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363 results for “EMT”
Functional antagonism between STAT3 and SMAD4 regulates EMT
<p>Oncogenic mutations in KRAS are among the most common in cancer. Classical models suggest that loss of epithelial characteristics and the acquisition of mesenchymal traits are associated with cancer aggressiveness and therapy resistance. We identify STAT3 as a genetic modifier of TGF-beta-induced epithelial to mesenchymal transition in mutant KRAS tumors. RNA sequencing was performed with murine cells expressing mutant KRAS either overexpressing hyperactive STAT3Y640, or CRISPR-mediated knockout of STAT3, SMAD4, or KRAS. Excel files of differential expression compared to control mutant RAS cells or fpkm files are provided.</p>
Flow Cytometry data from: "The EMT transcription factor Zeb1 is essential for HSPC differentiation that acts synergistically with Zeb2 in fine-tuning hematopoietic lineage fidelity"
<p>Abstract:</p> <p>The Zeb2 transcription factor has been demonstrated to play important roles in hematopoiesis and leukemic transformation. Zeb1 is a close family member of Zeb2 but has remained more enigmatic concerning its roles in hematopoiesis. Here we show using conditional loss of function approaches and bone marrow reconstitution experiments that Zeb1 plays cell autonomous role in hematopoietic lineage differentiation, particularly as a positive regulator of monocyte development in addition to its previously reported important role in T-cell differentiation. Analysis of existing single cell RNAseq data of early hematopoiesis has revealed distinctive expression differences between Zeb1 and Zeb2 in HSPC differentiation with Zeb2 being more highly and broadly expressed that Zeb1 except at a key transition point (ST-HSCàMPP1) whereby Zeb1 appears to be the dominantly expressed family member. Inducible deletion of both Zeb1 and Zeb2 using a tamoxifen inducible Cre-mediated approach leads to acute bone marrow failure at this transition point with increased long-term and shortterm hematopoietic stem cell numbers and an accompanying decrease in all hematopoietic lineage differentiation. Bioinformatics analysis of RNAseq data has revealed that Zeb2 acts predominantly as a transcriptional repressor involved in restraining mature hematopoietic lineage gene expression programs from being expressed too early in hematopoietic stem and progenitor cells (HSPCs). Zeb1 appears to fine tune this repressive role during hematopoiesis to ensure hematopoietic lineage fidelity. Analysis of ROSA26 locus based transgenic models has revealed that Zeb1 as well as Zeb2 overexpression within the hematopoietic system can drive extramedullary hematopoiesis/splenomegaly and enhanced monocyte development. Finally, deletion of Zeb2 alone or Zeb1/2 together was found to enhance survival in secondary MLL-AF9 AML models attesting to the oncogenic role of Zeb1/2 in AML.</p> <p> </p> <p>Flow cytometric and Hematocrit analysis methods: </p> <p><br> Cells were stained with antibodies listed in the provided Supplemental Table (Antibodies.xlsx) according to the manufacturer guidelines. Flow cytometric analyses were performed on the LSRII and Fortessa X-20 cytometer (BD Biosciences) and the results were analysed by FACSDiva or FlowJo software (BD Biosciences). Cells for MLL-AF9 experiments and RNA-seq were stained and sorted on Influx or FACSAria Fusion sorters (BD Biosciences) at AMREP Flow Cytometry Core Facility and FlowCore, Monash University. <br> Submandibular blood samples were collected into EDTA-coated tubes, and hematology parameters were measured using a HemaVet 950FS automated blood analysis machine (Drew Scientific).</p>
Functional antagonism between STAT3 and SMAD4 regulates EMT
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Data from: Long-term severe hypoxia adaptation induces non-canonical EMT and a novel Wilms Tumor 1 (WT1) isoform
<p>The majority of cancer deaths are caused by solid tumors, where the four most prevalent cancers (breast, lung, colorectal and prostate) account for more than 60% of all cases (1). Tumor cell heterogeneity driven by variable cancer microenvironments, such as hypoxia, is a key determinant of therapeutic outcome. We developed a novel culture protocol, termed the Long-Term Hypoxia (LTHY) time course, to recapitulate the gradual development of severe hypoxia seen in vivo to mimic conditions observed in primary tumors. Cells subjected to LTHY underwent a non-canonical epithelial to mesenchymal transition (EMT) based on miRNA and mRNA signatures as well as displayed EMT-like morphological changes. Concomitant to this, we report production of a novel truncated isoform of WT1 transcription factor (tWt1), a non-canonical EMT driver, with expression driven by a yet undescribed intronic promoter through hypoxia-responsive elements (HREs). We further demonstrated that tWt1 initiates translation from an intron-derived start codon, retains proper subcellular localization and DNA binding. A similar tWt1 is also expressed in LTHY-cultured human cancer cell lines as well as primary cancers and predicts long-term patient survival. Our study not only demonstrates the importance of culture conditions that better mimic those observed in primary cancers, especially with regards to hypoxia, but also identifies a novel isoform of WT1 which correlates with poor long-term survival in ovarian cancer.</p>
Progression of Renal Interstitial Fibrosis / Tubular Atrophy (IF/TA) According to Epithelial-mesenchymal Transition (EMT) and Immunosuppressive Regimen (Everolimus Based Versus CNI Based) in de Novo R
ClinicalTrials.gov study NCT01079143. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Data from: Long-term severe hypoxia adaptation induces non-canonical EMT and a novel Wilms Tumor 1 (WT1) isoform
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Red rice bran polyphenols suppress invasive properties of HepG2 cells, possibly through Wnt/β-catenin-mediated EMT reversal.
<p>Data collection in its raw form is performed in a specific sequence dictated by the manuscript.</p>
SUKANTA EMT
<p>Source code for EMT simulation</p>
Data for: Link between glucose metabolism and EMT drives triple negative breast cancer migratory heterogeneity
<p>Intracellular and environmental cues result in heterogeneous cancer cell populations with different metabolic and migratory behaviors. While glucose metabolism and EMT have previously been linked, we aim to understand how this relationship fuels cancer cell migration. We show that while glycolysis drives single-cell migration in confining microtracks, fast and slow cells display different migratory sensitivities to glycolysis and oxidative phosphorylation inhibition. Phenotypic sorting of highly and weakly migratory subpopulations (MDA<sup>+</sup>, MDA<sup>-</sup>) reveals that more mesenchymal, highly migratory MDA<sup>+</sup> preferentially use glycolysis while more epithelial, weakly migratory MDA<sup>-</sup> utilize mitochondrial respiration. These phenotypes are plastic and MDA<sup>+</sup> can be made less glycolytic, mesenchymal, and migratory and MDA<sup>-</sup> can be made more glycolytic, mesenchymal, and migratory via modulation of glucose metabolism or EMT. These findings reveal an intrinsic link between EMT and glucose metabolism that controls migration. Identifying mechanisms fueling phenotypic heterogeneity is essential to develop targeted metastatic therapeutics.</p>
"High Levels of EMT-TFs for the Diagnosis of Colorectal Cancer (CRC)"
ClinicalTrials.gov study NCT04323813. IPD Sharing: NO. Countries: 1. Publications: 1.
Study on the Interplay Between Twist1 and Other EMT Regulators Through microRNA-29 Family.
ClinicalTrials.gov study NCT01927354. IPD Sharing: Not stated. Countries: 1. Publications: 50.
CTC, Free DNA, Stem Cells and EMT-related Antigens as Biomarkers of Activity of Cabazitaxel in CRPC.
ClinicalTrials.gov study NCT03381326. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Detection of High Expression Levels of EMT-Transcription Factor mRNAs in Patients With Pancreatic Cancer and Their Diagnostic Potential
ClinicalTrials.gov study NCT04323917. IPD Sharing: NO. Countries: 1. Publications: 1.
Pronostic and Predictive Value of EMT in Localized Lung Cancer
ClinicalTrials.gov study NCT03509779. IPD Sharing: NO. Countries: 1. Publications: 1.
Comparative Effects of IMT Vs EMT Along With AIT in COPD Patients
ClinicalTrials.gov study NCT06308302. IPD Sharing: NO. Countries: 1. Publications: 10.
Data for: Link between glucose metabolism and EMT drives triple negative breast cancer migratory heterogeneity
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Identification of the tumour transition states occurring during EMT
GEO Series GSE110587. Mus musculus. 31 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
CXCR4-LASP1-G9a-SNAIL Axis Drives NEPC Transdifferentiation via Induction of EMT and Downregulation of REST [331R]
GEO Series GSE296569. Homo sapiens. 4 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Gene expression profiling of NSCLC cell lines upon TGFb-induced epithelial-mesenchymal transition (EMT)
GEO Series GSE49644. Homo sapiens. 18 samples. Type: Expression profiling by array.
Epigenomic disorder and partial EMT impair luminal progenitor integrity in Brca1-associated breast tumorigenesis
GEO Series GSE288315. Mus musculus. 6 samples. Type: Other.
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