Gastric hyperplasia in mice lacking the putative Cdc42 effector IQGAP1. Li S, Wang Q, Chakladar A, Bronson RT, Bernards A. Downregulation of IQGAP1 inhibits epithelial-mesenchymal transition via the HIF1α/VEGF-A signaling pathway in gastric cancer. Liu J, Ni X, Li Y, Chen M, Chen W, Wu Y, et al. IQGAP1 promotes pancreatic cancer progression and epithelial-mesenchymal transition (EMT) through Wnt/β-catenin signaling. Hu W, Wang Z, Zhang S, Lu X, Wu J, Yu K, et al. A molecular rheostat at the interface of cancer and diabetes. IQGAPs in cancer: A family of scaffold proteins underlying tumorigenesis. Nuclear F-actin counteracts nuclear deformation and promotes fork repair during replication stress. Lamm N, Read MN, Nobis M, Van Ly D, Page SG, Masamsetti VP, et al. IQGAP1 binds to yes-associated protein (YAP) and modulates its transcriptional activity. Sayedyahossein S, Li Z, Hedman AC, Morgan CJ, Sacks DB. IQGAPs choreograph cellular signaling from the membrane to the nucleus. IQGAP1 translocates to the nucleus in early S-phase and contributes to cell cycle progression after DNA replication arrest. Johnson M, Sharma M, Brocardo MG, Henderson BR. Direct interaction between hnRNP-M and CDC5L/PLRG1 proteins affects alternative splice site choice. Llères D, Denegri M, Biggiogera M, Ajuh P, Lamond AI. Large-scale proteomic analysis of the human spliceosome. Rappsilber J, Ryder U, Lamond AI, Mann M. The ATAC acetyltransferase complex coordinates MAP kinases to regulate JNK target genes. Suganuma T, Mushegian A, Swanson SK, Abmayr SM, Florens L, Washburn MP, et al. Disorder targets misorder in nuclear quality control degradation: a disordered ubiquitin ligase directly recognizes its misfolded substrates. Rosenbaum JC, Fredrickson EK, Oeser ML, Garrett-Engele CM, Locke MN, Richardson LA, et al. Signalling scaffolds and local organization of cellular behaviour. Alternative splicing and cancer: insights, opportunities, and challenges from an expanding view of the transcriptome. Comprehensive analysis of alternative splicing across tumors from 8,705 patients. Kahles A, Lehmann K-V, Toussaint NC, Hüser M, Stark SG, Sachsenberg T, et al. The cancer spliceome: reprograming of alternative splicing in cancer. Aberrant RNA splicing in cancer expression changes and driver mutations of splicing factor genes. Sveen A, Kilpinen S, Ruusulehto A, Lothe RA, Skotheim RI. Hallmarks of alternative splicing in cancer. Splicing regulation: From a parts list of regulatory elements to an integrated splicing code. Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing. Pan Q, Shai O, Lee LJ, Frey BJ, Blencowe BJ. Overall, we reveal a missing link between stress signals and AS regulation. Genome-wide analyses reveal that IQGAP1 and hnRNPM co-regulate the AS of a cell cycle-related RNA regulon in gastric cancer cells, thus favouring the accelerated proliferation phenotype of gastric cancer cells. IQGAP1 controls hnRNPM’s sumoylation, subnuclear localisation and the relevant response of the AS machinery to heat-induced stress. We show that in gastric cancer cells, a nuclear pool of IQGAP1 acts as a tethering module for a group of spliceosome components, including hnRNPM, a splicing factor critical for the response of the spliceosome to heat-shock. Here, we report that a cytosolic scaffold protein, IQGAP1, performs this task in response to heat-induced signals. In response to oncogenic signals, Alternative Splicing (AS) regulators such as SR and hnRNP proteins show altered expression levels, subnuclear distribution and/or post-translational modification status, but the link between signals and these changes remains unknown.
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