Project description:Tumor resistance to anti-cancer drugs is a major huddle in chemotherapy. To identify cancer genes that contribute to chemoresistance, B16 mouse melanoma cells were used as a model. We used microarrays to decipher the specific gene regulation in doxorubicine treated B16 mouse melanoma cells. Keywords: Time course
Project description:It is known that ubiquitination is important for T cell receptor (TCR) signaling during T cell activation but the breadth of ubiquitination events triggered during TCR signaling is not completely understood. This dataset utilizes di-glycine remnant profiling combined with mass spectrometry to identify a global landscape of ubiquitination events downstream of the TCR and to quantify changes ubiquitin abundance in response to TCR stimulation. Additionally, whole cell proteomics data were generated to measure protein abundances during TCR stimulation. Mouse primary T cells were isolated, proliferated and either remained resting or stimulated with CD3/CD28 to activate downstream signaling through the TCR and co-stimulatory pathways. Di-glycine remnant profiling and whole cell proteomics was performed on rested cells and cells that had undergone CD3/CD28 TCR stimulation for 4 hours. These data were analyzed to identify the ubiquitination events during TCR activation and to quantify the change in peptide-based ubiquitin abundance and total protein abundance over the course of the 4 hour TCR stimulation. Integration of di-glycine and whole cell proteomics was used to generate protein-specific predictions of whether ubiquitination events downstream of TCR signaling lead to a decrease in associated protein abundance. The analysis of these data suggests that T cell activation leads to an increase in ubiquitination that is not associated with proteasomal or lysosomal degradation.
Project description:Analysis of gene expression patterns in cancer improved the understanding the mechanisms underlying the process of metastatic progression. Recent studies have attributed an important role to B-1 cells, a subset of B lymphocytes, in melanoma progression. It was already demonstrated that in vitro interaction between B16 melanoma cells and B-1 lymphocytes induced increase in metastatic potential of B16 lineage. In this study we used a microarray approach to assess gene expression profile in B16 melanoma cells after contacting B-1 lymphocytes (B16B1).
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.