"Global Functional Genomics Reveals GRK5 as a Therapeutic Target for Cystic Fibrosis", CFTR interactomes

<em>A tidy selection of published CFTR interactomes (or CFTR-related omics datasets)</em> Collects data from the original online sources, converts gene/protein identifiers into a standard tidy format and updates the identifiers. The Uniprot ID is taken as reference and all other identifiers are genereated from them. This causes some datasets to end up with less genes/proteins than reported. Datasets included <strong>Botelho (2021)</strong> - CFTR traffic regulators Botelho <em>et al</em> (2022), submitted <strong>Pankow (2015)</strong> - CFTR interactome Pankow <em>et al</em> (2015) deltaF508 CFTR interactome remodelling promotes rescue of cystic fibrosis. <em>Nature</em>. 528, 510--516. https://doi.org/10.1038/nature15729 <strong>Canato (2018)</strong> - CFTR interactome Canato <em>et al</em> (2018) Proteomic interaction profiling reveals KIFC1 as a factor involved in early targeting of F508del-CFTR to degradation. <em>Cell Mol Life Sci</em>. 75(24):4495-4509. https://doi.org/10.1007/s00018-018-2896-7 <strong>Santos (2019)</strong> - CFTR interactome Santos <em>et al</em> (2019) Folding Status Is Determinant over Traffic-Competence in Defining CFTR Interactors in the Endoplasmic Reticulum. <em>Cells</em>. 8(4):353. https://doi.org/10.3390/cells8040353 <strong>Hutt (2018)</strong> - CFTR interactome Hutt <em>et al</em> (2018) A Proteomic Variant Approach (ProVarA) for Personalized Medicine of Inherited and Somatic Disease. <em>J Mol Biol</em>. 430: 2951-2973. https://doi.org/10.1016/j.jmb.2018.06.017 <strong>Rauniyar (2014)</strong> - CFTR proteome Rauniyar <em>et al</em> (2014) Quantitative Proteomic Profiling Reveals Differentially Regulated Proteins in Cystic Fibrosis Cells. <em>J Proteome Res</em>. 13(11): 4668-4675. https://doi.org/10.1021/pr500370g <strong>Almaça (2013)</strong> - ENaC regulome Almaça <em>et al</em> (2013) High-content siRNA screen reveals global ENaC regulators and potential cystic fibrosis therapy targets. <em>Cell</em>. 154(6):1390-400. https://doi.org/10.1016/j.cell.2013.08.045 <strong>Tomati (2018)</strong> - CFTR regulome Tomati <em>et al</em> (2018) High-throughput screening identifies FAU protein as a regulator of mutant cystic fibrosis transmembrane conductance regulator channel. <em>J Biol Chem</em>. 293(4):1203-1217. https://doi.org/10.1074/jbc.m117.816595 <strong>Simpson (2012)</strong> - Secretome Simpson <em>et al</em> (2012) Genome-wide RNAi screening identifies human proteins with a regulatory function in the early secretory pathway. <em>Nature Cell Biology</em>. 14, 764-774. https://doi.org/10.1038/ncb2510 <strong>Wang (2006)</strong> - CFTR interactome Wang <em>et al</em> (2006) Hsp90 Cochaperone Aha1 Downregulation Rescues Misfolding of CFTR in Cystic Fibrosis. <em>Cell</em>. 127(4):803-815. https://doi.org/10.1016/j.cell.2006.09.043 <strong>Reilly (2017)</strong> - CFTR interactome Reilly <em>et al</em> (2017) Targeting the PI3K/Akt/mTOR signalling pathway in Cystic Fibrosis. <em>Sci Rep</em>. 9;7(1):7642. https://doi.org/10.1038/s41598-017-06588-z <strong>Gilchrist (2006)</strong> - Secretome Gilchrist <em>et al</em> (2006) Quantitative Proteomics Analysis of the Secretory Pathway. <em>Cell</em>. 127(6):1265-1281. https://doi.org/10.1016/j.cell.2006.10.036 <strong>Pankow (2019)</strong> - CFTR interactome Pankow <em>et al</em> (2019) A posttranslational modification code for CFTR maturation is altered in cystic fibrosis. <em>Science Signaling</em>. 12(562):eaan7984. https://doi.org/10.1126/scisignal.aan7984 <strong>Dang (2020)</strong> - CF lung disease modifier genes Dang <em>et al</em> (2020) Mining GWAS and eQTL data for CF lung disease modifiers by gene expression imputation. <em>PLoS One</em>. 15(11):e0239189. https://doi.org/10.1371/journal.pone.0239189 <strong>Hodos (2020)</strong> - CF genomic meta-analysis Hodos <em>et al</em> (2020) Integrative genomic meta-analysis reveals novel molecular insights into cystic fibrosis and deltaF508-CFTR rescue. <em>Sci Rep</em> 10(1):20553. http://dx.doi.org/10.1038/s41598-020-76347-0