A new analysis of distributed faulty node detection in DTNS

Previously proposed solutions suffer from long delays in identifying and dividing nodes producing faulty data. This is unsuitable to DTNs where nodes meet only rarely. This proposes a completely conveyed and essentially implementable way to deal with enable each DTN node to quickly distinguish whether its sensors are delivering flawed information. The dynamical conduct of the proposed algorithm is approximated by some persistent time state conditions, whose balance is portrayed. The nearness of getting out of hand nodes, attempting to bother the faulty node recognition process, is additionally considered

Genomic Promoter Analysis Predicts Functional Transcription Factor Binding

Background. The computational identification of functional transcription factor binding sites (TFBSs) remains a major challenge of computational biology. Results. We have analyzed the conserved promoter sequences for the complete set of human RefSeq genes using our conserved transcription factor binding site (CONFAC) software. CONFAC identified 16296 human-mouse ortholog gene pairs, and of those pairs, 9107 genes contained conserved TFBS in the 3 kb proximal promoter and first intron. To attempt to predict in vivo occupancy of transcription factor binding sites, we developed a novel marginal effect isolator algorithm that builds upon Bayesian methods for multigroup TFBS filtering and predicted the in vivo occupancy of two transcription factors with an overall accuracy of 84%. Conclusion. Our analyses show that integration of chromatin immunoprecipitation data with conserved TFBS analysis can be used to generate accurate predictions of functional TFBS. They also show that TFBS cooccurrence can be used to predict transcription factor binding to promoters in vivo

Cross-platform expression profiling demonstrates that SV40 small tumor antigen activates Notch, Hedgehog, and Wnt signaling in human cells

BACKGROUND: We previously analyzed human embryonic kidney (HEK) cell lines for the effects that simian virus 40 (SV40) small tumor antigen (ST) has on gene expression using Affymetrix U133 GeneChips. To cross-validate and extend our initial findings, we sought to compare the expression profiles of these cell lines using an alternative microarray platform. METHODS: We have analyzed matched cell lines with and without expression of SV40 ST using an Applied Biosystems (AB) microarray platform that uses single 60-mer oligonucleotides and single-color quantitative chemiluminescence for detection. RESULTS: While we were able to previously identify only 456 genes affected by ST with the Affymetrix platform, we identified 1927 individual genes with the AB platform. Additional technical replicates increased the number of identified genes to 3478 genes and confirmed the changes in 278 (61%) of our original set of 456 genes. Among the 3200 genes newly identified as affected by SV40 ST, we confirmed 20 by QRTPCR including several components of the Wnt, Notch, and Hedgehog signaling pathways, consistent with SV40 ST activation of these developmental pathways. While inhibitors of Notch activation had no effect on cell survival, cyclopamine had a potent killing effect on cells expressing SV40 ST. CONCLUSIONS: These data show that SV40 ST expression alters cell survival pathways to sensitize cells to the killing effect of Hedgehog pathway inhibitors

Automation of comparative genomic promoter analysis of DNA microarray datasets

M.S.Committee Chair: Roger M. Wartel

Metastasis-associated protein 1/histone deacetylase 4-nucleosome remodeling and deacetylase complex regulates phosphatase and tensin homolog gene expression and function

Metastasis-associated protein 1 (MTA1) is widely overexpressed in human cancers and is associated with malignant phenotypic changes contributing to morbidity in the associated diseases. Here we discovered for the first time that MTA1, a master chromatin modifier, transcriptionally represses the expression of phosphatase and tensin homolog (PTEN), a tumor suppressor gene, by recruiting class II histone deacetylase 4 (HDAC4) along with the transcription factor Yin-Yang 1 (YY1) onto the PTEN promoter. We also found evidence of an inverse correlation between the expression levels of MTA1 and PTEN in physiologically relevant breast cancer microarray datasets. We found that MTA1 up-regulation leads to a decreased expression of PTEN protein and stimulation of PI3K as well as phosphorylation of its signaling targets. Accordingly, selective down-regulation of MTA1 in breast cancer cells increases PTEN expression and inhibits stimulation of the PI3K/AKT signaling. Collectively, these findings provide a mechanistic role for MTA1 in transcriptional repression of PTEN, leading to modulation of the resulting signaling pathways

Antitumor activities of cyclopamine and γ-secretase inhibitor against HEKTER-LUK and HEKTER-ST cell lines

<p><b>Copyright information:</b></p><p>Taken from "Cross-platform expression profiling demonstrates that SV40 small tumor antigen activates Notch, Hedgehog, and Wnt signaling in human cells"</p><p>BMC Cancer 2006;6():54-54.</p><p>Published online 7 Mar 2006</p><p>PMCID:PMC1420312.</p><p>Copyright © 2006 Ali-Seyed et al; licensee BioMed Central Ltd.</p> Survival of HEK-TERV and HEK-TERST cells determined by MTT assay after treatment with vehicle, 2.4μM Cyclopamine or 1 nM γ-secretase inhibitor for 72 hrs. Mean and standard error are shown for each treatment. Percent cell survival was computed relative to untreated cells. Survival of HEK-TERST cells determined by Trypan Blue exclusion assay after treatment of 1 × 10cells with vehicle, 2.4μM Cyclopamine or 1 nM γ-secretase inhibitor for 72 hrs