Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome.

@article{Toyooka2004LossOT,
  title={Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome.},
  author={Kazuhito Toyo-oka and Shinji Hirotsune and Michael J Gambello and Z Q Zhou and Lorin E Olson and Michael G. Rosenfeld and Robert N. Eisenman and Peter J. Hurlin and Anthony Wynshaw-Boris},
  journal={Human molecular genetics},
  year={2004},
  volume={13 10},
  pages={1057-67}
}
The Mnt gene encodes a Mad-family bHLH transcription factor located on human 17p13.3. Mnt is one of 20 genes deleted in a heterozygous fashion in Miller-Dieker syndrome (MDS), a contiguous gene syndrome that consists of severe neuronal migration defects and craniofacial dysmorphic features. Mnt can inhibit Myc-dependent cell transformation and is hypothesized to counterbalance the effects of c-Myc on growth and proliferation in vivo by competing with Myc for binding to Max and by repressing… CONTINUE READING
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