Affinage

MNT

Max-binding protein MNT · UniProt Q99583

Length
582 aa
Mass
62.3 kDa
Annotated
2026-04-28
100 papers in source corpus 18 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MNT is a bHLHZip transcriptional repressor that functions as the principal physiological antagonist of MYC-family oncoproteins by competing for heterodimerization with MAX and occupancy of E-box elements on shared target gene promoters. MNT:MAX heterodimers recruit the mSin3-HDAC co-repressor complex through a 13-amino-acid N-terminal Sin3-interaction domain (SID), maintaining transcriptional repression of proliferative genes such as cyclin D2, CDK4, and ODC in quiescent cells; mitogenic signaling triggers MNT phosphorylation that disrupts mSin3 binding, while E6AP-mediated ubiquitin-proteasomal degradation and miR-210-dependent post-transcriptional suppression further relieve MNT repression to permit MYC-driven gene activation (PMID:9000049, PMID:16103876, PMID:26506232, PMID:19652553). Genetic deletion of Mnt in mice phenocopies MYC overexpression—accelerating proliferation, enhancing apoptosis, bypassing senescence, and causing mammary adenocarcinomas and T-cell lymphomas—establishing MNT as a bona fide tumor suppressor; paradoxically, in MYC-driven lymphomagenesis MNT is required to suppress BIM-dependent apoptosis, so its loss prevents MYC-driven lymphoma (PMID:12970171, PMID:16507988, PMID:31978211). In MAX-deficient contexts, MNT forms homodimers or MNT:MLX heterodimers and redistributes to the cytoplasm, where it supports proliferation through MAX-independent gene regulation (PMID:31919096).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 1997 High

    The founding question—how MYC-MAX transcriptional activation is counterbalanced—was answered by the identification of MNT as a MAX-interacting bHLHZip repressor that recruits mSin3 corepressors via a discrete SID to E-box elements, and whose SID deletion converts it from repressor to activator/oncoprotein.

    Evidence Interaction mating, co-immunoprecipitation, E-box reporter assays, deletion mutagenesis, and primary cell transformation assays in multiple labs

    PMID:9000049 PMID:9184233

    Open questions at the time
    • No genome-wide target gene identification
    • Mechanism by which SID-deleted MNT activates transcription undefined
    • In vivo relevance as tumor suppressor not yet tested genetically
  2. 2003 High

    Whether MNT loss alone is sufficient to phenocopy MYC gain was resolved: Mnt-knockout MEFs showed premature S-phase entry, CDK4/cyclin E upregulation, apoptosis, senescence bypass, and Ras-mediated transformation, while conditional mammary knockout produced adenocarcinomas, establishing MNT as a tumor suppressor in vivo.

    Evidence Mnt gene knockout mice, MEF cell cycle and apoptosis analysis, conditional Cre-lox mammary deletion

    PMID:12970171

    Open questions at the time
    • Identity of direct versus indirect MNT target genes genome-wide unknown
    • Whether tumor suppression requires MAX dimerization not tested
  3. 2004 High

    The dynamic occupancy model was demonstrated: ChIP showed that quiescent cells harbor MAX:MNT on E-box promoters (e.g., ODC) and mitogens trigger a switch to MYC:MAX; stable MNT RNAi alone was sufficient to transform fibroblasts with Ras even without c-Myc.

    Evidence ChIP for occupancy switch, stable retroviral RNAi, transformation assay in MEFs, Mnt-null mouse perinatal phenotyping

    PMID:14749372 PMID:15028671

    Open questions at the time
    • Kinetics and signaling pathway driving the occupancy switch not defined
    • Whether MNT loss fully recapitulates all MYC targets unresolved
  4. 2005 High

    The mechanism by which mitogenic signals inactivate MNT repression was identified: phosphorylation of MNT upon serum stimulation disrupts the MNT-mSin3 interaction and reduces associated HDAC activity, derepressing targets such as cyclin D2; double knockout of Mnt and c-Myc rescued proliferative defects of c-Myc loss, confirming epistatic antagonism.

    Evidence Co-IP, ChIP, phosphorylation analysis, HDAC activity assays, Cre-lox double-KO MEFs

    PMID:15866886 PMID:16103876

    Open questions at the time
    • Identity of the kinase(s) phosphorylating MNT unknown
    • Phosphorylation site mapping incomplete
    • Structural basis of phosphorylation-induced SID-mSin3 dissociation undefined
  5. 2006 High

    Tissue-specific consequences of MNT loss were mapped: conditional deletion in T cells caused increased apoptosis, disrupted development, Th1 skewing, and eventual T-cell lymphoma; in mammary gland, Mnt loss disrupted involution and produced tumors with expression profiles resembling MMTV-c-Myc tumors.

    Evidence Cre-lox conditional KO in T cells and mammary epithelium, FACS, ChIP-chip promoter arrays, expression arrays

    PMID:16507988 PMID:16740691

    Open questions at the time
    • Cell-type-specific MNT target genes not fully catalogued
    • Mechanism of disrupted involution not molecularly resolved
  6. 2009 High

    Post-transcriptional regulation of MNT was established: miR-210 targets MNT mRNA via 3′UTR sites, and MNT knockdown phenocopies miR-210 overexpression in bypassing hypoxia-induced cell cycle arrest in a MYC-dependent manner; separately, a physiological MNT-to-MYC promoter occupancy switch on p53 and cyclin D1 was demonstrated during cholestasis-induced hepatocyte apoptosis.

    Evidence 3′UTR reporter assays, siRNA knockdown, microarray, cell cycle analysis; ChIP/EMSA, in vivo lentiviral MYC siRNA

    PMID:19086036 PMID:19652553

    Open questions at the time
    • Whether miR-210 regulation of MNT is operative in non-hypoxic physiological contexts unknown
    • Additional miRNAs targeting MNT not systematically explored
  7. 2012 High

    The paradox of MNT's dual role was clarified: while MNT loss alone increases apoptosis (tumor suppressor), in the context of MYC-driven T-cell expansion MNT is required to restrain MYC-induced ROS-mediated apoptosis, so MNT loss prevents MYC-driven thymoma.

    Evidence Conditional Mnt KO crossed with Myc transgenic mice, ROS measurement, apoptosis assays, tumor incidence

    PMID:23150551

    Open questions at the time
    • Direct transcriptional targets mediating ROS regulation by MNT not identified
    • Whether this anti-apoptotic role extends to non-T-cell tumors unclear at this point
  8. 2016 Medium

    Proteasomal control of MNT protein levels was established: E6AP (UBE3A) physically associates with MNT and promotes its ubiquitination and degradation; a catalytically inactive E6AP mutant stabilizes MNT, and E6AP overexpression opposes MNT-dependent myeloid differentiation.

    Evidence Co-immunoprecipitation with wild-type and C843A mutant E6AP, proteasome inhibitor experiments, differentiation assays

    PMID:26506232

    Open questions at the time
    • Ubiquitination sites on MNT not mapped
    • Whether E6AP regulation of MNT operates in all tissues unknown
    • Reciprocal validation in E6AP-knockout cells not shown
  9. 2020 High

    Two breakthroughs resolved MAX-independent functions and the in vivo apoptotic paradox: in MAX-deficient cells MNT forms homodimers and MNT-MLX heterodimers that redistribute to the cytoplasm and regulate cell cycle/DNA repair genes independently of MAX; in Eμ-Myc B-cell lymphomagenesis MNT suppresses BIM-dependent apoptosis, so its deletion prevents lymphoma by unleashing MYC-driven apoptosis.

    Evidence ChIP, RNA-seq, Co-IP and localization in MAX-null cells; Cre-lox and inducible KO in Eμ-Myc mouse model, BIM protein analysis, transplantation

    PMID:31919096 PMID:31978211

    Open questions at the time
    • Genomic targets of MNT homodimers and MNT-MLX dimers not fully defined
    • Whether cytoplasmic MNT has non-transcriptional functions unknown
    • Structural basis for MNT homodimerization not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the kinase(s) phosphorylating MNT, the structural basis of SID–mSin3 regulation by phosphorylation, the full genome-wide target repertoire specific to MNT homodimers versus MNT-MLX versus MNT-MAX, and whether MNT's context-dependent pro-survival versus tumor-suppressive functions can be therapeutically exploited.
  • No kinase responsible for MNT phosphorylation identified
  • No structural model of MNT or MNT-MAX complex available
  • Therapeutic relevance of modulating MNT in MYC-driven cancers untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0003677 DNA binding 5
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 1
Pathway
R-HSA-74160 Gene expression (Transcription) 7 R-HSA-1640170 Cell Cycle 5 R-HSA-5357801 Programmed Cell Death 4 R-HSA-1643685 Disease 3 R-HSA-4839726 Chromatin organization 3
Partners
HDAC1MAXMLXMYCSIN3ASIN3BUBE3A
Complex memberships
MNT-MAX heterodimerMNT-MAX-mSin3-HDAC co-repressor complexMNT-MLX heterodimer

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 MNT (Mnt) heterodimerizes with Max via its bHLHZip domain and the Mnt:Max complex acts as a transcriptional repressor at CACGTG E-box sites; repression maps to a 13-amino-acid N-terminal Sin3 interaction domain (SID) that mediates interaction with mSin3 corepressor proteins, and deletion of the SID converts Mnt from a repressor to a transcriptional activator. Interaction mating, co-immunoprecipitation, reporter gene assays, deletion mutagenesis, in vivo complex detection Genes & development High 9000049
1997 MNT (Rox) heterodimerizes with Max and shows a novel DNA-binding specificity, preferring CACGCG over the canonical CACGTG E-box; Rox represses transcription through its N-terminus interacting with the Sin3 co-repressor; expression is high in quiescent fibroblasts and decreases upon cell cycle entry. Interaction mating, co-immunoprecipitation, bandshift/EMSA assays, reporter transcription assays in HEK293 and yeast The EMBO journal High 9184233
1997 Mnt:Max heterodimers efficiently suppress Myc-dependent transcriptional activation from CACGTG-containing promoters; wild-type Mnt suppresses Myc+Ras co-transformation of primary cells, whereas Mnt with a SID deletion cooperates with Ras to transform cells in the absence of Myc, indicating overlapping target gene sets. Reporter gene assays, primary cell transformation assay, transgenic mouse embryo lethal phenotype Genes & development High 9000049
2003 Deletion of the Mnt gene in MEFs causes premature S-phase entry, accelerated proliferation, upregulation of Cdk4 and cyclin E, increased apoptosis, escape from senescence, and transformability by oncogenic Ras alone; conditional Mnt knockout in breast epithelium leads to adenocarcinomas, demonstrating Mnt as a tumor suppressor and Myc antagonist in vivo. Mnt gene knockout in mice, MEF cell cycle analysis, BrdU incorporation, Western blot, Cre-lox conditional knockout The EMBO journal High 12970171
2004 In quiescent cells, the Odc E-box elements are occupied by Max:Mnt repressor complexes; upon mitogen stimulation these are displaced by Myc:Max complexes. Stable RNAi knockdown of Mnt triggers Myc target gene expression, accelerates proliferation and apoptosis, and is sufficient to transform primary fibroblasts with Ras even in the absence of c-myc. Chromatin immunoprecipitation (ChIP), stable retroviral RNAi, transformation assay, cell cycle analysis Molecular and cellular biology High 14749372
2005 During G0-to-S-phase transition, c-Myc induction leads to a transient decrease in Mnt-Max complexes and a switch in the ratio of Mnt-Max to c-Myc-Max on shared target gene promoters; Mnt overexpression suppresses cell cycle entry, and simultaneous Cre-lox deletion of both Mnt and c-Myc in MEFs rescues the proliferative block caused by c-Myc ablation alone. Co-immunoprecipitation, ChIP, Cre-lox double knockout MEFs, flow cytometry The Journal of cell biology High 15866886
2005 Mnt is phosphorylated upon serum-stimulated cell cycle re-entry, and this phosphorylation disrupts the Mnt-mSin3 interaction, reducing Mnt-associated HDAC activity; Mnt binds the cyclin D2 promoter (a Myc target) in quiescent cells, and RNAi-mediated Mnt knockdown upregulates cyclin D2 in growth-arrested fibroblasts. Co-immunoprecipitation, ChIP, RNAi, HDAC activity assay, Western blot phosphorylation analysis Oncogene High 16103876
2009 miR-210 targets MNT mRNA via multiple binding sites in its 3' UTR; MNT knockdown phenocopies miR-210 overexpression (bypass of hypoxia-induced cell cycle arrest), and loss of MYC abolishes this effect, placing MNT as a key node through which miR-210 exerts a MYC-like transcriptional response in hypoxia. 3' UTR reporter assays, siRNA knockdown, microarray expression analysis, cell cycle analysis Cell cycle (Georgetown, Tex.) High 19652553
2009 During cholestasis, expression of MNT decreases while c-Myc increases; nuclear E-box binding by Mnt to the p53 and cyclin D1 promoters decreases while Myc binding increases; this Mnt-to-Myc switch is responsible for p53 and cyclin D1 upregulation and hepatocyte apoptosis, as demonstrated by Myc siRNA protection experiments. ChIP/EMSA, siRNA knockdown of c-Myc, lentiviral c-Myc siRNA in vivo, promoter activity assays Hepatology (Baltimore, Md.) High 19086036
2011 Max-Mnt-Sin3a-HDAC complexes occupy and repress E-box-containing genes promoting cell cycle arrest and apoptosis in proliferating cells; inhibition of PI3-kinase leads to loss of Max/Mnt binding and transcriptional induction by MITF and USF1 as well as FoxO at these loci. Chromatin immunoprecipitation, siRNA knockdown, reporter gene assays The Journal of biological chemistry Medium 21873430
2012 Conditional deletion of Mnt in T cells reveals that Mnt does not require Myc to induce apoptosis, but ectopic Myc expression dramatically increases death of Mnt-deficient T cells; Myc-driven T-cell proliferative expansion and thymoma formation are prevented in the absence of Mnt; tumor suppression by Mnt loss is linked to increased ROS-mediated apoptosis. Cre-lox conditional KO in T cells, in vivo tumor incidence, apoptosis assays, ROS measurement Proceedings of the National Academy of Sciences of the United States of America High 23150551
2016 The E3 ubiquitin ligase E6AP (UBE3A) physically associates with MNT and promotes its ubiquitin-mediated proteasomal degradation; catalytically inactive E6AP (C843A) stabilizes MNT instead; wild-type E6AP overexpression impedes ATRA-mediated myeloid differentiation whereas MNT overexpression promotes G0-G1 arrest and myeloid differentiation. Co-immunoprecipitation, proteasome inhibitor experiments, MNT overexpression/knockdown, flow cytometry, differentiation assays Oncotarget Medium 26506232
2020 MNT autoregulates its own expression: MNT-MAX dimers bind E-boxes on the MNT promoter and repress it; in MAX-deficient cells, MNT is overexpressed and redistributed to the cytoplasm, forms homodimers and MNT-MLX dimers, and supports cell proliferation by regulating genes involved in cell cycle and DNA repair independently of MAX. ChIP, RNA-sequencing, co-immunoprecipitation, siRNA knockdown, immunofluorescence localization in MAX-deficient cells The Journal of biological chemistry High 31919096
2020 MNT synergizes with MYC in B lymphoid cells by suppressing MYC-driven apoptosis primarily through reducing pro-apoptotic BIM levels; homozygous Mnt deletion in Eμ-Myc mice greatly reduces lymphoma incidence by enhancing apoptosis; induction of Mnt deletion in fully malignant Eμ-Myc lymphoma cells extends recipient survival. Cre-lox conditional/inducible KO in Eμ-Myc mouse model, tumor incidence, apoptosis measurement, BIM protein level analysis, transplantation experiments Blood High 31978211
2004 Loss of Mnt in mice produces severely runted pups that die perinatally with reduced c-Myc and N-Myc levels and craniofacial defects including cleft palate, demonstrating essential roles in embryonic growth and linking Mnt haploinsufficiency to Miller-Dieker syndrome features. Mnt null mouse generation, genetic and histological phenotyping, Western blot Human molecular genetics Medium 15028671
2006 Conditional deletion of Mnt in T cells causes increased apoptosis of thymic T cells, disrupts T-cell development, skews toward Th1 cytokine production, enhances proliferation of activated CD4+ T cells, and ultimately leads to T-cell lymphoma, demonstrating roles in T-cell immune homeostasis and tumor suppression. Cre-lox conditional KO, FACS, cytokine profiling, histology, tumor incidence Molecular and cellular biology High 16507988
2008 In parous mammary glands, Mnt is upregulated and forms HDAC1/c-Myc/Mnt/Max complexes on promoters of Myc target genes (ornithine decarboxylase, cyclin D2, TGFβ1); these complexes act as transcriptional repressors and are disassembled in serum-stimulated cells, providing a mechanism for parity-induced protection against carcinogenesis. Co-immunoprecipitation, ChIP, Western blot, mammary carcinogenesis rat model Cancer science Medium 18271930
2006 Mnt-deficient mammary glands show severely disrupted involution with reduced apoptosis; promoter array analysis demonstrates that Mnt and c-Myc bind similar promoters in mammary tumors, and mRNA expression patterns in Mnt-KO mammary tumors resemble those in MMTV-c-Myc transgenic tumors, confirming Mnt as a functional Myc antagonist in the mammary gland. Cre-lox conditional KO, mammary gland histology, promoter array (ChIP-chip), oligonucleotide expression arrays Cancer research High 16740691
1998 The human ROX/MNT gene encodes a bHLHZip protein that heterodimerizes with Max, represses transcription in an E-box reporter system, and its expression is down-regulated in proliferating cells; the gene maps to chromosome 17p13.3, a region frequently deleted in human malignancies. Co-immunoprecipitation, reporter gene assays, Northern blot cell-cycle expression analysis Genomics Medium 9598315

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Genomic binding by the Drosophila Myc, Max, Mad/Mnt transcription factor network. Genes & development 332 12695332
1999 Epigenetic spreading of the Drosophila dosage compensation complex from roX RNA genes into flanking chromatin. Cell 261 10481915
2009 MicroRNA miR-210 modulates cellular response to hypoxia through the MYC antagonist MNT. Cell cycle (Georgetown, Tex.) 231 19652553
1997 Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites. Genes & development 223 9000049
2002 The roX genes encode redundant male-specific lethal transcripts required for targeting of the MSL complex. The EMBO journal 208 11867536
1998 Rex-1, a gene encoding a transcription factor expressed in the early embryo, is regulated via Oct-3/4 and Oct-6 binding to an octamer site and a novel protein, Rox-1, binding to an adjacent site. Molecular and cellular biology 206 9528758
2001 Non-independence of Mnt repressor-operator interaction determined by a new quantitative multiple fluorescence relative affinity (QuMFRA) assay. Nucleic acids research 143 11410653
2000 Ordered assembly of roX RNAs into MSL complexes on the dosage-compensated X chromosome in Drosophila. Current biology : CB 141 10679323
2013 Tandem stem-loops in roX RNAs act together to mediate X chromosome dosage compensation in Drosophila. Molecular cell 136 23870142
1997 Rox, a novel bHLHZip protein expressed in quiescent cells that heterodimerizes with Max, binds a non-canonical E box and acts as a transcriptional repressor. The EMBO journal 126 9184233
2002 Extent of chromatin spreading determined by roX RNA recruitment of MSL proteins. Science (New York, N.Y.) 110 12446910
2003 Local spreading of MSL complexes from roX genes on the Drosophila X chromosome. Genes & development 88 12782651
2012 The bHLH protein ROX acts in concert with RAX1 and LAS to modulate axillary meristem formation in Arabidopsis. The Plant journal : for cell and molecular biology 85 22372440
2008 ECVAM retrospective validation of in vitro micronucleus test (MNT). Mutagenesis 85 18326866
2006 roX RNAs are required for increased expression of X-linked genes in Drosophila melanogaster males. Genetics 74 17028315
1985 The bacteriophage P22 arc and mnt repressors. Overproduction, purification, and properties. The Journal of biological chemistry 74 2995361
2013 ATP-dependent roX RNA remodeling by the helicase maleless enables specific association of MSL proteins. Molecular cell 73 23870143
2004 Mnt loss triggers Myc transcription targets, proliferation, apoptosis, and transformation. Molecular and cellular biology 73 14749372
2003 Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis. The EMBO journal 73 12970171
1987 Bacteriophage P22 Mnt repressor. DNA binding and effects on transcription in vitro. Journal of molecular biology 73 3656414
2006 Of Myc and Mnt. Journal of cell science 68 16410546
2005 Mnt-Max to Myc-Max complex switching regulates cell cycle entry. The Journal of cell biology 68 15866886
1997 Quantitative specificity of the Mnt repressor. Journal of molecular biology 68 9268651
2003 Sequence-specific targeting of Drosophila roX genes by the MSL dosage compensation complex. Molecular cell 64 12718883
1989 DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues. Proceedings of the National Academy of Sciences of the United States of America 62 2644643
1994 Solution structure of dimeric Mnt repressor (1-76). Biochemistry 57 7999761
2018 Rox, a Rifamycin Resistance Enzyme with an Unprecedented Mechanism of Action. Cell chemical biology 55 29398560
1999 The tetramerization domain of the Mnt repressor consists of two right-handed coiled coils. Nature structural biology 52 10426954
1989 The Arc and Mnt repressors. A new class of sequence-specific DNA-binding protein. The Journal of biological chemistry 52 2917965
2004 Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome. Human molecular genetics 49 15028671
2017 One-Step Synthesis of Rox-DNA Functionalized CdZnTeS Quantum Dots for the Visual Detection of Hydrogen Peroxide and Blood Glucose. Analytical chemistry 48 29019392
2007 Incorporation of the noncoding roX RNAs alters the chromatin-binding specificity of the Drosophila MSL1/MSL2 complex. Molecular and cellular biology 48 18086881
2009 Switch from Mnt-Max to Myc-Max induces p53 and cyclin D1 expression and apoptosis during cholestasis in mouse and human hepatocytes. Hepatology (Baltimore, Md.) 47 19086036
2003 Initiation of dosage compensation in Drosophila embryos depends on expression of the roX RNAs. Mechanisms of development 47 12915227
2018 Melatonin and Its Metabolites Ameliorate UVR-Induced Mitochondrial Oxidative Stress in Human MNT-1 Melanoma Cells. International journal of molecular sciences 46 30487387
2009 MNT and MutaMouse studies to define the in vivo dose response relations of the genotoxicity of EMS and ENU. Toxicology letters 45 19446969
1986 Analysis of forward mutations induced by N-methyl-N'-nitro-N-nitrosoguanidine in the bacteriophage P22 mnt repressor gene. Journal of bacteriology 43 3957871
2009 Monooxygenation of rifampicin catalyzed by the rox gene product of Nocardia farcinica: structure elucidation, gene identification and role in drug resistance. The Journal of antibiotics 42 19942945
2019 Microenvironment-regulated lncRNA-HAL is able to promote stemness in breast cancer cells. Biochimica et biophysica acta. Molecular cell research 41 31401107
2009 Characterization and DNA-interaction studies of 1,1-dicyano-2,2-ethylene dithiolate Ni(II) mixed-ligand complexes with 2-amino-5-methyl thiazole, 2-amino-2-thiazoline and imidazole. Crystal structure of [Ni(i-MNT)(2a-5mt)(2)]. Bioorganic & medicinal chemistry 41 19608424
2004 Sequence-specific targeting of MSL complex regulates transcription of the roX RNA genes. The EMBO journal 41 15229655
2020 The rOX-stars of inflammation: links between the inflammasome and mitochondrial meltdown. Clinical & translational immunology 40 32055400
2009 roX RNAs: non-coding regulators of the male X chromosome in flies. RNA biology 40 19229132
2005 Genomic binding and transcriptional regulation by the Drosophila Myc and Mnt transcription factors. Cold Spring Harbor symposia on quantitative biology 39 16869766
2020 Novel polyadenylylation-dependent neutralization mechanism of the HEPN/MNT toxin/antitoxin system. Nucleic acids research 38 33045733
2019 Melatonin exerts oncostatic capacity and decreases melanogenesis in human MNT-1 melanoma cells. Journal of pineal research 36 31532834
2008 Regulation of histone H4 Lys16 acetylation by predicted alternative secondary structures in roX noncoding RNAs. Molecular and cellular biology 36 18541664
2015 Identification and characterization of a HEPN-MNT family type II toxin-antitoxin in Shewanella oneidensis. Microbial biotechnology 35 26112399
2004 Drosophila male-specific lethal 2 protein controls sex-specific expression of the roX genes. Genetics 34 15126401
2012 A critical role for Mnt in Myc-driven T-cell proliferation and oncogenesis. Proceedings of the National Academy of Sciences of the United States of America 33 23150551
2012 Induction of melanogenesis by rapamycin in human MNT-1 melanoma cells. Annals of dermatology 32 22577264
2011 The E-box binding factors Max/Mnt, MITF, and USF1 act coordinately with FoxO to regulate expression of proapoptotic and cell cycle control genes by phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 signaling. The Journal of biological chemistry 32 21873430
2007 Regional control of chromatin organization by noncoding roX RNAs and the NURF remodeling complex in Drosophila melanogaster. Genetics 32 17507677
2006 Mnt-deficient mammary glands exhibit impaired involution and tumors with characteristics of myc overexpression. Cancer research 32 16740691
2001 Recruitment of the male-specific lethal (MSL) dosage compensation complex to an autosomally integrated roX chromatin entry site correlates with an increased expression of an adjacent reporter gene in male Drosophila. The Journal of biological chemistry 32 11402038
1997 Mnt: a novel Max-interacting protein and Myc antagonist. Current topics in microbiology and immunology 32 9308234
2021 The ROX index has greater predictive validity than NEWS2 for deterioration in Covid-19. EClinicalMedicine 31 33937729
2015 Medical Nutrition Therapy for Patients With Advanced Systemic Sclerosis (MNT PASS): A Pilot Intervention Study. JPEN. Journal of parenteral and enteral nutrition 31 26209221
2013 ULK1 regulates melanin levels in MNT-1 cells independently of mTORC1. PloS one 31 24066173
2006 Chemistry of [Et4N][MoIV(SPh)(PPh3)(mnt)2] as an analogue of dissimilatory nitrate reductase with its inactivation on substitution of thiolate by chloride. Journal of the American Chemical Society 30 16568972
2004 Analysis of transcripts from 17p13.3 in medulloblastoma suggests ROX/MNT as a potential tumour suppressor gene. European journal of cancer (Oxford, England : 1990) 29 15519529
1995 Domains of Mnt repressor: roles in tetramer formation, protein stability, and operator DNA binding. Biochemistry 29 7548071
2020 Development and survival of MYC-driven lymphomas require the MYC antagonist MNT to curb MYC-induced apoptosis. Blood 28 31978211
2014 The activities of MYC, MNT and the MAX-interactome in lymphocyte proliferation and oncogenesis. Biochimica et biophysica acta 28 24731854
1989 Identification of functionally important residues in the DNA binding region of the mnt repressor. The Journal of biological chemistry 28 2668272
2005 Mnt transcriptional repressor is functionally regulated during cell cycle progression. Oncogene 27 16103876
2004 Path to equality strewn with roX. Developmental biology 27 15081354
1992 Biochemical and genetic analysis of operator contacts made by residues within the beta-sheet DNA binding motif of Mnt repressor. The EMBO journal 27 1740107
2006 Inflammatory disease and lymphomagenesis caused by deletion of the Myc antagonist Mnt in T cells. Molecular and cellular biology 26 16507988
2018 Structure-function analyses reveal the molecular architecture and neutralization mechanism of a bacterial HEPN-MNT toxin-antitoxin system. The Journal of biological chemistry 25 29555683
2018 Rox-DNA Functionalized Silicon Nanodots for Ratiometric Detection of Mercury Ions in Live Cells. Analytical chemistry 25 30014694
2017 MNT and Emerging Concepts of MNT-MYC Antagonism. Genes 25 28230739
2016 The essential Drosophila CLAMP protein differentially regulates non-coding roX RNAs in male and females. Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology 25 27995349
2014 Non-coding roX RNAs prevent the binding of the MSL-complex to heterochromatic regions. PLoS genetics 25 25501352
2000 Dosage compensation rox! Current opinion in cell biology 25 10801462
1999 Analysis of the Max-binding protein MNT in human medulloblastomas. International journal of cancer 25 10446446
2017 RNA-DamID reveals cell-type-specific binding of roX RNAs at chromatin-entry sites. Nature structural & molecular biology 24 29323275
2007 Mnt takes control as key regulator of the myc/max/mxd network. Advances in cancer research 23 17419941
2004 Expression and DNA-binding activity of MYCN/Max and Mnt/Max during induced differentiation of human neuroblastoma cells. Journal of cellular biochemistry 22 15258910
2013 TAILOR: transgene activation and inactivation using lox and rox in zebrafish. PloS one 21 24391998
2021 Hyperthermia Enhances Doxorubicin Therapeutic Efficacy against A375 and MNT-1 Melanoma Cells. International journal of molecular sciences 20 35008457
2015 Novel Heterotypic Rox Sites for Combinatorial Dre Recombination Strategies. G3 (Bethesda, Md.) 20 26715092
2010 MSL cis-spreading from roX gene up-regulates the neighboring genes. Biochemical and biophysical research communications 19 20654579
1995 Dramatic changes in DNA-binding specificity caused by single residue substitutions in an Arc/Mnt hybrid repressor. Nature structural biology 19 8846224
1991 Specificity of the Mnt protein determined by binding to randomized operators. Proceedings of the National Academy of Sciences of the United States of America 19 2062848
1988 The Mnt repressor of bacteriophage P22: role of C-terminal residues in operator binding and tetramer formation. Biochemistry 19 3288281
1998 The human ROX gene: genomic structure and mutation analysis in human breast tumors. Genomics 18 9598315
2022 Combined Therapy with Dacarbazine and Hyperthermia Induces Cytotoxicity in A375 and MNT-1 Melanoma Cells. International journal of molecular sciences 17 35408947
2016 Proteomic discovery of MNT as a novel interacting partner of E3 ubiquitin ligase E6AP and a key mediator of myeloid differentiation. Oncotarget 17 26506232
2004 Photoelectron spectroscopy of the doubly-charged anions [MIVO(mnt)2]2- (M = Mo, W; mnt = S2C2(CN)2(2-): access to the ground and excited states of the [MVO(mnt)2]- anion. Journal of the American Chemical Society 17 15099095
1998 Molecular analysis of a Myc antagonist, ROX/Mnt, at 17p13.3 in human lung cancers. Japanese journal of cancer research : Gann 17 9617337
2011 OX40 engagement stabilizes Mxd4 and Mnt protein levels in antigen-stimulated T cells leading to an increase in cell survival. European journal of immunology 16 21400495
2021 The Multiple Faces of MNT and Its Role as a MYC Modulator. Cancers 15 34572909
2020 The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells. The Journal of biological chemistry 15 31919096
2019 Structural insights reveal the specific recognition of roX RNA by the dsRNA-binding domains of the RNA helicase MLE and its indispensable role in dosage compensation in Drosophila. Nucleic acids research 14 30649456
2004 Evidence of mnt-myc antagonism revealed by mnt gene deletion. Cell cycle (Georgetown, Tex.) 14 14712062
2004 Quantitative modeling of DNA-protein interactions: effects of amino acid substitutions on binding specificity of the Mnt repressor. Nucleic acids research 14 15289576
1993 Specificity of the Mnt protein. Independent effects of mutations at different positions in the operator. Journal of molecular biology 14 8445649
2008 Induction of a novel histone deacetylase 1/c-Myc/Mnt/Max complex formation is implicated in parity-induced refractoriness to mammary carcinogenesis. Cancer science 13 18271930
2001 Contributions of distinct quaternary contacts to cooperative operator binding by Mnt repressor. Proceedings of the National Academy of Sciences of the United States of America 13 11226234