RNA-seq was performed to compare expression pattern of musles taken form two mice strains- mdx and mdx/Runx1f/f, which are double KO carrting a muscle specific ablation of Runx1 using a Myf5-Cre. This comparison revealed the Runx1- responsive gene set in mdx muscles. we could cross this data with prior retrived datd from privous experiments found in this GEO quary, to pinpiont Runx1 target genes in muscle rgeneration Overall design: RNA was extracted form soleus muscles of 2 months old mice, n=3,4 for mdx and mdx/Runx1f/f, respectively . Differentially expressed genes were discovered using the DeSeq2 software
Genomic-wide transcriptional profiling in primary myoblasts reveals Runx1-regulated genes in muscle regeneration.
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Genomic-wide transcriptional profiling in primary myoblasts reveals Runx1-regulated genes in muscle regeneration.
Specimen part
View SamplesBone morphogenetic protein 4 (BMP4) is essential for lung development. To define its intracellular signaling mechanisms by which BMP4 regulates lung development, BMP-specific Smad1 or Smad5 was selectively knocked out in fetal mouse lung epithelial cells. Abrogation of lung epithelial-specific Smad1, but not Smad5, resulted in retardation of lung branching morphogenesis and reduced sacculation, accompanied by altered distal lung epithelial cell proliferation and differentiation, and consequently severe neonatal respiratory failure. By combining cDNA microarray with ChIP-chip analyses, Wnt inhibitory factor-1 (Wif1) was identified as a novel target gene of Smad1 in the developing mouse lung epithelial cells. Loss of Smad1 transcriptional activation of Wif1 expression was associated with reduced Wif1 expression and increased Wnt/beta-catenin signaling activity in lung epithelia, resulting in specific fetal lung abnormalities. Therefore, a novel regulatory loop of BMP4-Smad1-Wif1-Wnt/beta-catenin in coordinating BMP and Wnt pathways to control fetal lung development is suggested.
Smad1 and its target gene Wif1 coordinate BMP and Wnt signaling activities to regulate fetal lung development.
Specimen part
View SamplesMDSC (myeloid-derived suppressor cells) can be differentiated in vitro using IL-6 and GM-CSF. To identify the specific role of IL-6 in this process, we used microarray to compare MDSC differentiated with IL-6 and GM-CSF to MDSC differentiated with GM-CSF alone. We have found genes and pathways that are up- or downregulated when IL-6 is present.
IL-6 regulates CCR5 expression and immunosuppressive capacity of MDSC in murine melanoma.
Specimen part, Treatment
View SamplesThe role of murine peroxisome proliferator-activated receptor-delta (PPARd) in mammary tumorigenesis was assessed. Microarrays were used to analyse global gene expression to determine changes in MMTV-PPARd transgenic mice versus wild-type mice and the effect of GW501516.
PPARδ induces estrogen receptor-positive mammary neoplasia through an inflammatory and metabolic phenotype linked to mTOR activation.
Specimen part, Treatment
View SamplesThe objective of this study was to understand the gene expression changes during granulosa cell tumor development in Smad1/5/8 mutant ovaries.
Conditional deletion of Smad1 and Smad5 in somatic cells of male and female gonads leads to metastatic tumor development in mice.
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View SamplesTo capture the Zeb2-dependent transcriptional changes in early cell state/fate decisions we performed RNA-seq on Zeb2 control and Zeb2 knockout cells. We chose three stages, which correspond in control ESCs to the naive pluripotent state (d0; very low amounts of Zeb2 mRNA), multipotent progenitors (d4, low Zeb2 mRNA/protein) and early neural progenitors (d6, high Zeb2 mRNA/protein), respectively. Overall design: Three biological replicates of Zeb2 control (Ctrl) and Zeb2 knockout (KO) samples on day 0, day 4 and day 6 of neural differentiation were used in this study (18 samples in total)
Zeb2 Regulates Cell Fate at the Exit from Epiblast State in Mouse Embryonic Stem Cells.
Cell line, Subject
View SamplesIn this study we determine the transcriptional profile by RNAseq of mESC in the absence of Smad1 and Smad5 and in subpopulation of mESC with different levels of BMP-SMAD activation. Overall design: Transcriptome analysis using RNAseq was performed on 3 biological replicates of BRE negative and positive mESC subpopulations, which were collected in pairs at 3 different times. Transcriptome analysis using RNAseq was performed on Smad1/5 floxed (FL) and knockout (KO) mESC. Two different parental cell lines were used. For each parental cell line we analyzed one Smad1/5 FL sample and two Smad1/5 KO samples, resulting in respectively two and four biological replicates for the FL and KO conditions.
BMP-SMAD Signaling Regulates Lineage Priming, but Is Dispensable for Self-Renewal in Mouse Embryonic Stem Cells.
No sample metadata fields
View SamplesZIP-3 has been shown to repress the mitochondrial-UPR response. To identify genes repressed by ZIP-3, we compared transcript profiles from wildtype, atfs-1(tm4919) and zip-3(gk3164) worms raised on control RNAi or spg-7 RNAi Overall design: RNA samples were prepared from wild-type(wt) and zip-3(gk3164)(mutant) worms fed either control RNAi or spg-7 RNAi. Worms were synchronized by bleaching, raised on NGM plates seeded with control RNAi or spg-7 RNAi till L4 stage and then harvested. Each experiment was performed in triplicate indicated as 1,2 and 3.
Mitochondrial UPR repression during <i>Pseudomonas aeruginosa</i> infection requires the bZIP protein ZIP-3.
Specimen part, Subject
View SamplesZIP-3 has been shown to repress the mitochondrial-UPR genes and immune response during P. aeruginosa infection. To identify genes repressed by ZIP-3, we compared transcript profiles from wildtype and zip-3(gk3164) worms raised on P. aeruginosa or E. coli. Overall design: RNA samples were prepared from wild-type(wt) and zip-3(gk3164)(mutant) worms fed either E. coli or P. aeruginosa. Worms were synchronized by bleaching, starved on empty NGM plates for 48h, transferred to E. coli or P. aeruginosa seeded NGM plates for 18h and then harvested. Each experiment was performed in triplicate indicated as 1,2 and 3.
Mitochondrial UPR repression during <i>Pseudomonas aeruginosa</i> infection requires the bZIP protein ZIP-3.
Specimen part, Subject
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