We searched for roles of ZEB1 during EMT by RNA-seq in breast cancer cells. Overall design: Expression of mRNA in a basal type breast cancer cell line MDA-231-D transfected with ZEB1/ZEB2 siRNAs and stimulated with TGF-beta for 24 h.
ZEB1-regulated inflammatory phenotype in breast cancer cells.
Specimen part, Cell line, Subject
View SamplesHere, we performed single nuclear RNA-seq (snRNA-seq) of control and Pitx2 deficient cardiac tissue 3 weeks post myocardial infarction. Next, unsupervised graph-based clustering of the combined snRNA-Seq data set mapped to both introns and exons, comprising 7848 cells. Overall, we identified nine transcriptionally distinct clusters representing all the major cardiac cell types, including cardiac fibroblasts (FB), cardiomyocytes (CM), endothelial cells (EC), vascular smooth muscle cells (SMC), macrophages (Mf), epicardial cells (EpiC), endocardial cells (EndoC), lymphatic endothelial cells (LEC), and mural cells or pericytes (PeC). Moreover, two distinct populations of fibroblasts, designated FB-1 and FB-2, were also identified. Overall design: Cardiac tissue dissociated, nuclei were isolated via density gradient centrifugation, and then ran through the 10X Chromium device to generate snRNA-seq libraries that were sequenced on an Illumina NextSeq 500.
<i>Pitx2</i> maintains mitochondrial function during regeneration to prevent myocardial fat deposition.
Specimen part, Subject, Time
View SamplesColon cancers typically contain tumor cell populations with differential WNT signaling activity. Colon cancer cells with high WNT-activity have been attributed increase tumorigenic potential and stem cell characteristics.
Differential WNT activity in colorectal cancer confers limited tumorigenic potential and is regulated by MAPK signaling.
Specimen part, Cell line
View SamplesIdiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear.
Comprehensive Screening of Gene Function and Networks by DNA Microarray Analysis in Japanese Patients with Idiopathic Portal Hypertension.
Specimen part, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Cell line, Treatment
View SamplesSmad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Treatment
View SamplesSmad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Cell type-specific target selection by combinatorial binding of Smad2/3 proteins and hepatocyte nuclear factor 4alpha in HepG2 cells.
Specimen part, Cell line, Treatment
View SamplesSmad2/3 are transcription factors that engage in TGF-beta-induced transcription. We determined and analyzed HepG2 and Hep3B-specific Smad2/3 binding sites by ChIP-chip. We used expression microarrays to compare the Smad2/3 and HNF4alpha binding sites identified by ChIP-chip or ChIP-seq, respectively, to TGF-beta-induced gene expressions.
Cell type-specific target selection by combinatorial binding of Smad2/3 proteins and hepatocyte nuclear factor 4alpha in HepG2 cells.
Specimen part, Cell line, Treatment
View SamplesEpigenetically silenced Ink4a-Arf locus is activated by loss of H3K27me3 in cellular senescence, where secreted factor expression is also involved. Here we analyzed epigenome and transcriptome alteration during Ras-induced senescence using mouse embryonic fibroblast (MEF). Seventeen genes with H3K27me3 loss and H3K4me3 gain showed marked upregulation, including p16Ink4a and Bmp2, a secreted factor for BMP/SMAD signal. Smad6, specific BMP/SMAD pathway inhibitor, was identified as the only one gene showing de novo H3K27 trimethylation with H3K4me3, resulting in strong repression. Ras-activated cells senesced with SMAD1/5/8 phosphorylation, and they escaped from senescence with decreased SMAD1/5/8 phosphorylation when introducing Smad6 or knocking-down Bmp2.
Activation of Bmp2-Smad1 signal and its regulation by coordinated alteration of H3K27 trimethylation in Ras-induced senescence.
Specimen part, Treatment
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