HSL is a key enzyme in in the mobilization of fatty acids from the triglyceride stores of white adipose tissue. In addition, it is expressed in mice liver. In the present microarray study, changes in the transcript profile of murine liver samples due to global HSL knockout were investigated.
Disturbed cholesterol homeostasis in hormone-sensitive lipase-null mice.
Sex, Specimen part
View SamplesThe embryo lethal adenosine methylase tDNA knockout line SALK_074069 was partially complemented with its cDNA driven by the embryo specific ABI3 promoter (A6 lines). The plants have reduced adenosine methylation and show pleiotropic phenotypes. Rosette leaves were harvested from 3 week old plants, both wild-type and mutant plants in triplicate and analysed using the Affymetrix ATH1 array.
Adenosine Methylation in Arabidopsis mRNA is Associated with the 3' End and Reduced Levels Cause Developmental Defects.
Age, Specimen part
View SamplesMethylation of mRNA at the N6 position of adenosin is known for a long time, but its function remains poorly understood. Here generated a null mutant in the catalytic subunit of the m6A mRNA methylosome, dIME4, in Drosophila to determine the impact of loss of m6A on gene expression using Illumina sequencing. Overall design: Since dIME4 is preferentially expressed in the nervous system and dIME4 null mutants are viable, we compared gene expression and alternative splicing in wild type (2 samples) and dIME4 mutants (3 samples) with genetic background matched w control females in neuron enriched head/thorax.
m<sup>6</sup>A potentiates Sxl alternative pre-mRNA splicing for robust Drosophila sex determination.
Specimen part, Cell line, Subject
View SamplesMethylation of mRNA at the N6 position of adenosin is known for a long time, but its function remains poorly understood. Here generated a null mutant in the catalytic subunit of the m6A mRNA methylosome, dIME4, in Drosophila to determine the impact of loss of m6A on gene expression using Illumina sequencing. Overall design: Since dIME4 is preferentially expressed in the nervous system and dIME4 null mutants are viable, we compared gene expression and alternative splicing in wild type (2 samples) and dIME4 mutants (3 samples) with genetic background matched w control females in neuron enriched head/thorax.
m<sup>6</sup>A potentiates Sxl alternative pre-mRNA splicing for robust Drosophila sex determination.
Specimen part, Cell line, Subject
View SamplesAnalysis of the transcriptome of mononuclear side population (SP) and main population (MP) cells of human fetal skeletal muscle from 12 human subjects of gestational age 14-18 weeks.
Regulation of myogenic progenitor proliferation in human fetal skeletal muscle by BMP4 and its antagonist Gremlin.
Specimen part
View SamplesFunctional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells.
ABCB5 maintains melanoma-initiating cells through a proinflammatory cytokine signaling circuit.
Specimen part, Cell line
View SamplesTo find BMAL1-regulated genes in mice pituitary gland we performed a differential microarray from wild-type vs Bmal1-/- knock-out mice
Chromatin remodeling as a mechanism for circadian prolactin transcription: rhythmic NONO and SFPQ recruitment to HLTF.
Sex, Specimen part
View SamplesIn order to gain insight into relative stability of transcripts in plants that lacked m6A, we performed global mapping of uncapped and cleaved transcripts Overall design: 2 replicates of GMUCT in Arabidopsis thaliana ecotype Col-0 ABI3:MTA (mta) plants. genome-wide mapping of uncapped and cleaved transcripts (GMUCT)
N<sup>6</sup>-Methyladenosine Inhibits Local Ribonucleolytic Cleavage to Stabilize mRNAs in Arabidopsis.
Specimen part, Subject
View SamplesGlucocorticoids remain the most widely used class of anti-inflammatory and immunosuppressive agents. They act primarily by binding to the glucocorticoid receptor, resulting in direct and indirect effects on gene expression. The current understanding of glucocorticoid effects on transcription in human cells is based mostly on studies of cancer cell lines, immortalized cell lines, or highly mixed populations of primary cells (such as peripheral blood mononuclear cells). To advance the understanding of the transcriptome-wide effects of glucocorticoids on highly pure populations of primary human cells, we performed RNA-seq on nine such cell populations at two time points after in vitro exposure to methylprednisolone or vehicle. Overall design: Nine cell types were studied: four hematopoietic (circulating B cells, CD4+ T cells, monocytes, and neutrophils) and five non-hematopoietic (endothelial cells, fibroblasts, myoblasts, osteoblasts, and preadipocytes). Each cell type was obtained from a separate cohort of 4 unrelated healthy human donors (4 biological replicates per cell type: BR1 - BR4). Cells form each donor were independently cultured and exposed in vitro to glucocorticoid or vehicle. Non-hematopoietic cells were incubated until the early plateau phase of growth, then exposed to methylprednisolone or vehicle. Hematopoietic cells were collected from peripheral blood, purified by magnetic selection (negative selection for B cells, CD4+ T cells and neutrophils; positive selection for monocytes). Purified B cells, CD4+ T cells, and monocytes were incubated overnight, then exposed to methylprednisolone or vehicle. Purified neutrophils were cultured for 4 hours, then exposed to methylprednisolone or vehicle. Ethanol was used as a vehicle for methylprednisolone. Estimated final concentrations were 8500 mcg/L (22.7 mcM) for methylprednisolone and 0.07% (15.57 mM) for ethanol (vehicle). For each cell type, samples were collected at two time points after treatment with methylprednisolone or vehicle: 2 hours and 6 hours. Samples were collected into TRIzol reagent and frozen at -80°C prior to RNA extraction. RNA-seq data for all samples is made available in this GEO Series.
Immune regulation by glucocorticoids can be linked to cell type-dependent transcriptional responses.
Specimen part, Subject, Time
View SamplesMelanoma growth is driven by malignant melanoma initiating cells (MMIC) identified by expression of the ATP-binding cassette (ABC) member, ABCB5. ABCB5+ melanoma subpopulations have been shown to overexpress the vasculogenic differentiation markers CD144 (VE-cadherin) and TIE-1 and are associated with CD31-negative vasculogenic mimicry (VM), an established biomarker associated with increased patient mortality. Here we identify a critical role for VEGFR-1 signaling in ABCB5+ MMIC-dependent VM and tumor growth. Global gene expression analyses, validated by mRNA and protein determinations, revealed preferential expression of VEGFR-1 on ABCB5+ tumor cells purified from clinical melanomas and established melanoma lines. In vitro, VEGF induced in a VEGFR-1-dependent manner expression of CD144 in ABCB5+ subpopulations that constitutively expressed VEGFR-1, but not in ABCB5- bulk populations that were predominantly VEGFR-1-negative. In vivo, melanomaspecific shRNA-mediated knockdown of VEGFR-1 blocked the development of ABCB5+ VM morphology and inhibited ABCB5+ VM-associated production of the secreted melanoma mitogen, laminin. Moreover, melanoma-specific VEGFR-1 knockdown markedly inhibited tumor growth (by >90%). Our results demonstrate that VEGFR-1 function in MMIC regulates VM and associated laminin production, and show that this function represents one mechanism through which MMIC promote tumor growth.
VEGFR-1 expressed by malignant melanoma-initiating cells is required for tumor growth.
Specimen part
View Samples