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Gene Review

Sim2  -  single-minded homolog 2 (Drosophila)

Mus musculus

Synonyms: SIM transcription factor, Single-minded homolog 2, bHLHe15, mSIM
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Disease relevance of Sim2


Psychiatry related information on Sim2


High impact information on Sim2


Biological context of Sim2


Anatomical context of Sim2

  • Sim2s is expressed at high levels in kidney and skeletal muscle; however, the ratio of Sim2 to Sim2s mRNA differs between these tissues [1].
  • Mice homozygous for the disrupted allele (Sim2 -/-) exhibit a cleft of the secondary palate and malformations of the tongue and pterygoid processes of the sphenoid bone [4].
  • These craniofacial malformations are the most probable cause of aerophagia (air swallowing with subsequent accumulation of air in the gastrointestinal tract) and postnatal death exhibited by Sim2 -/- mice [4].
  • Sim2 is a member of the basic helix-loop-helix PAS transcription factor gene family and is evolutionarily related to the Drosophila single-minded gene, a key regulator of central nervous system midline development [4].
  • To explore how Sim2 influences spatial memory, a DNA plasmid-encoding mouse Sim2 (mSim2) wrapped with liposome was bilaterally injected into the hippocampus of rats [5].

Associations of Sim2 with chemical compounds


Other interactions of Sim2

  • Genetically, Sim1 acts upstream of Sim2 and partially compensates for the loss of Sim2 [7].
  • Similar to full-length Sim2, Sim2s interacts with Arnt and to a lesser extent, Arnt2 [1].
  • Comparative expression studies at the anterior hypothalamus at early stages reveal that there are separate pools of Trh cells with distinctive molecular codes defined by Sim1 and Sim2 expression [7].
  • In addition, alterations in the Sim-2 expression domain in ventral prosencephalon, rostral to p1, provide novel evidence for Wnt-1 function in this region [9].
  • It is concluded that Sim2 may play an important role in the pathogenesis of DS by inhibiting the cell cycle, which is related to the decreased expression of cyclin E and increased expression of p27 [8].

Analytical, diagnostic and therapeutic context of Sim2

  • In an effort to determine the biological roles of Sim2 in mammalian development, we disrupted the murine Sim2 gene through gene targeting [4].


  1. Differential Transcriptional Regulation by Mouse Single-minded 2s. Metz, R.P., Kwak, H.I., Gustafson, T., Laffin, B., Porter, W.W. J. Biol. Chem. (2006) [Pubmed]
  2. Mice trisomic for a bacterial artificial chromosome with the single-minded 2 gene (Sim2) show phenotypes similar to some of those present in the partial trisomy 16 mouse models of Down syndrome. Chrast, R., Scott, H.S., Madani, R., Huber, L., Wolfer, D.P., Prinz, M., Aguzzi, A., Lipp, H.P., Antonarakis, S.E. Hum. Mol. Genet. (2000) [Pubmed]
  3. Sim2 mutants have developmental defects not overlapping with those of Sim1 mutants. Goshu, E., Jin, H., Fasnacht, R., Sepenski, M., Michaud, J.L., Fan, C.M. Mol. Cell. Biol. (2002) [Pubmed]
  4. Craniofacial abnormalities resulting from targeted disruption of the murine Sim2 gene. Shamblott, M.J., Bugg, E.M., Lawler, A.M., Gearhart, J.D. Dev. Dyn. (2002) [Pubmed]
  5. Effects of overexpression of Sim2 on spatial memory and expression of synapsin I in rat hippocampus. Meng, X., Peng, B., Shi, J., Zheng, Y., Chen, H., Zhang, J., Li, L., Zhang, C. Cell Biol. Int. (2006) [Pubmed]
  6. Members of the bHLH-PAS family regulate Shh transcription in forebrain regions of the mouse CNS. Epstein, D.J., Martinu, L., Michaud, J.L., Losos, K.M., Fan, C., Joyner, A.L. Development (2000) [Pubmed]
  7. Sim2 contributes to neuroendocrine hormone gene expression in the anterior hypothalamus. Goshu, E., Jin, H., Lovejoy, J., Marion, J.F., Michaud, J.L., Fan, C.M. Mol. Endocrinol. (2004) [Pubmed]
  8. Effect of mouse Sim2 gene on the cell cycle of PC12 cells. Meng, X., Shi, J., Peng, B., Zou, X., Zhang, C. Cell Biol. Int. (2006) [Pubmed]
  9. Early deletion of neuromeres in Wnt-1-/- mutant mice: evaluation by morphological and molecular markers. Mastick, G.S., Fan, C.M., Tessier-Lavigne, M., Serbedzija, G.N., McMahon, A.P., Easter, S.S. J. Comp. Neurol. (1996) [Pubmed]
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