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The lack of any induction of tissue damage in our chimera experiments allowed us to observe trogocytosis only.

By labeling our chimera with the red fluorescent protein, mCherry (a gift of Roger Tsien[12]) we generated a non-targeted "cAMP sponge" construct.

Finally, we used our chimera system to investigate whether the tolerogenic influence of LCs was retained with a stronger adjuvant.

Our chimera detection criteria differ from previous studies in taking self chimeras into account and allowing short overlap between query coverages.

Given the prevalence in our chimera data set of entire DNA-binding domains in the absence of transcriptional activation domains, we suspect that such chimeras compete with the parental transcription factors, thus exerting dominant negative effects (Fig. 2).

In our chimera data set, 1,643 chimeras had a correct frame for two parental proteins that ensured a directed translation without a stop codon at the junction site of chimeras.

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All three of our chimeras that fit this description were essentially non-functional, while reciprocal mouse ORF2 chimeras maintained retrotransposition competence.

8d,  17 Similar to WT Ure2, 10 our chimeras retained their enzyme activities after fibril formation.

Thus far, we did not observe any phenotypic changes in our chimeras or their offspring that could be attributed to a particular CNV; however, this remains a possibility.

Two of these α-helices are fully replaced by our chimeras, SC(140 148) and SC(153 165), and display defective HDL binding.

The prion domain of Ure2 was attached to the N terminus of AP or HRP, both of which have widespread applications in clinical and immunodiagnostic use and can be assessed for activity using simple colorimetric, fluorescent, or luminescent assays even at low (single molecule) concentrations, which raises the possibility of using our chimeras to probe the assembly and subunit structure of Ure2.

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