To identify cellular and genetic abnormalities involved in interstrand cross link repair-deficient bone marrow failure and its transformation to leukemia, we used an Ercc1 hypomorphic mouse model (Ercc1 -/d).
ICL-induced miR139-3p and miR199a-3p have opposite roles in hematopoietic cell expansion and leukemic transformation.
Age, Specimen part
View SamplesmRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated Overall design: mRNA profiles of 8 weeks old C57BL/6 mice 2 days after infections with 5e7 pfu of various strains of murine norovirus (MNV) or 1e8 pfu of T1L reovirus were evauated
Murine Norovirus Infection Induces T<sub>H</sub>1 Inflammatory Responses to Dietary Antigens.
Age, Specimen part, Cell line, Subject
View SamplesWe overexpressed the spliced form of transcription factor XBP1 in mature F442A adipocytes by adenoviral infection. Control virus expressed GFP alone.
The role of adipocyte XBP1 in metabolic regulation during lactation.
Specimen part, Cell line
View SamplesWe find that treating mesenchymal NAMEC8 cells with cholera toxin (CTx) to elevate intracellular cAMP levels and activate PKA induces a mesenchymal-to-epithelial transition whereby the cells assume an epithelial state (N8-CTx). NAMEC8 cells undergo epigenetic reprogramming triggered by active PHF2, a histone demethylase, which demethylates H3K9me2 and H3K9me3 regions of epithelial genes silencing in the mesenchymal state Overall design: Performing RNASeq with HMLE (immortalized human mammary epithelial cells), their mesenchymal CD44hi counterparts, NAMEC8 and the CTx-reverted versions of NAMEC8 a.k.a N8-CTx
Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability.
No sample metadata fields
View SamplesUsing the recently described CD104+/CD44hi antigen combination we demonstrate that tumorigenicity depends on individual cells residing in a hybrid E/M state. Acquisition of this E/M hybrid state is facilitated by the differential expression of EMT- TFs, like Snail accompanied by the expression of adult stem-cell programs. Transition from the highly tumorigenic E/M state to a fully mesenchymal phenotype, achieved by constitutive ectopic expression of Zeb1, is sufficient to drive cells out of the E/M hybrid state into an extreme mesenchymal (xM) state, which is accompanied by a substantial loss of tumorigenicity and a switch from canonical to non-canonical Wnt signaling. Overall design: Performing RNASeq with HMLE (immortalized human mammary epithelial cells) in different EMT stages, either in the E state the hybrid E/M state or the extreme mesenchymal (xM) state as determined by sorting for CD104 and CD44. And performing RNASeq with HMLE cells locked in the xE state by Zeb1KO (xE-SCC-Zeb1KO), from there transferred to the hybrid E/M state by Snail overexpression (E-SCC-Zeb1KOSn) or rescued and transitioned to an xM state with CRISPR resistant Zeb1 wobble mutant (mt) (E-SCC-Zeb1KOSnZmt).
Acquisition of a hybrid E/M state is essential for tumorigenicity of basal breast cancer cells.
Specimen part, Subject
View SamplesWe report the gene expression profiles of normal epithelial and carcinoma cell populations that differ in their relative levels of integrin-beta 4 expression. ITGB4 high, mesenchymal subtype, triple-negative breast cancer cells were found to be more epithelial than related ITGB4 low cells. Overall design: RNA-seq was used to compare the expression of mesenchymal-like carcinoma cell subtypes isolated from polyclonal cell populations. Isolated cell populations that had high levels of ITGB4 were found to be more epithelial than those with low levels, despite the fact that they were within the mesenchymal-like cell state spectrum.
Integrin-β4 identifies cancer stem cell-enriched populations of partially mesenchymal carcinoma cells.
Specimen part, Cell line, Subject
View SamplesThe EMT program allows epithelial cells to become endowed with motility, invasiveness and stem cell traits. We investigated difference in signaling networks that are differentially utilized in EMTed and non-EMTed cells, thereby identifying therapeutic targets that are unique to EMT/cancer stem cells.
Protein kinase C α is a central signaling node and therapeutic target for breast cancer stem cells.
No sample metadata fields
View SamplesGlobal expression analysis of neural crest-like skin-derived precursors (SKPs) and Sox2-positive follicle dermal cells that SKPs originate from.
SKPs derive from hair follicle precursors and exhibit properties of adult dermal stem cells.
Specimen part
View SamplesComparison of gene expression profile of HEK293 cells stably expressing a shRNA control (SilX-CT) or a shRNA against BAHD1 (SilX-BAHD1)
Overexpression of the Heterochromatinization Factor BAHD1 in HEK293 Cells Differentially Reshapes the DNA Methylome on Autosomes and X Chromosome.
Cell line
View SamplesComparison of gene expression profile of HEK293-CT cells and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)
Overexpression of the Heterochromatinization Factor BAHD1 in HEK293 Cells Differentially Reshapes the DNA Methylome on Autosomes and X Chromosome.
Cell line, Treatment
View Samples