We made the novel observation, that ARID3B Fl induces apoptosis when overexpressed in ovarian cancer cells while ARID3B Sh does not. Although ARID3B is overexpressed in ovarian, we have demonstrated that one of the splice forms induces cell death. We predict that the subcellular localization of ARID3B may contribute to this discrepancy since ovarian tumors have high levels of cytoplasmic ARID3B Fl. Furthermore, we propose that ARID3B may be reminiscent of cMyc that is both oncogenic and promotes apoptosis. Further work will address how localization and dosage of ARID3B regulates tumor cell growth and survival. These studies clearly identify a function for ARID3B Fl and it may be useful in increasing chemosensitivity in ovarian cancer cells and thereby improving therapeutic response. In recent years, RNAi screens have become a useful method for identifying genetic regulators of a range of biological processes. A commonly used approach for performing RNAi screens in mammalian cells is arrayed screening, in which individual RNAi triggers are distributed across individual wells in multi-well culture plates and phenotypes are screened on a well-by-well basis. An alternative approach is to perform pooled RNAi screens in which hundreds or thousands of different shRNAs are introduced into a population of cells. These cells are then selected for the phenotype of interest and examined for proviral shRNA abundance compared to a control. The main advantage to pooled 3,4,5-Trimethoxyphenylacetic acid screening is that the experiments do not require expensive automation, storage of large arrayed RNAi collections or well-by-well analysis. In addition, by using this approach RNAi screening can be applied to study phenotypes that take longer to develop because shRNAs integrate into the genome. Pooled shRNA screens have been successfully used to identify genetic regulators of cell proliferation and survival, tumorigenicity, adhesion, migration, drug modulation and even cancer phenotypes in mouse models. Retroviral and lentiviral shRNA libraries have been used for pooled shRNA screening. With both of these viral delivery methods, cells are transduced and shRNAs stably integrate into the genomes of the host cells. The transduced cells are subsequently subjected to phenotypic selection and/or selective pressure. Cells expressing shRNAs targeting genes involved in the phenotype are enriched or depleted relative to the control population of transduced cells. In order to identify these shRNAs of interest, proviral shRNAs or their associated molecular barcodes are PCR-amplified from genomic DNA isolated from the cell populations, and the relative abundance of the individual shRNAs is compared between control and selected cell populations using custom microarrays or next generation sequencing. Although it is clear that factors influencing each of these experimental steps may have effects on the quality of the screen and the biological significance of the hits obtained from the screen, a thorough analysis of the technical considerations for performing successful and reproducible pooled shRNA screens has only recently begun to emerge. One of the critical considerations of pooled lentiviral shRNA screening is the extent to which any given shRNA construct in a pooled library will be represented throughout the screening process. It is plausible that identification of shRNAs that are enriched Folinic acid calcium salt pentahydrate during the selection process would have a less stringent requirement of average fold representation than identification of shRNAs that are depleted during the selection process. The average shRNA fold representation at transduction varies among published screens. For example, while some groups transduce cells with enough viral particles such that each shRNA in the library is represented by at least 1 000 copies, other groups have used equivalents of 10 to 20 copies per shRNA.