Fig. S1. Signalling pathways potentially regulating β-catenin levels in B-13 cells. Expression levels of selected transcripts relative to B-13 cells. RNA from the indicated cell type/treatment was converted to cDNA, labelled and hybridized to the Affymetrix Rat RG-U34A GeneChips as described (Wallace et al., 2009). Probesets intensities were averaged using Microarray Suite 5.0 (Affymetrix), the mean of each array was globally normalised to 500 and these data were imported into GeneSpring v6.0 (Silicon Genetics). The following normalisations were applied: data transformation of measurements below 0.01 to 0.01; per-chip and per-gene normalisations. Gene lists were created in GeneSpring by filtering for differences in fold expression between pair wise treatments combinations.

Fig. S2. Signalling pathways potentially regulating β-catenin levels in B-13 cells. The NCBI Unigene web site identifies 72 EST sequences that align with the rat Sgk1 gene. These were examined and 3 transcripts were identified − Sgk1a (reference Sgk1 gene sequence for the rat) and two alternatively spliced transcripts (Sgk1b and Sgk1c) resulting in three transcripts containing different 5′ ends through use of alternative first exons. The first start (ATG) codon in each of the two additional transcripts is in frame with the Sgk1a transcript, predicting three SGK1 proteins with different N-terminal domains (see bottom panel).

Fig. S3. Structure of SGK1A proteins. (A) Schematic diagram of human SGK1A indicating position of phosphorylated residues (Pearce et al., 2010). (B) Clustal alignment of rat SGK1A and human SGK1A proteins. Green residues indicate site of phosphorylation, red residues indicate site of mutation to create KD mutants. *, residues are identical; colon, conserved substitutions; full stop, semi-conserved substitutions.