First of all we have localized the three selenoproteins chosen in the human genome. Thanks to the different on-line databases, overalls to ensembl database, we have seen the exact location of every selenoprotein, the number of pb that form the selenoprotein, the number of exons and also in which tissue are they characteristic.

At the same time we have found the different selenocysteines in the peptide sequence, thanks to ensembl database that has been a very good tool to obtain our results. The database being correctly annotated, the search of the selenocysteins as a "U" was possible, instead of seeing it as a codon stop.

The SNPs were localized in the peptid sequence and we found out that no one was affecting the SecIS structure, or the near regions to it, or the aminoacid sequence. For this reason we continue our study to analize the human ests. In blastn est_human database we obtained few hits (100 maximum), due to this fact the search was faster but we can extract few conclusion in our project.

The programming was a heavy job, we made 3 different programs in order to obtain a collection of all the sequences with SNPs that we wanted to analyze and an output with the position and changes of each SNP that we applied to the query sequence of the selenoprotein.
We were able to obtain the results which we were looking for, and thanks to them we could continue with our study.

The SecIs structure elements were also analyzed for seing if they were affected by SNPs.

The last one step in our project was to observe any relation between the selenoproteins chosen and some kind or specific disease. We only obtain results from the SEPN.

Selenoprotein I has no relevant results, and we have not found any SNP that could alter the operation on the protein. More studies should be done to obtain more concluding results.

Selenoprotein N has two isoforms, and both were analyzed obtaining results for both. Both isoforms differ in the number of selenocysteines and only the first one was associated to a disease (muscular distrophy) due to the mutation which alters the TGA codon.
One possible SecIS structure alteration has been found in our project that could be related to a disease but the est hit corresponding to it was coming from a normal cell. That suggests that there is no relation between this alteration of the SecIS element of the SELN and a disease.

Selenoprotein O is the one that contains more SNPs. We have found a lot of hits from est sequences containing a lot of SNPs related to neuroblastoma and we can correlate the alterations of SecIS structures to this kind of disease.

To obtain the best results a new project should be done obtaining and comparing information from more than one database. More concluding facts could be discovered.