Research Focus
My group is interested in signalling pathways that promote colorectal tumorigenesis and we study (i) the alternative splice variant Rac1b overexpressed in tumours, (ii) the effect of activated b-catenin/TCF signalling on splicing, (iii) the effect on splicing of exonic missense mutations diagnosed by our department in colorectal tumour suppressor genes, and (iv) the role of a novel cell-cycle regulating protein that co-immunoprecipitates with cdc5L and Prp19.
Publications
- Matos, P., Oliveira, C., Velho, S., Gonçalves, V., da Costa, L.T., Moyer, M.P., Seruca, R. and Jordan, P. (2008). B-RafV600E cooperates with alternative spliced Rac1b to sustain colorectal cancer cell survival. Gastroenterology 135, 899-906.
- Vieira, L., Sousa, A.C., Matos, P., Marques, B., Alaiz, H., Ribeiro, M.J., Braga, P., da Silva, M.G., Jordan, P. (2006). Three-way translocation involves MLL, MLLT3, and a novel cell cycle control gene, FLJ10374, in the pathogenesis of acute myeloid leukemia with t(9;11;19)(p22;q23;p13.3). Genes Chromosomes Cancer 45, 455-469.
- Matos, P., Collard, J. and Jordan, P. (2003). Tumor-related alternative- spliced Rac1b is not regulated by Rho-GDI and exhibits selective downstream signaling. Journal of Biological Chemistry 278, 50442-50448.
- Clarke, L.A., Veiga, I., Isidro, G., Jordan, P., Silva Ramos, J., Castedo, S. and Boavida, M.G. (2000). Pathological exon skipping in an HNPCC proband with hMLH1 splice acceptor site mutation. Genes Chromosomes Cancer 29, 367-370.
Key lab techniques:
Lab contact: peter.jordan@insa.min-saude.pt [1]
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