Intermittent turbulence, noisy fluctuations and wavy structures in the Venusian magnetosheath and wake

Recent research has shown that distinct physical regions in the Venusian induced magnetosphere are recognizable from the variations of strength of the magnetic field and its wave/fluctuation activity. In this paper the statistical properties of magnetic fluctuations are investigated in the Venusian magnetosheath and wake regions. The main goal is to identify the characteristic scaling features of fluctuations along Venus Express (VEX) trajectory and to understand the specific circumstances of the occurrence of different types of scalings. For the latter task we also use the results of measurements from the previous missions to Venus. Our main result is that the changing character of physical interactions between the solar wind and the planetary obstacle is leading to different types of spectral scaling in the near-Venusian space. Noisy fluctuations are observed in the magnetosheath, wavy structures near the terminator and in the nightside near-planet wake. Multi-scale turbulence is observed at the magnetosheath boundary layer and near the quasi-parallel bow shock. Magnetosheath boundary layer turbulence is associated with an average magnetic field which is nearly aligned with the Sun-Venus line. Noisy magnetic fluctuations are well described with the Gaussian statistics. Both magnetosheath boundary layer and near shock turbulence statistics exhibit non-Gaussian features and intermittency over small spatio-temporal scales. The occurrence of turbulence near magnetosheath boundaries can be responsible for the local heating of plasma observed by previous missions

KPNB1 (karyopherin (importin) beta 1)

Review on KPNB1 (karyopherin (importin) beta 1), with data on DNA, on the protein encoded, and where the gene is implicated

Growth inhibition of non-small cell lung cancer cells by AP-1 blockade using a cJun dominant-negative mutant

cJun, a major constituent of AP-1 transcription factor transducing multiple mitogen growth signals, is frequently overexpressed in non-small cell lung cancers (NSCLCs). The purpose of this study is to determine the effects of AP-1 blockade on the growth of NSCLC cells using a cJun dominant-negative mutant, TAM67. Transiently transfected TAM67 inhibited AP-1 transcriptional activity in NSCLC cell lines, NCI-H1299 (H1299), A549 and NCI-H520 (H520). The colony-forming efficiency of H1299 and A549 was reduced by TAM67, while that of H520 was not. To elucidate the effects of TAM67 on the growth of H1299, we established H1299 clone cells that expressed TAM67 under the control of a doxycycline-inducible promoter. In the H1299 clone cells, the induced TAM67 inhibited anchorage-dependent growth by promoting G1 cell-cycle block, but not by apoptosis. The induced TAM67 decreased the expression of a cell-cycle regulatory protein, cyclin A. TAM67 also inhibited anchorage-independent growth of these cells. Furthermore, TAM67 reduced growth of established xenograft tumours from these cells in nude mice. These results suggest that AP-1 plays an essential role in the growth of at least some of NSCLC cells

Simultaneous blockade of AP-1 and phosphatidylinositol 3-kinase pathway in non-small cell lung cancer cells

c-Jun is a major constituent of AP-1 transcription factor that transduces multiple mitogen growth signals, and it is frequently overexpressed in non-small cell lung cancers (NSCLCs). Earlier, we showed that blocking AP-1 by the overexpression of a c-Jun dominant-negative mutant, TAM67, inhibited NSCLC cell growth. The phosphatidylinositol 3-kinase (PI3K)/Akt signal transduction pathway is important in transformation, proliferation, survival and metastasis of NSCLC cells. In this study, we used NCI-H1299 Tet-on clone cells that express TAM67 under the control of inducible promoter to determine the effects of inhibition of AP-1 and PI3K on cell growth. The PI3K inhibitor, LY294002, produced a dose-dependent inhibition of growth in H1299 cells and that inhibition was enhanced by TAM67. TAM67 increased dephosphorylation of Akt induced by LY294002 and reduced the TPA response element DNA-binding of phosphorylated c-Jun. TAM67 increased G1 cell cycle blockade induced by LY294002, which was partially associated with cyclin A decrease and p27Kip1 accumulation. Furthermore, TAM67 and LY294002 act, at least additively, to inhibit anchorage-independent growth of the H1299 cells. These results suggest that AP-1 and PI3K/Akt pathways play an essential role in the growth of some NSCLC cells

RegNetB: Predicting Relevant Regulator-Gene Relationships in Localized Prostate Tumor Samples

<p>Abstract</p> <p>Background</p> <p>A central question in cancer biology is what changes cause a healthy cell to form a tumor. Gene expression data could provide insight into this question, but it is difficult to distinguish between a gene that causes a change in gene expression from a gene that is affected by this change. Furthermore, the proteins that regulate gene expression are often themselves not regulated at the transcriptional level. Here we propose a Bayesian modeling framework we term RegNetB that uses mechanistic information about the gene regulatory network to distinguish between factors that cause a change in expression and genes that are affected by the change. We test this framework using human gene expression data describing localized prostate cancer progression.</p> <p>Results</p> <p>The top regulatory relationships identified by RegNetB include the regulation of RLN1, RLN2, by PAX4, the regulation of ACPP (PAP) by JUN, BACH1 and BACH2, and the co-regulation of PGC and GDF15 by MAZ and TAF8. These target genes are known to participate in tumor progression, but the suggested regulatory roles of PAX4, BACH1, BACH2, MAZ and TAF8 in the process is new.</p> <p>Conclusion</p> <p>Integrating gene expression data and regulatory topologies can aid in identifying potentially causal mechanisms for observed changes in gene expression.</p