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Gene Review

Mnt  -  max binding protein

Mus musculus

Synonyms: Max-binding protein MNT, Myc antagonist MNT, Protein ROX, Rox, bHLHd3
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Disease relevance of Mnt

  • Transcription repression by Mnt maps to a 13-amino-acid amino-terminal region related to the Sin3 interaction domain (SID) of Mad proteins [1].
  • Finally, most mice lacking Mnt in T cells ultimately succumbed to T-cell lymphoma [2].
  • An exception is P19 embryonal carcinoma cells, where Mnt is expressed and in a complex with Max, but Myc proteins are not detected [3].

High impact information on Mnt

  • Furthermore, wild-type Mnt suppresses Myc+Ras cotransformation of primary cells, whereas Mnt containing a SID deletion cooperates with Ras in the absence of Myc to transform cells [1].
  • These results demonstrate that Mnt-Myc antagonism plays a fundamental role in regulating cell cycle entry and proliferation [4].
  • Since mice lacking Mnt were born severely runted and typically died within several days of birth, mouse embryo fibroblasts (MEFs) derived from these mice and conditional Mnt knockout mice were used in this study [5].
  • Consistent with Mnt functioning as a tumor suppressor, conditional inactivation of Mnt in breast epithelium led to adenocarinomas [5].
  • These results demonstrate a unique negative regulatory role for Mnt in governing key Myc functions associated with cell proliferation and tumorigenesis [5].

Biological context of Mnt

  • Like MEFs that overexpress Myc, Mnt(-/-) MEFs were prone to apoptosis, efficiently escaped senescence and could be transformed with oncogenic Ras alone [5].
  • In the absence of Mnt, MEFs prematurely entered the S phase of the cell cycle and proliferated more rapidly than Mnt(+/+) MEFs [5].
  • The transcriptional orientation and intergenic distance of Lis1 and Mnt/Rox were ascertained by fragmentation analysis of a mouse yeast artificial chromosome containing both genes [6].
  • The basic-helix-loop-helix-leucine zipper (bHLHZip) proteins Myc, Mad and Mnt are part of a transcription activation/repression system involved in the regulation of cell proliferation [7].
  • The disruption of immune homeostasis is linked to a strong skewing toward production of T-helper 1 (Th1) cytokines and enhanced proliferation of activated Mnt-deficient CD4+ T cells [2].

Anatomical context of Mnt

  • Furthermore, simultaneous Cre-Lox mediated deletion of Mnt and c-Myc in mouse embryo fibroblasts rescued the cell cycle entry and proliferative block caused by c-Myc ablation alone [4].
  • Here we show that conditional deletion of Mnt in T cells leads to tumor formation but also causes inflammatory disease [2].
  • Deletion of Mnt caused increased apoptosis of thymic T cells and interfered with T-cell development yet led to spleen, liver, and lymph node enlargement [2].
  • Mnt-deficient mammary glands exhibit impaired involution and tumors with characteristics of myc overexpression [8].

Physical interactions of Mnt


Regulatory relationships of Mnt

  • Mnt loss triggers Myc transcription targets, proliferation, apoptosis, and transformation [10].

Other interactions of Mnt

  • Interestingly, bandshift assays demonstrate that the Rox-Max heterodimer shows a novel DNA binding specificity, having a higher affinity for the CACGCG site compared with the canonical E box CACGTG site [11].
  • Our data suggest a model in which phosphorylation of Mnt at cell cycle entry results in disruption of Mnt-mSin3-HDAC1 interaction, which allows induction of Myc target genes by release of Mnt-mediated transcriptional repression [9].

Analytical, diagnostic and therapeutic context of Mnt


  1. Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites. Hurlin, P.J., Quéva, C., Eisenman, R.N. Genes Dev. (1997) [Pubmed]
  2. Inflammatory disease and lymphomagenesis caused by deletion of the Myc antagonist Mnt in T cells. Dezfouli, S., Bakke, A., Huang, J., Wynshaw-Boris, A., Hurlin, P.J. Mol. Cell. Biol. (2006) [Pubmed]
  3. Mnt: a novel Max-interacting protein and Myc antagonist. Hurlin, P.J., Qúeva, C., Eisenman, R.N. Curr. Top. Microbiol. Immunol. (1997) [Pubmed]
  4. Mnt-Max to Myc-Max complex switching regulates cell cycle entry. Walker, W., Zhou, Z.Q., Ota, S., Wynshaw-Boris, A., Hurlin, P.J. J. Cell Biol. (2005) [Pubmed]
  5. Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis. Hurlin, P.J., Zhou, Z.Q., Toyo-oka, K., Ota, S., Walker, W.L., Hirotsune, S., Wynshaw-Boris, A. EMBO J. (2003) [Pubmed]
  6. Genomic organization of the murine Miller-Dieker/lissencephaly region: conservation of linkage with the human region. Hirotsune, S., Pack, S.D., Chong, S.S., Robbins, C.M., Pavan, W.J., Ledbetter, D.H., Wynshaw-Boris, A. Genome Res. (1997) [Pubmed]
  7. Mga, a dual-specificity transcription factor that interacts with Max and contains a T-domain DNA-binding motif. Hurlin, P.J., Steingrìmsson, E., Copeland, N.G., Jenkins, N.A., Eisenman, R.N. EMBO J. (1999) [Pubmed]
  8. Mnt-deficient mammary glands exhibit impaired involution and tumors with characteristics of myc overexpression. Toyo-oka, K., Bowen, T.J., Hirotsune, S., Li, Z., Jain, S., Ota, S., Escoubet-Lozach, L., Lozach, L.E., Garcia-Bassets, I., Bassett, I.G., Lozach, J., Rosenfeld, M.G., Glass, C.K., Eisenman, R., Ren, B., Hurlin, P., Wynshaw-Boris, A. Cancer Res. (2006) [Pubmed]
  9. Mnt transcriptional repressor is functionally regulated during cell cycle progression. Popov, N., Wahlström, T., Hurlin, P.J., Henriksson, M. Oncogene (2005) [Pubmed]
  10. Mnt loss triggers Myc transcription targets, proliferation, apoptosis, and transformation. Nilsson, J.A., Maclean, K.H., Keller, U.B., Pendeville, H., Baudino, T.A., Cleveland, J.L. Mol. Cell. Biol. (2004) [Pubmed]
  11. 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. Meroni, G., Reymond, A., Alcalay, M., Borsani, G., Tanigami, A., Tonlorenzi, R., Nigro, C.L., Messali, S., Zollo, M., Ledbetter, D.H., Brent, R., Ballabio, A., Carrozzo, R. EMBO J. (1997) [Pubmed]
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