This SuperSeries is composed of the SubSeries listed below.
Tumor-Derived Retinoic Acid Regulates Intratumoral Monocyte Differentiation to Promote Immune Suppression.
Specimen part, Treatment
View SamplesRetinoic acid signaling regulates monocyte differentiation into dendritic cells or macrophages. We used microarrays to uncover gene expression changes associated with retinoic acid exposure in human monocytes.
Tumor-Derived Retinoic Acid Regulates Intratumoral Monocyte Differentiation to Promote Immune Suppression.
Specimen part, Treatment
View SamplesThe microenvironment has profound effect on macrophage phenotype. Here we examine the phenotype of macrophages infiltrating murine undifferentiated pleomorphic sarcomas. We used microarray to examine gene expression profile of tumor-associated macrophages in murine undifferentiated pleomorphic sarcomas.
Tumor-Derived Retinoic Acid Regulates Intratumoral Monocyte Differentiation to Promote Immune Suppression.
Specimen part
View SamplesExamine the possible pro-inflammatory gene effects of alloantibody and complement on endothelial cells
Alloantibody and complement promote T cell-mediated cardiac allograft vasculopathy through noncanonical nuclear factor-κB signaling in endothelial cells.
Specimen part, Treatment
View SamplesAnalysis of transcriptional differences between control and RA-treated cells during cardiac differentiation. The hypothesis tested in these samples is that addition of RA during differentiation towards atrial-like cardiomyocytes while control cells treated with DMSO result in ventricular-like cardiomyocytes. Overall design: NKX2.5 (eGFP/w)-hESCs were differentiated to cardiomyocytes with spin EB protocol, with the addition of RA or DMSO. Cells were sorted at day-31 based on GFP resulting in CTplus, CTminus, RAplus or RAminus goups. RNA was isolated from each of these fractions for sequencing.
KeyGenes, a Tool to Probe Tissue Differentiation Using a Human Fetal Transcriptional Atlas.
No sample metadata fields
View SamplesAdenosine binds to 4 G protein-coupled receptors located on the cardiomyocyte (A1-R, A2a-R, A2b-R and A3-R) and modulates cardiac function during both ischemia and load-induced stress. While the role of adenosine receptor-subtypes has been well defined in the setting of ischemia-reperfusion, far less is known regarding their roles in protecting the heart during other forms of cardiac stress.
Identification of candidate long noncoding RNAs associated with left ventricular hypertrophy.
Specimen part
View SamplesWe reported that both conventional and adipose-specific Naa10p deletions in mice result in increased energy expenditure, thermogenesis, beige adipocyte differentiation and activation. Mechanistically, Naa10p acetylates the N-terminus of Pgc1α and prevents it from interacting with Ppar𝛾 to activate key genes, such as Ucp1, involved in beige adipocyte function. We used microarrays to profile the gene expression changes by Naa10p KO in inguinal white adipose tissues (iWATs) derived from mice fed with high fat diet for 15 weeks.
Naa10p Inhibits Beige Adipocyte-Mediated Thermogenesis through N-α-acetylation of Pgc1α.
Sex, Specimen part
View SamplesUsing 5 differents approaches, including RNA sequencing, we demonstrated that macrophages that specifically infiltrate renal tumors, express the immunosuppressive transcription factor Foxp3. Overall design: Examination of the Foxp3 mRNA expression in 3 different cell subsets (including CD4 T cells (CD4), type-1 macrophages (M1) and type-2 macrophages (M2))
Foxp3 expression in macrophages associated with RENCA tumors in mice.
No sample metadata fields
View SamplesDNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. Overall design: RNAseq of untreated HMEC-hTERT cells, siCtrl, siMBD2 or DAC treated HMLER cells, siCtrl or siMBD2 treated HME-ZEB1-RAS and HME-shP53-RAS cells, in duplicates.
Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells.
No sample metadata fields
View SamplesCD4 T cells can differentiate into a hetergenous population of effector T cells. A population of cytotoxic CD4 T cells can be generated against influenza challenge, however identifying these cells have been challenging. The expression of NKG2A/C/E on CD4 T cells identifies CD4 T cells with cytotoxic potential thus allowing further characterization of this subset of CD4 effector cells.
NKG2C/E Marks the Unique Cytotoxic CD4 T Cell Subset, ThCTL, Generated by Influenza Infection.
Specimen part
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