This SuperSeries is composed of the SubSeries listed below.
MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.
Specimen part, Cell line
View SamplesColorectal carcinoma (CRC) is one of the most common cancers worldwide. Re-evaluating our current knowledge on CRC and developing novel therapeutic strategies is still crucial. Accumulating evidence suggests that cancer cells possess characters reminiscent of those of normal stem cells. Unveiling small RNAs responsible for cell stemness and chemoradioresistance should eventually lead to the development of novel therapeutic approaches. Overall design: Expression profiles of parental CRC cells and cancer spheres expanded under stem cell medium cultivation were generated for identifying key regulators.
MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.
No sample metadata fields
View SamplesmiRNAs exert various biological functions by targeting different cellular targets. Studying miR-146a functions in colon cancer cells helps to understand colorectal cancer (CRC) malignancy and progression.
MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.
Cell line
View SamplesWe use rAPOBEC-XTEN-Cas9n-UGI (BE3) to introduce a point mutation (R17H) into 8 loci of Hist1H3 by a single sgRNA and a pre-stop codon into Carm1 in early mouse embryo, and both strategies resulted in developmental defects in pre-implantation embryos and fetal stages with smaller or developmental-delayed embryos. Transcriptomic analysis revealed that Yap1 and cell cycle signaling pathways were dysregulated in Carm1 pre-stop and H3R17H embryos, and Yap1 overexpression could rescue the developmental defects. Our results establish the direct regulatory relationship between Carm1-mediated site-specific histone modifications and mouse embryo development, and we also demonstrate that Hippo-Yap1 acts downstream of Carm1-mediated H3R17me2a to regulate the embryonic development and size determination. Overall design: Examination of RNA expression profiles of E4.5 WT/H3R17H/Carm1-/- mouse embryos by deep sequencing.
Base-Editing-Mediated R17H Substitution in Histone H3 Reveals Methylation-Dependent Regulation of Yap Signaling and Early Mouse Embryo Development.
Age, Specimen part, Subject
View SamplesIt is important to reveal the regulatory mechanism of OsMYB30 gene which participated in cold response.
The OsMYB30 Transcription Factor Suppresses Cold Tolerance by Interacting with a JAZ Protein and Suppressing β-Amylase Expression.
Specimen part, Treatment
View SamplesFind the casual relationship between gene expression network and cellular phenotype at single cell resolution. We collected donated human pre-implatation embryos, and the embryonic stem cells derived from them, isolate individual cells, prepared single cell cDNAs, and sequenced them by HiSeq2000. Then we analyzed the expression of known RefSeq genes. Overall design: We get transcriptome of 124 individual cells from human pre-implantation embryos and human embryonic stem cells by applying single cell RNA-seq technique we recently developed[1][2][3][4]. We did in-depth bioinformatic analysis to these data and found very dynamic expression of protein-coding genes. [1] Tang, F. et al. (2010a) Tracing the Derivation of Embryonic Stem Cells from the Inner Cell Mass by Single-Cell RNA-Seq Analysis. Cell Stem Cell 6, 468-478. [2] Tang, F. et al. (2010b) RNA-Seq analysis to capture the transcriptome landscape of a single cell. Nat Protocols 5, 516-535. [3] Tang, F. et al. (2009) mRNA-Seq whole-transcriptome analysis of a single cell. Nat Meth 6, 377-382. [4] Tang, F. et al. (2011) Development and applications of single-cell transcriptome analysis. Nat Meth 8, S6-S11.
Single-cell RNA-Seq profiling of human preimplantation embryos and embryonic stem cells.
Specimen part, Subject
View SamplesAn in-depth analysis of miRNomes in 3 human myeloid leukemia cell lines was carried out to comprehensively identify miRNAs that distinguish acute and chronic myeloid leukemias and relate to myeloid cell differentiation. Overall design: Characterization the miRNomes in 3 myeloid leukemia cell lines.
Characterization of miRNomes in acute and chronic myeloid leukemia cell lines.
Specimen part, Disease, Cell line, Subject
View Samplestranscriptional profile of both macrophages and endothelial end cells between three different lesion stages (uninjured control , upon macrophage arrival , and during macrophage traction). Overall design: Examination of gene expression different in 2 cell types.
Macrophages Mediate the Repair of Brain Vascular Rupture through Direct Physical Adhesion and Mechanical Traction.
No sample metadata fields
View SamplesPneumonic plague is the most deadly form of infection caused by Yersinia pestis and can progress extremely fast. However, our understanding on the host transcriptomic response to pneumonic plague is insufficient. Here, we used RNA-sequencing technology to analyze transcriptomic responses in mice infected with fully virulent strain 201 or EV76, a live attenuated vaccine strain lacking the pigmentation locus. Approximately 600 differentially expressed genes (DEGs) were detected in lungs from both 201- and EV76-infected mice at 12 hours post-infection (hpi). DEGs in lungs of 201-infected mice exceeded 2,000 at 48 hpi, accompanied by sustained large numbers of DEGs in the liver and spleen; however, limited DEGs were detected in those organs of EV-infected mice. Remarkably, DEGs in lungs were significantly enriched in critical immune responses pathways in EV76-infected but not 201-infected mice, including antigen processing and presentation, T cell receptor signaling among others. Pathological and bacterial load analyses confirmed the rapid systemic dissemination of 201-infection and the confined EV76-infection in lungs. Our results demonstrate that fully virulent Y. pestis strongly inhibits both the innate and adaptive immune responses that are substantially stimulated in a self-limited infection, which update our holistic views on the transcriptomic response to pneumonic plague. Overall design: We used RNA-sequencing technology to analyze transcriptomic responses in lungs, spleen and liver of mice infected with fully virulent strain 201 or EV76 at 12, 48 and 72 hpi.
Host transcriptomic responses to pneumonic plague reveal that Yersinia pestis inhibits both the initial adaptive and innate immune responses in mice.
Sex, Specimen part, Cell line, Subject, Time
View SamplesCF patients suffer from chronic and recurrent respiratory tract infections which eventually lead to lung failure followed by death. Pseudomonas aeruginosa is one of the major pathogens for CF patients and is the principal cause of mortality and morbidity in CF patients.
Bacterial adaptation during chronic infection revealed by independent component analysis of transcriptomic data.
No sample metadata fields
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