TL;DR: It is shown that activation protein 1 (AP-1) activates the miR-21 transcription in conjugation with the SWI/SNF complex, after PMA stimulation, through the conserved AP-1 and PU.1 binding sites in the promoter identified here.
TL;DR: The identification of widespread chromatin changes during SCLC progression reveals an unexpected global reprogramming during metastatic progression, and indicates that Nfib is necessary and sufficient to increase chromatin accessibility at a large subset of the intergenic regions.
TL;DR: It is shown that Nfib-deficient mice possess unique defects in lung maturation and exhibit callosal agenesis and forebrain defects that are similar to, but more severe than, those seen in Nfia- deficient animals.
Abstract: The phylogenetically conserved nuclear factor I (NFI) gene family encodes site-specific transcription factors essential for the development of a number of organ systems. We showed previously that Nfia-deficient mice exhibit agenesis of the corpus callosum and other forebrain defects, whereas Nfic-deficient mice have agenesis of molar tooth roots and severe incisor defects. Here we show that Nfib-deficient mice possess unique defects in lung maturation and exhibit callosal agenesis and forebrain defects that are similar to, but more severe than, those seen in Nfia-deficient animals. In addition, loss of Nfib results in defects in basilar pons formation and hippocampus development that are not seen in Nfia-deficient mice. Heterozygous Nfib-deficient animals also exhibit callosal agenesis and delayed lung maturation, indicating haploinsufficiency at the Nfib locus. The similarity in brain defects in Nfia- and Nfib-deficient animals suggests that these two genes may cooperate in late fetal forebrain development, while Nfib is essential for late fetal lung maturation and development of the pons.
TL;DR: In this article, the authors carried out an experiment as part of a larger project involving 16,000 small business owners/members of the National Federation of Independent Business (NFIB) and found that none of the six treatments examined improved response rates enough to warrant its routine use over the alternative, nor did any combinations of treatments help.
Abstract: Mail surveys of small business owners have notoriously low response rates, creating the potential for substantial error in surveys of this population and diminishing the credibility of research conducted on small firms. The author recently carried out an experiment as part of a larger project involving 16,000 small business owner/members of the National Federation of Independent Business (NFIB). The experiment's purpose was to ascertain survey treatments that might enhance mail survey response among small business owners. Results showed that none of the six treatments examined improved response rates enough to warrant its routine use over the alternative, nor did any combinations of treatments help. The implication is that commonly used treatments, for example prenotification, often are unproductive.
TL;DR: Interestingly, tumors with MYB and MYBL1 translocations displayed similar gene expression profiles, and the combined MyB and MyBL1 expression correlated with outcome, suggesting that the related MYB proteins are interchangeable oncogenic drivers in ACC.
Abstract: Adenoid Cystic Carcinoma (ACC), the second most common malignancy of salivary glands, is a rare tumor with bleak prognosis for which therapeutic targets are unavailable. We used RNA-sequencing (RNA-seq) to analyze low-quality RNA from archival, formaldehyde-fixed, paraffin-embedded samples. In addition to detecting the most common ACC translocation, t(6;9) fusing the MYB proto-oncogene to NFIB, we also detected previously unknown t(8;9) and t(8;14) translocations fusing the MYBL1 gene to the NFIB and RAD51B genes, respectively. RNA-seq provided information about gene fusions, alternative RNA splicing and gene expression signatures. Interestingly, tumors with MYB and MYBL1 translocations displayed similar gene expression profiles, and the combined MYB and MYBL1 expression correlated with outcome, suggesting that the related Myb proteins are interchangeable oncogenic drivers in ACC. Our results provide important details about the biology of ACC and illustrate how archival tissue samples can be used for detailed molecular analyses of rare tumors.