The mean systolic and diastolic blood pressures were higher among those with any target organ involvement compared to those without any damage. In addition, immunolabelled cells free of phagocytosed bacteria were also observed, suggesting that Spod-11-tox expression was not associated to phagocytosis. Recently, it has become clear that ERM proteins play an important role in the function of mature lymphocytes. In this study, we have analyzed for the first time the expression patterns of ERM proteins in lymphoid tissues and conducted the first analysis of the role of ezrin in lymphoid development. We found that ezrin expression is high during early thymocyte development, while moesin expression is low, raising the possibility that ezrin plays a unique role in early thymocyte development. Germline deletion of ezrin results in profound pathology in lymphoid development. However, further analysis showed that most of these defects are stress-induced, presumably arising as a secondary consequence of previously identified defects in the gut. We conclude that ezrin is dispensable for lymphoid development, most likely due to redundancy with moesin. The relatively high hit rate in the primary screen and low validation rate point to a number of potential caveats with using an overexpression screen for the heat shock response. First, the heat shock response is part of the cell’s protein quality control system and the false positives in the context of the primary screen may be due to nonspecific activation of the heat shock response via overexpressed or misfolded protein. The overexpressed or misfolded protein may act as a chaperone substrate and compete with HSF1 for binding Torin 1 1222998-36-8 resulting in nonspecific activation of the heat shock response. Second, the use of a native promoter instead of synthetic response elements may have also inflated the number of hits in the screen since a promoter is typically regulated by multiple transcription factors that either bind simultaneously as a complex to a regulatory region or in a sequential manner. This dynamic interplay may be artificially affected in an overexpression screen leading to a high number of hits and lower validation rate. Finally, the use of a mixed fulllength gene library containing both human and mouse clones may have contributed to the lower than expected validation rate. Although dramatic species differences haven’t been observed in other overexpression screening efforts, it is possible that orthologs may play different roles in the heath shock response in each species. In summary, a series of functional genomic screens were used to identify PRKCI as an regulator of the mammalian heat shock response. Although follow-up studies and literature searches suggest that PRKCI is an indirect regulator of the signaling pathway, additional studies will be required to confirm the precise mechanism of HSF1 regulation.