| 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
|