Possibly indirectly regulated by PAD2 via crosstalk with PAD4. Subsequent findings directly demonstrating that PADs regulate gene Axitinib clinical trial activity in the mammary gland epithelium would likely lead to the identification of new regulatory pathways important for mammary function. Unlike MazF that cleaves mRNAs only at ACA sequences, ChpK also cleaves at sequences ACU and ACG. These interactions spread across the membrane, underlying that a profound reorganization occurred at the membrane after infection. In infected females, there were less interactions between proteins encoded by modulated genes at the membrane level than in males, but the interconnection between the cytosol and the nucleus was apparently more developed. Our findings also have implications for iPSC and it is striking that we found N-Myc regulating 3 other known iPSC-related genes, lin28b, klf2, and klf4. These data suggest a model in which overexpressed myc enhances iPSC formation in fibroblasts at least in part by turning on klf family and lin28b gene expression, and through inducing expression of lif. Notably our data also provide the first model for why overexpressed myc, although a potent enhancer of iPSC formation, may not be formally required for the process: if expression levels of klf and lin28 as well as other pluripotency-related genes are high enough, myc may become more dispensable since it is no longer required to turn on their expression. Endogenous lif expression may also be dispensable since ectopic LIF is often added to iPSC media. The presence of an iPSC-related gene expression program in neuroblastoma also raises the concern of the tumorigenicity of iPSC. In our previous model, we proposed that myc genes were most likely contributing to tumorigenesis and perhaps iPSC formation through both gene specific and global chromatin events. Our new findings confirm an important role for Myc’s gene specific, classical transcription factor function in neuroblastoma. The potential contributions of a more global Myc chromatin function to neuroblastoma genesis and delineating the mechanisms by which Myc contributes to iPSC biology await future study. Particularly important will be functional genomics assays addressing Myc chromatin function, not just binding, in iPSC and in additional types of tumors. YoeB was also initially thought to function as an endoribonuclease cleaving translated mRNAs. However, recently YoeB was found to be specifically associated with the 50S ribosomal subunit of E. coli and thereby it primarily inhibits translation initiation. YafQ of the dinJ-yafQ system has been recently shown to be a toxin that functions different from other TA toxins. Of note, most of these residues with high CRES are located in or near the pore in the 3D homology model of CaMdr1p, thus validating their relevance.