Affinage

Showing MNT — ROX is a alias.

MNT

Max-binding protein MNT · UniProt Q99583

Length
582 aa
Mass
62.3 kDa
Annotated
2026-06-10
100 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MNT (ROX/MXD6) is a bHLHZip transcriptional repressor that heterodimerizes with MAX to bind E-box sequences and antagonize MYC-MAX–driven transcription, functioning as a brake on MYC-dependent proliferation and oncogenesis (PMID:9000049, PMID:15866886). Repression depends on a 13-amino-acid N-terminal Sin3 interaction domain (SID) that recruits mSIN3-HDAC co-repressor complexes; deleting the SID converts MNT from a repressor and tumor suppressor into a transcriptional activator and cooperating oncogene (PMID:9000049, PMID:9184233). MNT-MAX preferentially occupies the non-canonical CACGCG E-box and is constitutively present in quiescent and proliferating cells, where MYC induction at cell cycle entry transiently switches promoter occupancy from MNT-MAX to MYC-MAX at shared targets such as Cdk4, cyclin D2, and Odc (PMID:9184233, PMID:14749372, PMID:15866886). Loss of MNT phenocopies MYC overexpression—premature S-phase entry, upregulation of Cdk4 and cyclin E, escape from senescence, and Ras-driven transformation independent of c-Myc—and genetic deletion produces adenocarcinoma and T-cell lymphoma in vivo, establishing MNT as a tumor suppressor (PMID:12970171, PMID:14749372, PMID:16507988). Paradoxically, MNT also restrains MYC-induced apoptosis: in Eμ-Myc lymphoma its deletion enhances apoptosis by failing to suppress pro-apoptotic BIM, so MNT loss reduces lymphoma incidence and extends survival of established tumors (PMID:23150551, PMID:31978211). MNT activity is set post-translationally—cell-cycle-entry phosphorylation disrupts the MNT-mSIN3 interaction and lowers associated HDAC activity, E6AP-mediated ubiquitination drives its proteasomal degradation, and OX40 signaling stabilizes it in T cells (PMID:16103876, PMID:26506232, PMID:21400495). MNT also autoregulates its promoter via an E-box, and in MAX-deficient cells relocalizes to the cytoplasm and forms MNT homodimers and MNT-MLX heterodimers that regulate cell cycle and DNA repair genes, remaining required for proliferation even without MAX (PMID:31919096).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1997 High

    Established MNT's core biochemical identity: how a MAX partner could oppose rather than mimic MYC, and which protein element confers repression.

    Evidence Two-hybrid, co-IP, EMSA, reporter assays and SID mutagenesis defining MNT-MAX dimers as E-box repressors that recruit Sin3

    PMID:9000049 PMID:9184233

    Open questions at the time
    • Endogenous promoter occupancy not yet shown
    • In vivo physiological role undefined
  2. 2003 High

    Tested whether MNT physiologically restrains proliferation, resolving its role as a tumor suppressor that phenocopies MYC when lost.

    Evidence Conditional knockout MEFs and breast epithelium with cell cycle, ChIP, and Ras transformation readouts

    PMID:12970171

    Open questions at the time
    • Apoptosis-suppressing role not yet appreciated
    • Direct target gene set incompletely mapped
  3. 2004 High

    Defined the dynamic MNT-MAX/MYC-MAX promoter switch and showed MNT can repress MYC targets independently of MYC itself.

    Evidence ChIP occupancy at Odc, stable RNAi, and transformation assays in c-myc-null MEFs

    PMID:14749372

    Open questions at the time
    • Mechanism of complex displacement not resolved
    • MYC-independent target scope unclear
  4. 2004 Medium

    Addressed MNT's developmental requirement, revealing perinatal lethality and craniofacial defects and an upstream influence on Myc protein levels.

    Evidence Germline/conditional knockout mice with histopathology and Myc western blots

    PMID:15028671

    Open questions at the time
    • Mechanism by which MNT loss reduces Myc protein not defined
    • Single lab
  5. 2005 High

    Connected signaling to MNT function by showing cell-cycle-entry phosphorylation dismantles the MNT-mSIN3 repressor complex, and confirmed direct MNT-MYC antagonism genetically.

    Evidence Co-IP, HDAC assays, ChIP at cyclin D2, and Mnt/c-Myc double-knockout rescue of cell cycle block

    PMID:15866886 PMID:16103876

    Open questions at the time
    • Kinase responsible for MNT phosphorylation not identified
    • Phosphosite mapping incomplete
  6. 2006 High

    Extended MNT tumor suppression to specific lineages and linked its loss to overlapping MYC target gene programs.

    Evidence T-cell and mammary conditional knockouts with cytokine profiling, ChIP-chip promoter arrays, and expression profiling

    PMID:16507988 PMID:16740691

    Open questions at the time
    • Whether lymphoma arises from proliferation or apoptosis defect not yet separated
    • Direct targets driving phenotype not isolated
  7. 2009 Medium

    Placed MNT within stress and hypoxia signaling axes by identifying upstream regulators and context-specific promoter switches.

    Evidence miR-210 3'UTR reporter and MYC epistasis in hypoxia; EMSA promoter switch at p53/cyclin D1 with in vivo c-myc siRNA in cholestasis

    PMID:19086036 PMID:19652553

    Open questions at the time
    • No in vitro reconstitution of miR-210–MNT binding
    • Promoter-switch causality inferred from correlation in vivo
  8. 2011 Medium

    Defined post-translational control of MNT abundance/localization by survival signaling, and linked PI3K signaling to MNT repressor occupancy.

    Evidence OX40-driven stabilization and nuclear translocation with siRNA survival readout; ChIP and PI3K inhibition controlling Max/Mnt promoter binding

    PMID:21400495 PMID:21873430

    Open questions at the time
    • Direct kinase/ligase intermediates between signaling and MNT not all defined
    • Single-lab signaling placements
  9. 2012 High

    Reframed MNT's dominant physiological role as suppression of MYC-induced apoptosis, mediated by ROS, rather than purely proliferation control.

    Evidence T-cell conditional Mnt knockout in Myc-transgenic mice with ROS and apoptosis assays and MEF transformation refractoriness

    PMID:23150551

    Open questions at the time
    • Molecular link between MNT and ROS unresolved
    • Apoptotic effectors not yet identified
  10. 2016 Medium

    Identified an E3 ligase controlling MNT turnover, providing a druggable node for restoring MNT in differentiation.

    Evidence Co-IP, proteasome inhibition, E6AP catalytic mutant, and ATRA/E6AP knockdown in HL60 myeloid differentiation

    PMID:26506232

    Open questions at the time
    • Ubiquitination sites on MNT not mapped
    • Single-lab finding
  11. 2020 High

    Pinned down the apoptosis mechanism to BIM and revealed MAX-independent MNT functions, broadening the regulatory model.

    Evidence Inducible Mnt deletion in Eμ-Myc lymphoma with BIM measurement and survival; ChIP/RNA-seq/localization in MAX-deficient cells

    PMID:31919096 PMID:31978211

    Open questions at the time
    • How MNT represses BIM mechanistically not fully defined
    • Functional importance of MNT homodimers/MNT-MLX in normal cells unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How MNT integrates its repressor and apoptosis-suppressing functions—and the molecular link between MNT, ROS, and BIM regulation—remains unresolved.
  • No structural model of MNT-MAX–SIN3 assembly on chromatin
  • Direct mechanism connecting MNT to BIM/ROS undefined
  • Kinase and full ligase network controlling MNT not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 5 GO:0003677 DNA binding 3 GO:0060090 molecular adaptor activity 3
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 1
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1640170 Cell Cycle 2 R-HSA-4839726 Chromatin organization 2 R-HSA-5357801 Programmed Cell Death 2
Partners
HDAC1MAXMLXMYCSIN3AUBE3A
Complex memberships
MNT-MAX heterodimermSIN3-HDAC co-repressor complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 MNT (Rox/Mnt) heterodimerizes with Max via bHLHZip domains, and the Mnt:Max heterodimer binds CACGTG E-box sequences and acts as a transcriptional repressor. Transcriptional repression maps to a 13-amino-acid N-terminal Sin3 interaction domain (SID); deletion of SID converts Mnt from a repressor to an activator and from a suppressor of Myc+Ras cotransformation to a cooperating oncogene. Interaction mating (two-hybrid), co-immunoprecipitation, reporter gene transcription assays, mutagenesis of SID domain, primary cell transformation assay Genes & development High 9000049
1997 Rox (human MNT ortholog) heterodimerizes with Max and weakly homodimerizes; the Rox-Max heterodimer preferentially binds the non-canonical CACGCG site over the canonical CACGTG E-box. Rox represses transcription in human HEK293 cells and yeast, and repression in yeast is mediated through interaction of its N-terminus with the Sin3 co-repressor. Interaction mating (two-hybrid), co-immunoprecipitation, electrophoretic mobility shift assay (EMSA), reporter gene transcription assays The EMBO journal High 9184233
2003 Deletion of Mnt in mouse embryo fibroblasts (MEFs) causes premature S-phase entry and faster proliferation linked to upregulation of Cdk4 and cyclin E; Cdk4 is a direct target of Mnt-Myc antagonism. Mnt-null MEFs are prone to apoptosis, bypass senescence, and can be transformed by oncogenic Ras alone, phenocopying Myc overexpression. Conditional deletion of Mnt in breast epithelium leads to adenocarcinomas. Conditional knockout (Cre/lox) mice, MEF proliferation and cell cycle assays, flow cytometry, ChIP, transformation assay with oncogenic Ras The EMBO journal High 12970171
2004 In quiescent cells, Mnt-Max complexes occupy E-boxes (e.g., at the Odc gene); upon cell proliferation, Myc-Max complexes displace Mnt-Max. Stable RNAi knockdown of Mnt triggers Myc target gene expression, accelerated proliferation, apoptosis, and transformation of primary fibroblasts with Ras even in cells lacking c-myc, establishing Mnt as a transcriptional repressor of Myc target genes that functions partly independently of Myc. Chromatin immunoprecipitation (ChIP), stable retroviral RNAi, luciferase reporter assay, proliferation and transformation assays, c-myc null MEFs Molecular and cellular biology High 14749372
2005 Mnt is phosphorylated upon serum-stimulated cell cycle re-entry; this phosphorylation disrupts the Mnt-mSin3 interaction and reduces Mnt-associated HDAC activity. Mnt binds and recruits mSin3 to the Myc target gene cyclin D2 in quiescent fibroblasts, repressing it; RNAi-mediated reduction of Mnt upregulates cyclin D2 in growth-arrested cells. Co-immunoprecipitation, HDAC activity assay, ChIP, RNAi knockdown, western blot for phosphorylation, serum stimulation cell cycle model Oncogene High 16103876
2005 c-Myc induction during G0-to-S transition causes a transient switch in the ratio of Mnt-Max to Myc-Max on shared target gene promoters. Mnt overexpression suppresses cell cycle entry and proliferation. Simultaneous Cre-lox deletion of both Mnt and c-Myc in MEFs rescues the cell cycle block caused by c-Myc ablation alone, demonstrating direct Mnt-Myc antagonism in cell cycle entry. ChIP, co-immunoprecipitation, retroviral overexpression, conditional double knockout (Cre/lox), proliferation and cell cycle assays The Journal of cell biology High 15866886
2009 MNT mRNA contains multiple miR-210 binding sites in its 3′ UTR; miR-210 overexpression reduces MNT levels and the resulting MNT knockdown phenocopies miR-210 overexpression (bypass of hypoxia-induced cell cycle arrest). Loss of MYC abolishes the miR-210-mediated override, placing MNT downstream of miR-210 and upstream of MYC-dependent transcription in the hypoxia response. 3′ UTR reporter assays, siRNA knockdown, microarray gene expression profiling, cell cycle analysis, MYC knockout cell line epistasis Cell cycle (Georgetown, Tex.) Medium 19652553
2009 During cholestasis, a switch from Mnt-Max to Myc-Max binding at E-box elements in the p53 and cyclin D1 promoters is responsible for upregulation of p53 and cyclin D1 and hepatocyte apoptosis; lentiviral c-myc siRNA in bile duct-ligated mice prevented this switch and protected against apoptosis. Electrophoretic mobility shift assay (EMSA) for E-box binding, nuclear fractionation, promoter activity assays, lentiviral siRNA in vivo, bile duct ligation mouse model Hepatology (Baltimore, Md.) Medium 19086036
2006 Conditional deletion of Mnt in T cells causes increased apoptosis of thymic T cells, disrupted T-cell development, Th1 cytokine skewing, and ultimately T-cell lymphoma, demonstrating that Mnt is required for T-cell homeostasis and functions as a tumor suppressor in the T-cell lineage. Conditional Cre/lox knockout in T cells, flow cytometry, cytokine profiling, histopathology, in vivo tumor development Molecular and cellular biology High 16507988
2012 Deletion of Mnt in T cells prevented Myc-driven T-cell proliferative expansion and thymoma formation; tumor suppression was linked to increased apoptosis mediated by reactive oxygen species (ROS). Mnt-null MEFs were refractory to oncogenic transformation by Myc, redefining Mnt's dominant physiological role as suppression of apoptosis in Myc-driven oncogenesis. T-cell-specific conditional Mnt knockout in Myc-transgenic mice, ROS measurement, apoptosis assays, in vitro transformation assays with MEFs Proceedings of the National Academy of Sciences of the United States of America High 23150551
2006 Conditional loss of Mnt in mammary epithelium disrupts involution by reducing apoptosis and leads to hyperplastic ducts; promoter array analysis shows Mnt and c-Myc bind similar promoters, and mRNA expression profiles of Mnt-null mammary tumors resemble those of MMTV-c-Myc transgenic tumors, functionally linking Mnt loss to deregulated Myc target gene activation. Conditional Cre/lox knockout, promoter array (ChIP-chip), oligonucleotide expression arrays, histopathology Cancer research High 16740691
2016 E6AP (E6-associated protein), an E3 ubiquitin ligase, physically associates with MNT and promotes its ubiquitin-mediated proteasomal degradation; catalytically inactive E6AP (C843A mutant) stabilizes MNT rather than degrading it. ATRA treatment inhibits E6AP and stabilizes MNT, and E6AP knockdown restores MNT expression and promotes myeloid differentiation. Co-immunoprecipitation, proteasome inhibitor assays, catalytic mutant of E6AP, siRNA knockdown, western blot, myeloid differentiation assays (HL60 cells) Oncotarget Medium 26506232
2020 MNT autoregulates its own expression: MNT-MAX dimers bind and repress the MNT promoter via an E-box. In MAX-deficient cells, MNT relocalizes from nucleus to cytoplasm, forms homodimers and MNT-MLX heterodimers, and regulates cell cycle and DNA repair genes independently of MAX; MNT homodimers regulate transcription of some cell proliferation genes. MNT is required for cell proliferation even in the absence of MAX. ChIP, E-box deletion reporter assay, co-immunoprecipitation, RNA-seq in MAX-deficient cells, subcellular fractionation/localization, siRNA knockdown of MNT in MAX-null cells The Journal of biological chemistry High 31919096
2011 Max-Mnt-Sin3a-HDAC complexes repress transcription of pro-apoptotic and cell cycle arrest genes in proliferating cells; inhibition of PI3-kinase leads to loss of Max/Mnt binding at target gene promoters, enabling transcriptional induction by MITF and USF1 and FoxO, linking PI3K/Akt/GSK3 signaling to regulation of Mnt-dependent repressor complexes. Chromatin immunoprecipitation, RNA interference, promoter activity assays, PI3-kinase inhibitor treatment, identification of GSK3 phosphorylation sites on USF1 The Journal of biological chemistry Medium 21873430
2008 In parous mammary glands responding to carcinogen exposure, Mnt is upregulated and a novel HDAC1/c-Myc/Mnt/Max complex forms on promoters of Myc target genes (ornithine decarboxylase, cyclin D2, TGFβ1), repressing their transcription and blocking proliferative response; this complex disassembles in serum-stimulated cells. Co-immunoprecipitation, ChIP, western blot, in vivo carcinogen treatment model Cancer science Medium 18271930
2004 Loss of the Max-interacting protein Mnt in mice results in perinatal lethality, intrauterine growth restriction, and craniofacial defects including cleft palate; Mnt-deficient embryos show reduced c-Myc and N-Myc levels, placing Mnt upstream of Myc regulation in embryonic development. Germline and conditional knockout mice (Cre/lox), histopathology, western blot for Myc proteins Human molecular genetics Medium 15028671
2020 In Eμ-Myc mice, homozygous Mnt deletion greatly reduced lymphoma incidence by enhancing MYC-driven apoptosis, primarily by failing to suppress pro-apoptotic BIM levels. Inducible deletion of Mnt within established transplanted Eμ-Myc lymphoma cells significantly extended recipient survival, establishing that MNT suppresses MYC-driven apoptosis through reduction of BIM. Conditional and inducible Cre/lox Mnt deletion in Eμ-Myc transgenic mice, transplantation survival assay, BIM protein measurement, apoptosis assays Blood High 31978211
2011 OX40 engagement in antigen-stimulated T cells leads to increased protein stability of Mnt (and Mxd4), translocation to the nucleus, and increased cell survival; siRNA knockdown of Mnt led to increased cell death, demonstrating that Mnt stability contributes to OX40-mediated T-cell survival. Flow cytometry, nuclear fractionation, siRNA knockdown, protein stability assay, ex vivo antigen stimulation of murine T cells European journal of immunology Medium 21400495
2004 In neuroblastoma cells during retinoic-acid-induced differentiation, MYCN is rapidly downregulated and MYCN/Max DNA-binding activity decreases, while Mnt expression and Mnt/Max DNA-binding activity do not change significantly; overexpression of Mnt in MYCN-amplified cells does not block differentiation capacity, indicating that MYCN downregulation rather than changes in Mnt is essential for neuroblastoma differentiation. EMSA, western blot, flow cytometry, retroviral overexpression in neuroblastoma cells Journal of cellular biochemistry Medium 15258910
1999 Mnt protein interacts with Max to form a heterodimer that binds DNA specifically at E-box/CACGTG sequences in medulloblastoma cell lines; the functional bHLHZip domain is intact. No somatic mutations were found in the bHLHZip or SID regions in 44 medulloblastoma samples, making MNT an unlikely frequent target for 17p13.3 deletion-driven tumorigenesis in medulloblastoma. EMSA, RT-PCR, western blot, SSCP mutation analysis International journal of cancer Medium 10446446

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 262 10481915
2009 MicroRNA miR-210 modulates cellular response to hypoxia through the MYC antagonist MNT. Cell cycle (Georgetown, Tex.) 232 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 211 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 137 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.) 111 12446910
2003 Local spreading of MSL complexes from roX genes on the Drosophila X chromosome. Genes & development 88 12782651
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 75 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
1997 Quantitative specificity of the Mnt repressor. Journal of molecular biology 69 9268651
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
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
2018 Melatonin and Its Metabolites Ameliorate UVR-Induced Mitochondrial Oxidative Stress in Human MNT-1 Melanoma Cells. International journal of molecular sciences 47 30487387
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
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
2020 The rOX-stars of inflammation: links between the inflammasome and mitochondrial meltdown. Clinical & translational immunology 41 32055400
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 Novel polyadenylylation-dependent neutralization mechanism of the HEPN/MNT toxin/antitoxin system. Nucleic acids research 40 33045733
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
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 Induction of melanogenesis by rapamycin in human MNT-1 melanoma cells. Annals of dermatology 33 22577264
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
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 33 21873430
2007 Regional control of chromatin organization by noncoding roX RNAs and the NURF remodeling complex in Drosophila melanogaster. Genetics 33 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
2020 Development and survival of MYC-driven lymphomas require the MYC antagonist MNT to curb MYC-induced apoptosis. Blood 29 31978211
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
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
2018 Structure-function analyses reveal the molecular architecture and neutralization mechanism of a bacterial HEPN-MNT toxin-antitoxin system. The Journal of biological chemistry 26 29555683
2017 MNT and Emerging Concepts of MNT-MYC Antagonism. Genes 26 28230739
2006 Inflammatory disease and lymphomagenesis caused by deletion of the Myc antagonist Mnt in T cells. Molecular and cellular biology 26 16507988
2018 Rox-DNA Functionalized Silicon Nanodots for Ratiometric Detection of Mercury Ions in Live Cells. Analytical chemistry 25 30014694
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 24 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
2015 Novel Heterotypic Rox Sites for Combinatorial Dre Recombination Strategies. G3 (Bethesda, Md.) 21 26715092
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
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
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
2022 Combined Therapy with Dacarbazine and Hyperthermia Induces Cytotoxicity in A375 and MNT-1 Melanoma Cells. International journal of molecular sciences 16 35408947
2020 The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells. The Journal of biological chemistry 16 31919096
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
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
2007 Expression and mutation analysis of genes that encode the Myc antagonists Mad1, Mxi1 and Rox in acute leukaemia. Leukemia & lymphoma 12 17577784
2017 Mnt modulates Myc-driven lymphomagenesis. Cell death and differentiation 11 28800127

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