Affinage

MXI1

Max-interacting protein 1 · UniProt P50539

Length
228 aa
Mass
26.1 kDa
Annotated
2026-06-10
79 papers in source corpus 27 papers cited in narrative 27 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

MXI1 (Mxi1) is a bHLH-Zip transcriptional repressor that antagonizes the Myc oncogenic program and acts as a tumor suppressor (PMID:8425219, PMID:9624006). It heterodimerizes specifically with Max and binds the CACGTG E-box, occupying Myc-Max target sites as a transactivation-incompetent complex; deletion of its basic DNA-binding region attenuates suppression, establishing site occupancy rather than simple Max titration as the dominant antagonism mechanism (PMID:8425219, PMID:8202517). Active repression is conferred by a short amino-terminal SIN3-interacting domain (SID) that recruits mSin3 and associated co-repressors, dramatically augmenting anti-Myc activity; a Sin3-fusion substituting for the SID recapitulates full repression, and Mxi1 in turn assembles NCOR1/2, Sin3A/B, and HDAC1 on target promoters (PMID:7889571, PMID:8649810, PMID:41428087). Beyond E-box-dependent repression, Mxi1 directly represses the c-MYC P2 promoter through a Sin3-independent mechanism requiring its leucine zipper and C-terminal CK2 sites, and MYC reciprocally suppresses MXI1 via miRNA induction, forming a negative feedback loop (PMID:9872993, PMID:32680921). Functionally, Mxi1 inhibits Myc-driven target genes such as ODC, arrests the cell cycle, suppresses transformation and tumor growth, and its loss in mice causes multi-organ and prostate hyperplasia with enhanced tumorigenesis (PMID:8202517, PMID:8637719, PMID:9624006, PMID:11351349). Mxi1 abundance is controlled post-translationally: S6K1 phosphorylation at S160 and PRMT5-mediated arginine methylation both promote β-TrCP-dependent ubiquitin–proteasome degradation, UBE2O ubiquitinates Mxi1 at K46, and FUBP3 counteracts turnover by stabilizing the protein (PMID:29507620, PMID:32901121, PMID:35149174, PMID:41428087). Transcriptionally, MXI1 is a hypoxia-inducible HIF-1/HIF-2 target and is repressed by multiple oncogenic miRNAs (miR-24-3p, miR-27a-3p, miR-155, miR-191), linking it to hypoxic adaptation, erythroid differentiation, and glioma proliferation (PMID:16319523, PMID:19254710, PMID:21196494, PMID:23254855, PMID:24376632). Alternative promoter usage and splicing generate functionally distinct isoforms, notably the cytoplasmic Mxi1-0, which retains Max and E-box binding but cannot repress Myc targets, and Mxi1-SRalpha, which has higher Sin3 affinity yet paradoxically activates the MYC promoter (PMID:15548375, PMID:15467743, PMID:15809730).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1993 High

    Established the founding molecular identity of Mxi1 as a Max partner that occupies Myc-Max DNA sites without activating transcription, defining it as a candidate Myc antagonist.

    Evidence Yeast two-hybrid interaction trap and E-box DNA binding assays

    PMID:8425219

    Open questions at the time
    • Did not establish how repression is enforced beyond site occupancy
    • No in vivo functional role demonstrated
  2. 1994 High

    Distinguished between two competing suppression models, showing transactivation-incompetent Mxi1-Max site occupancy, not mere Max sequestration, drives suppression of Myc-induced transformation.

    Evidence Rat embryo fibroblast focus formation assay with basic-region deletion mutants

    PMID:8202517

    Open questions at the time
    • Did not identify the repressive co-factors recruited
    • Transformation readout indirect for endogenous transcription
  3. 1995 High

    Identified the SID as the module that converts passive site occupancy into active repression by recruiting mSin3, explaining why SID-lacking isoforms are weak repressors.

    Evidence Deletion mutagenesis, co-IP, and REF transformation assays

    PMID:7889571 PMID:8649810

    Open questions at the time
    • HDAC enzymatic activity not directly shown in these studies
    • Genome-wide target occupancy unmeasured
  4. 1998 High

    Provided definitive in vivo proof that Mxi1 is a tumor suppressor, with loss causing hyperplasia and accelerated tumorigenesis cooperating with Ink4a deficiency.

    Evidence Mxi1 knockout mice, carcinogen challenge, and genetic cross with Ink4a-deficient mice

    PMID:9624006

    Open questions at the time
    • Did not resolve which target genes mediate the phenotype
    • Tissue-specific contributions not dissected
  5. 1999 Medium

    Revealed a second, Sin3-independent repression mode in which Mxi1 directly silences the c-myc P2 promoter via its leucine zipper and C-terminal CK2 sites, coupling Mxi1 to S-phase entry control.

    Evidence Reporter assays, inducible expression, and cell cycle analysis

    PMID:9872993

    Open questions at the time
    • CK2 phosphorylation of Mxi1 not directly demonstrated
    • Mechanism of USF antagonism unresolved
  6. 2004 High

    Demonstrated isoform-dependent functional divergence, with cytoplasmic Mxi1-0 retaining Max/E-box/Sin3 binding yet failing to repress Myc, and Mxi1-SRalpha paradoxically activating the MYC promoter.

    Evidence Promoter-specific RT-PCR, co-IP, EMSA, fractionation, and reporter/REF transformation assays

    PMID:15467743 PMID:15548375

    Open questions at the time
    • Mechanism of Mxi1-0 cytoplasmic retention unknown
    • Basis for SRalpha activation versus repression undefined
  7. 2005 Medium

    Identified additional isoform complexity with Mxi-D, which binds Max and Sin3 but cannot bind E-box DNA, acting as a dominant-negative.

    Evidence GST pulldown, EMSA, reporter, and colony formation assays

    PMID:15809730

    Open questions at the time
    • Endogenous abundance and physiological relevance unclear
    • Dominant-negative mechanism in vivo untested
  8. 2006 Medium

    Placed Mxi1 in a developmental program, positioning it downstream of proneural/Sox and Notch inputs during neurogenesis.

    Evidence Xenopus loss- and gain-of-function with in situ hybridization

    PMID:16457797

    Open questions at the time
    • Direct transcriptional targets in neural cells unidentified
    • Mammalian relevance not established
  9. 2008 Medium

    Connected Mxi1 to hypoxic signaling, showing it is a HIF-1-induced transcriptional target that downregulates Myc targets and buffers Myc-driven hypoxic apoptosis.

    Evidence Northern/Western in ARNT-deficient cells, reporter and apoptosis assays; shRNA in pVHL-defective cells with xenografts

    PMID:16319523 PMID:19018165

    Open questions at the time
    • Context-dependent oncogenic versus suppressive roles unresolved
    • Direct HIF binding element on canonical MXI1 promoter not mapped here
  10. 2009 Medium

    Mapped direct HIF binding to the MXI1-0 promoter and showed the MXI1-0 isoform is the predominant hypoxia-induced form, with limited effect on MYC under hypoxia.

    Evidence ChIP, transactivation reporter, and siRNA/RT-PCR

    PMID:19254710

    Open questions at the time
    • Functional consequence of MXI1-0 induction under hypoxia incompletely defined
    • Isoform-specific targets unknown
  11. 2013 High

    Established post-transcriptional control of MXI1 by oncogenic miRNAs, showing miR-191, miR-24-3p/miR-27a-3p, and miR-155 directly target the 3'UTR to modulate erythroid maturation and tumor cell proliferation.

    Evidence 3'UTR luciferase reporters, miRNA/shRNA modulation, rescue experiments, and RNA-seq

    PMID:21196494 PMID:23254855 PMID:24376632

    Open questions at the time
    • Relative contribution of each miRNA in normal tissue unclear
    • Downstream Myc target sets in each context not fully mapped
  12. 2020 High

    Defined the post-translational degradation machinery for Mxi1, identifying S6K1-S160 phosphorylation and UBE2O-K46 ubiquitination as drivers of β-TrCP/proteasome turnover that regulate Myc suppression and radioresistance.

    Evidence In vitro kinase/ubiquitination assays, site-directed mutagenesis, and in vivo rescue in lung cancer models

    PMID:29507620 PMID:32901121

    Open questions at the time
    • Interplay between S6K1 and UBE2O pathways not resolved
    • Deubiquitinase counter-regulation unidentified at this stage
  13. 2020 Medium

    Closed the MYC-MXI1 regulatory circuit, showing MYC represses MXI1 via miRNAs while MXI1 binds and represses the MYC promoter, forming a negative feedback loop.

    Evidence ChIP at MYC promoter, reporter assays, and miRNA functional studies

    PMID:32680921

    Open questions at the time
    • Quantitative dynamics of the feedback loop unmodeled
    • FTO/m6A contribution mechanistically incomplete
  14. 2022 High

    Extended Mxi1 regulation to arginine methylation, showing PRMT5 methylates Mxi1 to enhance β-TrCP binding and degradation, linking Mxi1 stability to DNA damage repair and radiosensitivity.

    Evidence In vitro methylation/ubiquitination assays, co-IP, PRMT5 inhibition (EPZ015666), and in vivo functional assays

    PMID:35149174

    Open questions at the time
    • Specific methylated arginine residue(s) not pinpointed
    • Crosstalk with S160 phosphorylation undefined
  15. 2022 Medium

    Identified non-Myc target genes of Mxi1, showing direct repression of the miR-300 promoter feeds a KLF9/GADD34 axis controlling tumor immunosuppression.

    Evidence ChIP, dual-luciferase reporter, loss/gain-of-function, and in vivo tumor models

    PMID:35501353

    Open questions at the time
    • Direct co-repressor recruitment at miR-300 promoter not shown
    • Generalizability beyond lung cancer untested
  16. 2025 Medium

    Showed Mxi1 stabilization by FUBP3 and direct co-repressor (NCOR1/2, Sin3A/B, HDAC1) recruitment to the RRAS promoter blocks ERK signaling and CD8+ T cell immune escape, integrating Mxi1 into immune regulation.

    Evidence Co-IP, lentiviral knockdown/overexpression, ChIP with co-repressor mapping, and in vivo AMKL mouse model

    PMID:41428087

    Open questions at the time
    • FUBP3-Mxi1 interaction interface unmapped
    • Whether RRAS repression is E-box-dependent unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the distinct degradation inputs (S6K1, UBE2O, PRMT5, β-TrCP) and stabilizers (FUBP3) are integrated to set Mxi1 levels across tissues, and what determines isoform-specific localization and the activator-versus-repressor switch, remains unresolved.
  • No structural model of the Mxi1-Max-Sin3 repressive complex
  • Genome-wide direct target catalog incomplete
  • Mechanism of cytoplasmic retention of Mxi1-0 unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 4
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 1
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1643685 Disease 4 R-HSA-392499 Metabolism of proteins 3 R-HSA-8953897 Cellular responses to stimuli 2
Partners
HDAC1MAXNCOR1NCOR2PRMT5SIN3ASIN3BUBE2O
Complex memberships
Mxi1-Max heterodimermSin3-HDAC co-repressor complex

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 MXI1 (Mxi1) interacts specifically with Max to form heterodimers that efficiently bind to the Myc-Max consensus recognition site (CACGTG E-box). When bound to DNA in yeast, Mxi1 does not stimulate transcription, consistent with it being a transcriptional repressor that sequesters Max and competes with Myc-Max heterodimers for target sites. Yeast two-hybrid interaction trap, DNA binding assays Cell High 8425219
1995 A short amino-terminal alpha-helical domain of Mxi1 (the SIN3-interacting domain, SID) dramatically augments its transcriptional repressive and anti-Myc suppressive potential by mediating physical association with a mammalian homolog of the yeast transcriptional repressor SIN3 (mSin3B). Mxi1 isoforms lacking this domain are functionally weaker repressors. Deletion mutagenesis, co-immunoprecipitation, rat embryo fibroblast transformation assay, transient transfection reporter assays Cell High 7889571
1994 Mad and Mxi1 suppress Myc-induced transformation (c-Myc and N-Myc, but not E1a) in rat embryo fibroblast cooperation assays. Deletion of the basic region (DNA-binding domain) attenuates suppression, indicating that occupation of common DNA binding sites by transactivation-incompetent Mxi1-Max complexes is the dominant suppression mechanism over simple Max titration. Rat embryo fibroblast focus formation assay, basic-region deletion mutants Proceedings of the National Academy of Sciences of the United States of America High 8202517
1996 mSin3A physically associates with the strong-repression isoform of Mxi1 (Mxi1-SR) and both co-localize to the nucleus. A mSin3A–Mxi1 fusion protein in which the Sin3-interacting domain of Mxi1 is replaced by full-length mSin3A retains or exceeds Mxi1-SR repression activity, demonstrating that the amino-terminal domain of Mxi1-SR functions solely to recruit mSin3A (and related proteins) and that this recruitment is necessary for anti-Myc activity. Co-immunoprecipitation, nuclear localization by immunofluorescence, fusion protein rescue in REF transformation assay Oncogene High 8649810
1996 Overexpression of Mxi1 inhibits Myc/Max-dependent transcriptional induction of the ornithine decarboxylase (ODC) gene in a dose-dependent manner both in vivo (transfection) and in vitro. Mxi1 protein levels are up-regulated during quiescence and down-regulated following serum stimulation. Transient transfection reporter assays, Northern blot for ODC mRNA Oncogene Medium 8637719
1998 Mice lacking Mxi1 exhibit progressive, multisystem abnormalities including prostate epithelial hyperplasia, increased susceptibility to carcinogen-induced tumors, and enhanced tumorigenesis when also deficient in Ink4a, establishing Mxi1 as a tumor suppressor in vivo that engages the Myc network in a functionally relevant manner. Targeted gene deletion (knockout mouse), carcinogen treatment, genetic cross with Ink4a-deficient mice Nature High 9624006
1999 Mxi1 represses transcription from the major c-myc promoter P2 by targeting the core promoter elements and reversing activation by the constitutive transcription factor USF. This repression is independent of mSin3 binding but requires the Mxi1 leucine zipper and C-terminal sequences including putative CK2 phosphorylation sites. Zinc-inducible Mxi1 expression blocks serum-induced c-myc transcription and cell entry into S phase. Transient transfection reporter assays, stable inducible expression (metallothionein promoter), cell cycle analysis The Journal of biological chemistry Medium 9872993
1999 The MXI1 promoter is GC-rich, lacks a TATA box, and its activity is driven primarily by two proximal initiator sequences combined with nearby Sp1 and MED-1 sites. MXI1 promoter activity is repressed by high levels of AP2 transcription factor. Promoter cloning, deletion analysis, transient transfection reporter assays The Journal of biological chemistry Medium 10497252
2001 Expression of Mxi1 in DU145 prostate carcinoma cells via adenoviral vector reduces cell proliferation, reduces soft agar colony formation, and causes G2/M phase cell cycle arrest associated with elevated cyclin B and reduced c-MYC and MDM2 protein levels. Adenoviral Mxi1 expression, MTT proliferation assay, soft agar colony formation, flow cytometry cell cycle analysis, Western blot The Prostate Medium 11351349
2004 Mxi1-0, an alternatively transcribed Mxi1 isoform using an upstream exon with a unique N-terminal sequence, can bind Max and E-box DNA sites and interact with Sin3, but is predominantly localized to the cytoplasm (unlike nuclear Mxi1) and fails to repress c-Myc-dependent transcription. Its levels are higher in primary glioblastoma than normal brain, suggesting it may modulate Mxi1's Myc-inhibitory activity. RT-PCR/cloning, co-immunoprecipitation, EMSA (E-box binding), reporter assays, subcellular fractionation/immunofluorescence Neoplasia (New York, N.Y.) High 15548375
2004 A novel Mxi1 isoform, Mxi1-SRalpha, arises from its own promoter and encodes a unique Sin3-interacting domain with greater affinity for Sin3 adapter proteins than the related Mxi1-SRbeta isoform, conferring enhanced transcriptional repression in reporter assays. Unlike Mxi1-SRbeta, Mxi1-SRalpha activates rather than represses the MYC promoter, and is a less potent suppressor of Myc-induced cellular transformation. Promoter-specific RT-PCR, co-immunoprecipitation, transient transfection reporter assays, REF transformation assay Oncogene Medium 15467743
2005 Mxi1 is induced by hypoxia in a HIF-1-dependent manner (not induced in ARNT/HIF-1β-deficient cells), identifying it as a transcriptional target of the HIF-1 complex. Mxi1 induction during hypoxia contributes to downregulation of c-Myc target genes (e.g., ODC) and protects cells from c-Myc-dependent sensitization to hypoxia-induced apoptosis. Northern/Western blot in ARNT-deficient cells, reporter assays, apoptosis assays Cancer biology & therapy Medium 16319523
2006 In Xenopus, Mxi1 is positively regulated by Sox3, SoxD, and proneural genes, and negatively by the Notch pathway. Loss-of-function of Xmxi1 impairs establishment of a mature neural state, while overexpression causes ectopic Sox3 activation and transient inhibition of N-tubulin and cell cycle genes (XPak3, p27), placing Mxi1 between pan-neural and proneural gene programs in neurogenesis. Xenopus loss-of-function (antisense/dominant-negative), overexpression, in situ hybridization Developmental biology Medium 16457797
2007 Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) physically interacts with Mxi1-SRalpha and enhances its ability to activate the MYC promoter, contributing to the differential function of SRalpha versus SRbeta isoforms. Co-immunoprecipitation, transient transfection reporter assay The FEBS journal Low 17697116
2008 Mxi1 is overexpressed in primary clear cell renal cancers bearing VHL inactivation (constitutive HIF signaling). shRNA inhibition of Mxi1 in pVHL-defective kidney cancer cells alters cell cycle parameters, inhibits Matrigel invasion, and suppresses tumor formation in vivo, establishing Mxi1 as a downstream HIF target that contributes to renal carcinoma tumorigenesis. shRNA knockdown, flow cytometry, Matrigel invasion assay, xenograft tumor formation Cancer biology & therapy Medium 19018165
2009 HIF-1α (and HIF-2) directly binds and transactivates sequences near the MXI1-0 promoter, inducing the MXI1-0 isoform rapidly under hypoxia in neuroblastoma and breast cancer cells. Knockdown of MXI1 had limited effect on MYC/MYCN activity under hypoxia, suggesting the two MXI1 isoforms differ in their ability to antagonize MYC under hypoxic conditions. ChIP, transactivation reporter assay, siRNA knockdown, RT-PCR Experimental cell research Medium 19254710
2010 miR-191 directly targets Mxi1 (and Riok3) in erythroid cells. Knockdown of Mxi1 blocks erythroid enucleation and chromatin condensation, while miR-191 overexpression phenocopies this by suppressing Mxi1. Down-regulation of miR-191 during terminal erythroid differentiation is required to allow Mxi1 upregulation and enable enucleation. miRNA overexpression/knockdown, shRNA knockdown of Mxi1, luciferase 3′UTR reporter assay, RNA-seq Genes & development High 21196494
2012 miR-24-3p and miR-27a-3p directly target the MXI1 3′UTR (validated by luciferase reporter assay) and cooperate to suppress MXI1 expression, thereby promoting glioma cell proliferation. Rescue experiments confirm that MXI1 knockdown phenocopies miRNA overexpression. 3′UTR luciferase reporter assay, MTT proliferation assay, rescue experiments, bioinformatic target prediction International journal of oncology Medium 23254855
2013 miR-155 directly targets the MXI1 3′UTR (attenuates luciferase reporter activity) and decreases MXI1 mRNA and protein levels in glioma cells, promoting glioma cell proliferation. Rescue experiments confirm that miR-155-mediated proliferation promotion is through MXI1 suppression. 3′UTR luciferase reporter assay, MTT assay, EdU incorporation, rescue experiments PloS one Medium 24376632
2018 S6K1 phosphorylates Mxi1 at serine 160 (S160), which enables β-TrCP E3 ubiquitin ligase to bind, ubiquitinate, and degrade Mxi1. A phosphorylation-resistant Mxi1-S160A mutant is more stable, more effective at suppressing Myc transcriptional activity, and more effective at reducing radioresistance in lung cancer cells. In vitro kinase assay (S6K1 on Mxi1), in vivo ubiquitination assay, immunoprecipitation, stable cell lines expressing WT or S160A Mxi1, tandem affinity purification/mass spectrometry Theranostics High 29507620
2020 UBE2O, an E2/E3 hybrid ubiquitin-protein ligase, physically interacts with Mxi1 and promotes its ubiquitination and degradation specifically at lysine 46 (K46). Genetic or pharmacological blockade of UBE2O impairs lung cancer tumor progression and radioresistance, effects reversed by Mxi1 inhibition. Co-immunoprecipitation, in vivo ubiquitination assay, site-directed mutagenesis (K46), genetic knockdown/knockout, rescue experiments in vitro and in vivo Cell death and differentiation High 32901121
2020 MYC suppresses MXI1 expression via upregulation of miR-155 and the miR-23a~27a~24-2 cluster. In turn, MXI1 inhibits MYC expression by binding to the MYC promoter, forming a negative feedback loop. FTO (m6A RNA demethylase) regulates this loop by targeting MYC. Luciferase reporter assays, ChIP (Mxi1 binding to MYC promoter), miRNA overexpression, co-transfection rescue experiments Cancer research Medium 32680921
2022 PRMT5 arginine methyltransferase physically interacts with Mxi1 and methylates it, promoting binding of β-TrCP ubiquitin ligase to Mxi1 and thereby facilitating its ubiquitination and proteasomal degradation. Genetic or pharmacological blockade of PRMT5 increases Mxi1 stability, impairs DNA damage repair, and enhances radiosensitivity in lung cancer. Co-immunoprecipitation, in vitro methylation assay, in vivo ubiquitination assay, shRNA knockdown, pharmacological inhibition (EPZ015666), in vitro and in vivo functional assays Cancer letters High 35149174
2022 Mxi1 inhibits lung cancer progression by directly suppressing transcription of miR-300, which in turn derepresses KLF9, and KLF9 negatively regulates GADD34 expression. ChIP and dual-luciferase assays confirm direct Mxi1 binding at the miR-300 promoter. In vivo, silencing KLF9 promotes tumor growth via GADD34-mediated MDSC immunosuppression. ChIP assay, dual luciferase reporter assay, loss- and gain-of-function studies, in vivo tumor models Cell death & disease Medium 35501353
2005 A novel Mxi1 isoform (Mxi-D), lacking exon 3 (the basic region), can bind Max protein and the PAH2 region of mSin3 proteins (GST pulldown), but the Mxi-D/Max heterodimer cannot bind E-box DNA sequences (EMSA). Mxi-D represses transcription in reporter assays as strongly as full-length Mxi1, but cannot suppress c-Myc-induced clonal growth as effectively, suggesting it acts as a dominant-negative isoform. GST pulldown, EMSA, transient transfection reporter assay, colony formation assay International journal of oncology Medium 15809730
2017 Mxi1-0 regulates proliferation of HUVECs through ERK1/2 and IL-8 pathways. Mxi1-0 suppression decreased HUVEC proliferation, G2/M accumulation, IL-8 expression/secretion, and ERK1/2 activity; IL-8 neutralization abolished conditioned-medium-induced proliferation. ERK1/2 inhibition attenuated Mxi1-0-induced IL-8 autocrine production, indicating reciprocal activation between ERK1/2 and IL-8 downstream of Mxi1-0. siRNA knockdown, overexpression, ERK1/2 inhibitor (U0126), neutralizing antibody, flow cytometry, ELISA PloS one Low 28575053
2025 FUBP3 stabilizes Mxi1 protein by interacting with it, and Mxi1 in turn recruits NCOR1/2, Sin3A/B, and HDAC1 to co-repress RRAS transcription, thereby blocking RRAS-mediated ERK signaling. This FUBP3/MXI1/RRAS/MAPK axis suppresses CD8+ T cell immune escape in acute megakaryoblastic leukemia. Co-immunoprecipitation, lentiviral overexpression/knockdown, ChIP (Mxi1 at RRAS promoter with co-repressor recruitment), in vivo mouse AMKL model Cancer immunology, immunotherapy : CII Medium 41428087

Source papers

Stage 0 corpus · 79 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 Mxi1, a protein that specifically interacts with Max to bind Myc-Max recognition sites. Cell 747 8425219
1995 An amino-terminal domain of Mxi1 mediates anti-Myc oncogenic activity and interacts with a homolog of the yeast transcriptional repressor SIN3. Cell 352 7889571
2002 An Inv/Mxi-Spa-like type III protein secretion system in Burkholderia pseudomallei modulates intracellular behaviour of the pathogen. Molecular microbiology 239 12410823
1995 Mutation of the MXI1 gene in prostate cancer. Nature genetics 188 7773287
1995 Enhanced secretion through the Shigella flexneri Mxi-Spa translocon leads to assembly of extracellular proteins into macromolecular structures. Molecular microbiology 184 7565091
1998 Role of Mxi1 in ageing organ systems and the regulation of normal and neoplastic growth. Nature 172 9624006
1994 Expression of mad, mxi1, max and c-myc during induced differentiation of hematopoietic cells: opposite regulation of mad and c-myc. Oncogene 168 8134128
1994 Suppression of Myc, but not E1a, transformation activity by Max-associated proteins, Mad and Mxi1. Proceedings of the National Academy of Sciences of the United States of America 133 8202517
2020 FTO Inhibition Enhances the Antitumor Effect of Temozolomide by Targeting MYC-miR-155/23a Cluster-MXI1 Feedback Circuit in Glioma. Cancer research 118 32680921
1994 Mapping of two genes encoding members of a distinct subfamily of MAX interacting proteins: MAD to human chromosome 2 and mouse chromosome 6, and MXI1 to human chromosome 10 and mouse chromosome 19. Oncogene 110 8290278
2012 miR-24-3p and miR-27a-3p promote cell proliferation in glioma cells via cooperative regulation of MXI1. International journal of oncology 109 23254855
2010 miR-191 regulates mouse erythroblast enucleation by down-regulating Riok3 and Mxi1. Genes & development 103 21196494
2005 Mxi1 is induced by hypoxia in a HIF-1-dependent manner and protects cells from c-Myc-induced apoptosis. Cancer biology & therapy 103 16319523
1998 Repression by the Mad(Mxi1)-Sin3 complex. BioEssays : news and reviews in molecular, cellular and developmental biology 96 9819568
1997 MXI1, a putative tumor suppressor gene, suppresses growth of human glioblastoma cells. Cancer research 85 9354456
1993 Characterization of the Shigella flexneri ipgD and ipgF genes, which are located in the proximal part of the mxi locus. Infection and immunity 85 8478058
1999 A system for identifying post-invasion functions of invasion genes: requirements for the Mxi-Spa type III secretion pathway of Shigella flexneri in intercellular dissemination. Molecular microbiology 78 10564508
1998 Commonly occurring loss and mutation of the MXI1 gene in prostate cancer. Genes, chromosomes & cancer 70 9669667
2001 MxiM and MxiJ, base elements of the Mxi-Spa type III secretion system of Shigella, interact with and stabilize the MxiD secretin in the cell envelope. Journal of bacteriology 66 11717255
2000 Molecular analysis of PTEN and MXI1 in primary bladder carcinoma. International journal of cancer 63 11058880
2020 UBE2O targets Mxi1 for ubiquitination and degradation to promote lung cancer progression and radioresistance. Cell death and differentiation 62 32901121
1999 Two MAD tails: what the recent knockouts of Mad1 and Mxi1 tell us about the MYC/MAX/MAD network. Biochimica et biophysica acta 59 10382539
1999 Mxi1 is a repressor of the c-Myc promoter and reverses activation by USF. The Journal of biological chemistry 56 9872993
2013 MicroRNA-155 promotes glioma cell proliferation via the regulation of MXI1. PloS one 53 24376632
1998 Microsatellite deletion mapping on chromosome 10q and mutation analysis of MMAC1, FAS, and MXI1 in human glioblastoma multiforme. International journal of oncology 51 9499454
2007 IpgB1 and IpgB2, two homologous effectors secreted via the Mxi-Spa type III secretion apparatus, cooperate to mediate polarized cell invasion and inflammatory potential of Shigella flexenri. Microbes and infection 48 18316224
2001 Mxi1, a Myc antagonist, suppresses proliferation of DU145 human prostate cells. The Prostate 42 11351349
1994 Assignment of the human MAD and MXI1 genes to chromosomes 2p12-p13 and 10q24-q25. Genomics 42 7829091
1996 Overexpression of Mxi1 inhibits the induction of the human ornithine decarboxylase gene by the Myc/Max protein complex. Oncogene 41 8637719
1996 Mouse Sin3A interacts with and can functionally substitute for the amino-terminal repression of the Myc antagonist Mxi1. Oncogene 41 8649810
1999 The mxi-Spa type III secretory pathway of Shigella flexneri requires an outer membrane lipoprotein, MxiM, for invasin translocation. Infection and immunity 39 10085046
2018 S6K1 phosphorylation-dependent degradation of Mxi1 by β-Trcp ubiquitin ligase promotes Myc activation and radioresistance in lung cancer. Theranostics 36 29507620
1999 Expression of MXI1, a Myc antagonist, is regulated by Sp1 and AP2. The Journal of biological chemistry 33 10497252
1996 Genomic organization of human MXI1, a putative tumor suppressor gene. Genomics 33 8838813
1994 Evolutionary relationships and functional conservation among vertebrate Max-associated proteins: the zebra fish homolog of Mxi1. Oncogene 31 7936639
2022 Arginine methyltransferase PRMT5 methylates and destabilizes Mxi1 to confer radioresistance in non-small cell lung cancer. Cancer letters 29 35149174
1998 The MXI1 tumor suppressor gene is not mutated in primary prostate cancer. Oncology reports 28 9458379
1995 Redefinition of the coding sequence of the MXI1 gene and identification of a polymorphic repeat in the 3' non-coding region that allows the detection of loss of heterozygosity of chromosome 10q25 in glioblastomas. Human genetics 26 7789959
2006 Mxi1 is essential for neurogenesis in Xenopus and acts by bridging the pan-neural and proneural genes. Developmental biology 24 16457797
2009 HIF-1alpha induces MXI1 by alternate promoter usage in human neuroblastoma cells. Experimental cell research 23 19254710
2001 M-X-I motif of semliki forest virus capsid protein affects nucleocapsid assembly. Journal of virology 23 11312332
2001 Spa33, a cell surface-associated subunit of the Mxi-Spa type III secretory pathway of Shigella flexneri, regulates Ipa protein traffic. Infection and immunity 22 11254573
1997 No germline mutations in the dimerization domain of MXI1 in prostate cancer clusters. The CRC/BPG UK Familial Prostate Cancer Study Collaborators. Cancer Research Campaign/British Prostate Group. British journal of cancer 21 9376279
2020 A MXI1-NUTM1 fusion protein with MYC-like activity suggests a novel oncogenic mechanism in a subset of NUTM1-rearranged tumors. Laboratory investigation; a journal of technical methods and pathology 20 32873880
1997 Expression and subcellular localization of the Myc superfamily proteins: c-Myc, Max, Mad1 and Mxi1 in the epiphyseal plate cartilage chondrocytes of growing rats. Cellular and molecular biology (Noisy-le-Grand, France) 20 9130602
2004 Mxi1-0, an alternatively transcribed Mxi1 isoform, is overexpressed in glioblastomas. Neoplasia (New York, N.Y.) 19 15548375
2017 A positive feedback loop between ROS and Mxi1-0 promotes hypoxia-induced VEGF expression in human hepatocellular carcinoma cells. Cellular signalling 18 28065785
2003 Loss of heterozygosity in the MXI1 gene is a frequent occurrence in melanoma. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 18 14559981
1999 Mxi1 mutations in human neurofibrosarcomas. Japanese journal of cancer research : Gann 18 10470286
2018 FOXO3a-dependent up-regulation of Mxi1-0 promotes hypoxia-induced apoptosis in endothelial cells. Cellular signalling 17 30118760
2008 Inhibition of Mxi1 suppresses HIF-2alpha-dependent renal cancer tumorigenesis. Cancer biology & therapy 17 19018165
2007 Inactivation of Mxi1 induces Il-8 secretion activation in polycystic kidney. Biochemical and biophysical research communications 17 17350592
1995 Differential expression of c-myc, max and mxi1 in human myeloid leukemia cells during retrodifferentiation and cell death. Leukemia research 17 7500645
2022 Mxi1 participates in the progression of lung cancer via the microRNA-300/KLF9/GADD34 Axis. Cell death & disease 16 35501353
2011 Melanoma-associated genes, MXI1, FN1, and NME1, are hypoxia responsive in murine and human melanoma cells. Melanoma research 16 21912348
2004 Mxi1-SRalpha: a novel Mxi1 isoform with enhanced transcriptional repression potential. Oncogene 15 15467743
1996 Mxi1 tumor suppressor gene is not mutated in primary pancreatic adenocarcinoma. Cancer letters 15 8603382
2022 Mxi1-0 Promotes Hypoxic Pulmonary Hypertension Via ERK/c-Myc-dependent Proliferation of Arterial Smooth Muscle Cells. Frontiers in genetics 12 35401684
2007 Expression and mutation analysis of genes that encode the Myc antagonists Mad1, Mxi1 and Rox in acute leukaemia. Leukemia & lymphoma 12 17577784
2009 Identification of apolipoproteinA1 reduction in the polycystic kidney by proteomics analysis of the Mxi1-deficient mouse. Proteomics 11 19637234
2017 Functional relatedness in the Inv/Mxi-Spa type III secretion system family. Molecular microbiology 10 27997726
2013 N-Myc differentially regulates expression of MXI1 isoforms in neuroblastoma. Neoplasia (New York, N.Y.) 10 24403858
2023 Case report: NUT carcinoma with MXI1::NUTM1 fusion characterized by abdominopelvic lesions and ovarian masses in a middle-aged female. Frontiers in oncology 9 36741693
2000 Mxi1 is a potential cellular target of carcinogens and frequently mutated in experimental rat tumors and tumor cell lines. Pathology international 9 10849326
2015 Mxi1 and mxi1-0 antagonize N-myc function and independently mediate apoptosis in neuroblastoma. Translational oncology 8 25749179
2007 Differential effects of Mxi1-SRalpha and Mxi1-SRbeta in Myc antagonism. The FEBS journal 8 17697116
2005 Mxi1 isoforms are expressed in hematological cell lines and normal bone marrow. International journal of oncology 8 15809730
1996 Expression, regulation and polymorphism of the mxi1 genes. Gene 7 8918230
2015 CXCL10 expression induced by Mxi1 inactivation induces mesangial cell apoptosis in mouse Habu nephritis. Cellular signalling 6 25683914
2011 Mxi1 regulates cell proliferation through insulin-like growth factor binding protein-3. Biochemical and biophysical research communications 5 22008548
2017 Mxi1-0 regulates the growth of human umbilical vein endothelial cells through extracellular signal-regulated kinase 1/2 (ERK1/2) and interleukin-8 (IL-8)-dependent pathways. PloS one 4 28575053
1997 Detailed physical analysis of a 1.5-megabase YAC contig containing the MXI1 and ADRA2A genes. Genomics 4 9344667
2012 Over-expression of Mxi1 represses renal epithelial tubulogenesis through the reduction of matrix metalloproteinase 9. Biochemical and biophysical research communications 3 22342670
2020 Mxi-2 Dependent Regulation of p53 in Prostate Cancer. Anticancer research 2 32988877
1995 Cloning and sequencing of the murine Mxi1 cDNA. Gene 2 7835718
1999 c-Myc and Mxi1 immunoreactivities in the calcifying areas of the epiphyseal-plate cartilage matrix of growing rats. Bone 1 10375197
2025 FUBP3 mediates MXI1 stability to silence RRAS and hinder MAPK signaling in acute megakaryoblastic leukemia progression. Cancer immunology, immunotherapy : CII 0 41428087
2012 Mxi1 influences cyst formation in three-dimensional cell culture. BMB reports 0 22449707
2007 [Expression and mutation of myc antagonist genes Mad1, Mxi1 and Rox in leukemia cells]. Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 0 18457265

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