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:Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice.
Project description:Tmem100 was identified as a downstream gene of BMP9-ALK1 signaling. The signaling has been implicated in hereditary hemorrhagic telangiectasia. This study was designed to identify affected genes in TMEM100-deficiect mice. Tmem100 was inactivated in adult Tmem1002loxP/2loxP;ROSA26+/CreER mice by tamoxifen tereatment. Microarray data was obtained from the lungs isolated from tamoxifen treated control and mutant mice. Three control mice (Tmem1002loxP/2loxP) and three mutant mice (Tmem1002loxP/2loxP;ROSA26+/CreER) were treated with tamoxifen (two consecutive intraperitoneal injections, 0.1 mg/g of body weight) to activate CreER recombinase. Total RNAs were isolated from lungs 7 days after tamoxifen injection.
Project description:We demonstrate that the cell-surface molecule LRRC33 associates with proTGF-β1 and provides a milieu for a restricted subset of TGF-β-dependent functions. We deposit microglia transcriptional profiles from three Lrrc33+/+ mice and three Lrrc33-/- mice. In this dataset, we include the expression data obtained from microglia that were isolated from 3 Lrrc33+/+ mice and 3 Lrrc33-/- mice.