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W that a region of gH just prior to the transmembrane region is critical for function. Several criteria suggest that the truncated soluble complex that we are studying reflects the actual structure of the complex in the virion envelope. First, the gHt-gL complex was antigenically intact, as judged by its capacity to bind to MAbs 52S and 53S, which recognize gH conformation (49), as well as to the
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Racellular function.4 Indeed, in chimeric mice expressing a N-terminally truncated IL-33, the exclusion of IL-33 from the nucleus induced lethal inflammation, suggesting that its nuclear location acts as a sink, preventing its uncontrolled extracellular release. This IL-33 nuclear `docking' is even more important since its release is independent of prior processing either by caspase-1, caspase-8 (