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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RACRFEjMxUVp3R3BUZPFAy3JWF99-VtQftSQqQvvL5YUk#_4 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RACRFEjMxUVp3R3BUZPFAy3JWF99-VtQftSQqQvvL5YUk#_3 http://www.w3.org/ns/prov#value Supplemental Table I. Probe sets altered by nutlin-3a treatment. From results: Of ?40,000 human transcripts represented on the chip, 143 genes (166 probe sets) were found differentially expressed in HCT116 cells treated with nutlin-3a (Fig. 1D and Table 1, which is published as supporting information on the PNAS web site). The list included multiple genes previously shown to be affected by p53 activation (19?21), including 32 transcripts reported as directly regulated by p53. Changes in the expression of many genes may reflect the altered cell-cycle distribution in cells that arrest predominantly in G1 and G2 phases as a result of p53 activation (12). With the exception of a few genes that were marginally down-regulated in HCT116 cells, the inactive enantiomer did not significantly change the gene expression profile of both cell lines. Taken together, the data in Fig. 1 indicate that nutlin-3a is a highly selective MDM2 antagonist and p53 inducer. *Differential expression was determined as 3-fold altered in HCT116 treated with nutlin-3a vs. vehicle and P < 0.05, and no change (<1.5-fold change) in the H1299 cells or HCT116 treated with nutlin-3b. **Expression vaules are the average of three replicates of Affymetrix MAS5 signal intensities scaled to the median of the experiment. 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