We demonstrate by yeast two-hybrid, glutathione S-transferase pulldown, and mammalian reporter gene assays that ARNT requires its helix 2 domain but not its transactivation domain to interact with SRC-1. This indicates a novel mechanism of action for SRC-1. SRC-1 does not require its bHLH-PAS domain to interact with ARNT or AHR, but utilizes distinct domains proximal to its p300/CBP interaction domain. Taken together, these data support a role for the SRC family of transcriptional coactivators in TCDD-dependent gene regulation.

Chemical, electrical, and optical measurements were performed on n- and p-type β-silicon carbide crystals grown from pure or doped carbon-saturated silicon melts. Pure, transparent yellow crystals showed no detectable impurities and had carrier concentrations in the range of 1016 cm−3. Extensive twinning was observed. Uncorrected electron mobilities of 700–1000 cm2/V·sec were measured at room temperature. Intense injection electroluminescence, peaking at 2.28 eV and 2.0 eV, was observed in many diodes. Strong photoluminescence was observed in aluminum-doped crystals at 77°K and at room temperature when irradiated with uv light.

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Twinned β‐silicon carbide platelets with a (111) habit were grown from the walls of graphite crucibles in liquid silicon solutions with carbon concentrations below 0.1 a/o (atomic per cent). The observed crystal growth effects resulting from increasing the carbon solute transport rate by stirring the solution are described and correlated with boundary layer theory. Both forward growth of platelets into the solution and lateral growth of platelets were accelerated by stirring. However, crystal growth in the forward direction was eventually limited by a boundary layer region, beyond which the solution was no longer supersaturated. Because of the decrease in boundary layer thickness with increasing stirring speed, the terminal lengths of silicon carbide platelets decrease with increasing stirring speed.