Abstract
The mSim-1 and mSim-2 gene products are mammalian homologues of the Drosophila Sim gene. The dSim gene product transactivates through a DNA binding site known as the CNS midline enhancer (CME) element. We have investigated the transcriptional properties of mSIM-1 and mSIM-2 mediated through the CME element in concert with their dimerization partners, ARNT and ARNT-2. The mSIM-1/ARNT heterodimer transactivates reporter constructs via the ARNT carboxy-terminus. However, mSIM-2 quenches ARNT transactivation. We find that mSIM-2 competes with mSIM-1 for binding to ARNT, suggesting a possible antagonism between these transcription factors.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aryl Hydrocarbon Receptor Nuclear Translocator
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Base Sequence
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Basic Helix-Loop-Helix Transcription Factors
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Binding Sites / genetics
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Binding, Competitive
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Cell Line
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DNA / genetics
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DNA / metabolism
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DNA Primers / genetics
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DNA-Binding Proteins*
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Helix-Loop-Helix Motifs / genetics
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Humans
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Receptors, Aryl Hydrocarbon*
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
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Repressor Proteins / genetics*
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Repressor Proteins / metabolism*
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Transcription Factors / genetics*
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Transcription Factors / metabolism*
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Transcription, Genetic
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Transcriptional Activation
Substances
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ARNT protein, human
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ARNT2 protein, human
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Basic Helix-Loop-Helix Transcription Factors
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DNA Primers
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DNA-Binding Proteins
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Receptors, Aryl Hydrocarbon
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Recombinant Proteins
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Repressor Proteins
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SIM1 protein, human
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SIM2 protein, human
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Sim2 protein, mouse
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Transcription Factors
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Aryl Hydrocarbon Receptor Nuclear Translocator
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DNA