigenetically represses Ifna and Ifnb genes in lung epithelial cells by recruiting HDAC1 to their promoters; IAV infection induces Miz1 accumulation by promoting CUL4B-mediated ubiquitination and degradation of the E3 ligase Mule, thereby stabilizing Miz1, which limits type I IFN production and favors viral replication. ChIP (HDAC1 at Ifna/Ifnb promoters), Miz1 conditional KO, ubiquitination assays, CUL4B overexpression/knockdown, in vitro and in vivo IAV infection Science signaling High 38593156
2024 MIZ1 is specifically required for IgG1+ GC B cell survival during positive selection; mechanistically, MIZ1 activates TMBIM4, which regulates IP3R-mediated Ca2+ mobilization downstream of BCR signaling to prevent mitochondrial Ca2+ overload and apoptosis in IgG1+ GC B cells. CRISPR-Cas9 screen, conditional mouse genetics, ChIP, Ca2+ flux assays, mitochondrial dysfunction readouts Science immunology High 38579014
2025 ZBTB17/MIZ1 promotes peroxisome biogenesis by directly activating transcription of PEX13 (a key peroxisomal protein importer); knockdown of ZBTB17 reduces PEX13 expression and impairs peroxisomal protein import, leading to metabolic alterations including downregulated purine synthesis. CRISPR/Cas9 ubiquitin ligase library screen, ChIP at PEX13 promoter, reporter assays, metabolomics The Journal of cell biology High 40243840
2026 MIZ-1 directly regulates genes involved in BCR signal transduction and actin cytoskeleton dynamics (by ChIP-seq); Miz1ΔPOZ B cells show defective BCR-induced receptor clustering, impaired SYK/RAF1/AKT/ERK signaling, altered calcium flux, and mitochondrial respiration defects, leading to reduced follicular B cell survival. ChIP-seq, CRISPR, conditional KO, RNA-seq, Ca2+ flux, mitochondrial respiration assays, BCR crosslinking Frontiers in immunology High 41972179

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 479 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 281 16142238
2002 Negative regulation of the mammalian UV response by Myc through association with Miz-1. Molecular cell 264 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
2016 MYC/MIZ1-dependent gene repression inversely coordinates the circadian clock with cell cycle and proliferation. Nature communications 100 27339797
2010 The interaction between Myc and Miz1 is required to antagonize TGFbeta-dependent autocrine signaling during lymphoma formation and maintenance. Genes & development 100 20551174
2013 The role of MIZ-1 in MYC-dependent tumorigenesis. Cold Spring Harbor perspectives in medicine 90 24296348
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 85 21123453
2001 Transcription factor MIZ-1 is regulated via microtubule association. Molecular cell 79 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 73 21167753
2021 The zinc finger protein Miz1 suppresses liver tumorigenesis by restricting hepatocyte-driven macrophage activation and inflammation. Immunity 71 34038747
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 71 18923429
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
2023 A TNFα/Miz1-positive feedback loop inhibits mitophagy in hepatocytes and propagates non-alcoholic steatohepatitis. Journal of hepatology 57 37040844
2006 BCL2 is a downstream effector of MIZ-1 essential for blocking c-MYC-induced apoptosis. The Journal of biological chemistry 54 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 48 19001505
2013 Miz1 is required to maintain autophagic flux. Nature communications 47 24088869
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 47 9308237
1999 Zimp encodes a homologue of mouse Miz1 and PIAS3 and is an essential gene in Drosophila melanogaster. Gene 46 10095110
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
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 40 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
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 31 25468973
2003 Nramp1-mediated innate resistance to intraphagosomal pathogens is regulated by IRF-8, PU.1, and Miz-1. The Journal of biological chemistry 31 12904288
2007 A beta-sheet interaction interface directs the tetramerisation of the Miz-1 POZ domain. Journal of molecular biology 30 17880999
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 23 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 22 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
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 20 29217679
2004 Induction of G1 cell cycle arrest and P15INK4b expression by ECRG1 through interaction with Miz-1. Journal of cellular biochemistry 20 15095404
2019 Deletion of the Miz-1 POZ Domain Increases Efficacy of Cytarabine Treatment in T- and B-ALL/Lymphoma Mouse Models. Cancer research 18 31273062
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
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
2012 Miz1 is a critical repressor of cdkn1a during skin tumorigenesis. PloS one 15 22509363
2011 The proto-oncoprotein KR-POK represses transcriptional activation of CDKN1A by MIZ-1 through competitive binding. Oncogene 15 21804610
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 11 28266617
2022 Myc-Interacting Zinc Finger Protein 1 (Miz-1) Is Essential to Maintain Homeostasis and Immunocompetence of the B Cell Lineage. Biology 10 35453704
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
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
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 7 37698375
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
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 6 40372432
2024 Regulation of BCR-mediated Ca2+ mobilization by MIZ1-TMBIM4 safeguards IgG1+ GC B cell-positive selection. Science immunology 6 38579014
2024 Miz1 represses type I interferon production and limits viral clearance during influenza A virus infection. Science signaling 6 38593156
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
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
2024 Chromosome 8q24 amplification associated with human hepatocellular carcinoma predicts MYC/ZEB1/MIZ1 transcriptional regulation. Scientific reports 4 39424877
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
2021 MXD/MIZ1 transcription regulatory complexes activate the expression of MYC-repressed genes. FEBS letters 3 33914337
2021 Zinc Fingers 10 and 11 of Miz-1 undergo conformational exchange to achieve specific DNA binding. Structure (London, England : 1993) 3 34963061
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
2025 ZBTB17/MIZ1 promotes peroxisome biogenesis by transcriptional regulation of PEX13. The Journal of cell biology 1 40243840
2024 Unraveling Novel Strategies: Targeting Miz1 for Degradation to Enhance Antiviral Defense against Influenza A Virus. Journal of respiratory biology and translational medicine 1 39086612
2026 MIZ-1 controls transcriptional programs required for BCR signaling, actin dynamics, and naïve B cell survival. Frontiers in immunology 0 41972179
2026 BMI1 activated by ZBTB17 stabilizes SMAD2 to promote chondrocyte anabolism and alleviate osteoarthritis. Journal of advanced research 0 42070686

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