Additional file 1 of Analysis of multiple gene co-expression networks to discover interactions favoring CFTR biogenesis and ΔF508-CFTR rescue

Additional file 1. Table S1. Summary of differentially expressed genes across conditions in CFBE cells. Summary of up- and down-regulated differentially expressed genes in conditions vs. controls. Table S2. Differentially expressed genes in the miR-138/SIN3A condition. List of differentially expressed genes in the miR-138/SIN3A conditions vs. scrambled siRNA control. Table S3. Differentially expressed genes in the NEDD8/SYVN1 condition. List of differentially expressed genes in the NEDD8/SYVN1 conditions vs. scrambled siRNA control. Table S4. Differentially expressed genes in the temperature condition. List of differentially expressed genes in the temperature conditions vs. 37°C control. Table S5. CFTR interactome used as seed nodes. List of CFTR effectors and interactors used as seed nodes in the M-module analysis. Table S6. DsiRNA and primer sequences. List of siRNA and primer sequences used in the functional knockdown experiments to test for CFTR rescue. Table S7. Untested non-seed module genes. List of genes resulting from the M-module analysis that have not been previously tested or linked to CFTR. Table S8. Top 50 predicted gene ontology biological processes for CHURC1. List of biological processes associated with CHURC1 according to the ARChS4 software. Table S9. Top 50 predicted gene ontology biological processes for RPL15. List of biological processes associated with RPL15 according to the ARChS4 software. Table S10. Top 50 predicted gene ontology biological processes for GZF1. List of biological processes associated with GZF1 according to the ARChS4 software. Figure S1. Schematic showing intersection of differentially expressed genes across conditions. Controls and conditions are described in Table 1. Up arrows indicate up-regulated genes; down arrows indicate down-regulated genes. Significance is defined as FDR < 0.05. Figure S2. Representative transepithelial current tracings demonstrating the effects of individual gene knockdown on CFTR-dependent chloride current in CFBE cells. The Y-axis represents transepithelial current in µA and the X-axis represents time in seconds. The addition of the cAMP agonists forskolin and IBMX resulted in an increase in CFTR-dependent transepithelial chloride current in cells treated with DsiRNAs targeting: A) CHURC1 or B) RPL15. This increase in current was inhibited by the CFTR channel inhibitor GlyH-101. The tracing shown in C demonstrates that DsiRNA knockdown of THOC7 was ineffective in restoring CFTR-dependent chloride current.