Project description:Since acute deletion of host ATF4 caused a significant tumor-inhibitory phenotype, and since activated CAFs also play a critical role in the establishment of the metastatic niche we speculated that ATF4 deficiency could also result in an inhibitory effect on lung metastasis. Thus, we examined the impact of host ATF4 deletion in the pre-metastatic niche by analyzing gene expression changes on lungs from Atf4wt/wt and Atf4D/D mice at 4 weeks post tamoxifen treatment. Genome-wide microarray analysis identified 21 genes to be significantly downregulated in Atf4D/D lungs, including collagen-associated genes. Also, pathway analysis on the most dysregulated genes revealed defects on collagen formation, extracellular matrix organization and integrin cell surface interactions pathways.
Project description:We used microarrays to analyse the global program of gene expression in response to Influenza A (X31) infection in lungs from C57BL/6 wt, 129S7 wt and IFNAR-/- (129) mice.
Project description:We used microarrays to analyse the global program of gene expression in response to Influenza A (X31) infection in lungs from C57BL/6 wt, 129S7 wt and IFNAR-/- (129) mice. Mock- or 5 day influenza A (X31)-infected total lungs from mice with the indicated genotypes were collected and processed for expression profiling.
Project description:We used microarrays to analyse the global programme of gene expression in response to intranasal interferon treatment (IFNa4 and IFNl2) in lungs from C57BL/6 wt mice
Project description:This SuperSeries is composed of the following subset Series: GSE35979: Gene expression data from IL13-induced allergic airway inflammation of mice lungs GSE35980: MicroRNA expression data from IL13-induced allergic airway inflammation of mice lungs GSE37079: Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs Refer to individual Series
Project description:The hepatocyte growth factor (HGF)/c-Met signaling pathway is known to mediate vascularization. We have previously demonstrated that expression of a human HGF transgene in the small airways produced mice (HGF TG) that were more susceptible to the tobacco carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). We also have observed that HGF TG mice display significantly enhanced vascularization in the lungs that increases over time compared to wild-type (WT) littermates. To analyze which genes might contribute to increased vascularization from HGF overexpression in the airways, RNA and protein were isolated from whole lungs of individual HGF TG and WT adult mice. We profiled the mRNA expression of several hundred genes representative of six biological pathways involved in transformation, angiogenesis, and tumorigenesis using two commercial microarrays. Significant changes in expression over a 1.5-fold boundary were also observed in lung tumors derived from NNK-treated HGF TG mice.