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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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Interestingly, co-expression of DSCR1 strongly inhibited the induction of the IL-2 reporter by co-stimulation with PMA and ionophore. Similarly, DSCR1115-197, the truncated version of DSCR1 that retained CaNA binding activity, was able to act as a dose-dependent inhibitor, though not as efficiently as DSCR1 full-length. In contrast, co-expression of DSCR11-156, the mutant incapable of CaNA binding, had no effect on the activation assay, strongly suggesting that the inhibition caused by DSCR1 is mediated through calcineurin binding. ZAKI-4 was also able to inhibit calcineurin function, as measured by its ability to suppress IL-2 reporter activation (Fig. 5A).
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2014-07-03T14:29:51.347+02:00
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