Deep PIM kinase substrate profiling reveals new rational cotherapeutic strategies for acute myeloid leukemia.

Provirus integration site for Moloney murine leukemia virus (PIM) family serine/threonine kinases perform protumorigenic functions in hematologic malignancies and solid tumors by phosphorylating substrates involved in tumor metabolism, cell survival, metastasis, inflammation, and immune cell invasion. However, a comprehensive understanding of PIM kinase functions is currently lacking. Multiple small-molecule PIM kinase inhibitors are currently being evaluated as cotherapeutics in patients with cancer.

Sequence comparison of Francisella tularensis LVS, LVS-G and LVS-R.

Francisella tularensis is a gram-negative organism found in many regions of the world. F. tularensis can cause a fatal, febrile illness, although these natural tularemia infections are rare in the United States.

Distinct Patterns of Expression of Transcription Factors in Response to Interferonβ and Interferonλ1.

After viral infection, type I and III interferons (IFNs) are coexpressed by respiratory epithelial cells (RECs) and activate the ISGF3 transcription factor (TF) complex to induce expression of a cell-specific set of interferon-stimulated genes (ISGs). Type I and III IFNs share a canonical signaling pathway, suggesting that they are redundant. Animal and in vitro models, however, have shown that they are not redundant.