RNA Sequencing of Mrp8-Cre TGFbR2-fl/fl Lung Neutrophils
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ABSTRACT:
PROVIDER: PRJNA816345 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The goal of this study is to examine how the specific loss of TGFbR2 (under Mrp8 promoter for Cre recombinase) changes the transcriptome of neutrophils in the lung compared to their wildtype littermates.
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Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in palate development in order to discover candidate therapeutics for preventing and treating congenital birth defects. Here, we conducted gene expression profiling of embryonic palatal tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of cleft palate formation. To investigate the mechanism of cleft palate resulting from mutations in TGFBR2, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses using the palatal tissue of Tgfbr2fl/fl;Wnt1-Cre mice at embryonic day E13.5 (prior to palatal fusion, n=6 per genotype) and E14.5 (during palatal fusion, n=5 per genotype) to examine the genes regulated by Tgf-beta during palate formation.
2011-11-29 | E-GEOD-22989 | biostudies-arrayexpress
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tongue development in order to study the contribution of cranial neural crest (CNC) cells towards the patterning of cranial mesoderm for proper tongue formation. Here, we conducted gene expression profiling of embryonic tongue tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of microglossia, a common congenital birth defect which is frequently observed with several syndromic conditions. To investigate the mechanism of microglossia resulting from dysfunctional TGF-Beta signaling during muscle development, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses of tongue tissue of Tgfbr2fl/fl;Wnt1-Cre mutant mice and Tgfbr2fl/fl control mice at embryonic day E14.5 (n=3 per genotype) to examine the genes regulated by Tgf-beta during tongue muscle development.
2013-04-11 | E-GEOD-45968 | biostudies-arrayexpress
Project description:Transcriptional profiling of Twist2-Cre liver and Twist2-Cre/A20fl/fl liver
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Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.
2018-05-01 | E-MTAB-5833 | biostudies-arrayexpress
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in regulating the cellular metabolism of cranial neural crest (CNC) cells during palate development. Here, we conducted gene expression profiling of primary mouse embryonic palatal mesenchymal (MEPM) cells from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of cleft palate, which is among the most common congenital birth defects and observed in many syndromic conditions. To investigate the adverse effects of dysfunctional TGF-Beta signaling on the cellular metabolism of palatal mesenchyme during palatogenesis, we analyzed mice with a neural crest cell-specific conditional inactivation of Tgfbr2 (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses of primary mouse embryonic palatal mesenchymal cells of Tgfbr2fl/fl;Wnt1-Cre mutant mice and Tgfbr2fl/fl control mice, collected at embryonic day 13.5 (n=4 per genotype) and cultured with standard media (DMEM with supplements). Cells were collected after 2 passages.
2013-10-01 | E-GEOD-46150 | biostudies-arrayexpress
Project description:RNA-seq of colonic tissues from Hif1a(fl/fl) and Ncr1(Cre)Hif1a(fl/fl) mice
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Project description:Edothelial cells were FACS sorted as CD31+CD45- population from PYMT-BO1 transplant tumor bearing WT and Cdh-cre Myct1 fl/fl mice on Day 14 post tumor transplantation
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Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in epithelial cells as it pertains to the orientation of muscle fibers in the soft palate during embryogenesis. Here, we first conducted gene expression profiling of the anterior and posterior portions of the palate from wild-type mice. In addition, we also conducted gene expression profiling of the posterior palate in mutant mice with an epithelium-specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of submucosal cleft palate, which is a congenital birth defect commonly observed in many syndromic conditions. To investigate the adverse effects of dysfunctional TGF-Beta signaling on tissue-tissue interaction between the palatal epithelium and myofibers during palatogenesis, we analyzed mice with an epithelial cell-specific conditional inactivation of Tgfbr2 (Tgfbr2fl/fl;K14-Cre). We performed microarray analyses of anterior palatal tissue and posterior palatal tissue of E15.5 Tgfbr2fl/fl control mice (n=5, each region), and posterior palatal tissue of Tgfbr2fl/fl;K14-Cre mutant mice, collected at embryonic day 15.5 (n=5). Control samples and mutant samples are from separate litters.
2013-10-01 | E-GEOD-46211 | biostudies-arrayexpress
Project description:The abscence of TBR2 gene in human leads to microcephaly. This condition is mimicked by the specific ablation of the murine gene in developing cerebral cortex. Herein we compared gene expression in control and Tbr2 cKO in E14.5 cerebral cortices. This approach represents a useful tool to identify the molecular mechanisms at the basis of the phenotype. 6 samples, 3x Tbr2 +/+;Foxg1::Cre (control) and 3x Tbr2 fl/fl;Foxg1::Cre
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