Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most frequent cause of familial and sporadic Parkinsons disease (PD). Here, we investigated in parallel gene and microRNA transcriptome profiles of three different LRRK2 mouse models. Striatal tissue was isolated from adult LRRK2 knockout mice, as well as mice expressinghuman LRRK2 wildtype (hLRRK2-WT) or PD-associated R1441G mutation (hLRRK2-R1441G).
Gene and MicroRNA transcriptome analysis of Parkinson's related LRRK2 mouse models.
Age, Specimen part
View SamplesLivers from wild-type (WT) or Ppara knock-out (Ppara KO) C57Bl6 mice were used to prepare RNA which was then processed for analysis using MoGene-2_0-st Affymetrix microarrays according to standard procedures.
The logic of transcriptional regulator recruitment architecture at <i>cis</i>-regulatory modules controlling liver functions.
Sex, Specimen part
View SamplesIn an attempt to elucidate the molecular mechanisms underlying the multiple roles of L1 in endothelium, we checked whether manipulating its expression affected the transcriptome of lECs. To this purpose, we compared the gene expression profiles of L1-overexpressing and control lECs by Affymetrix, which revealed a remarkable effect of L1 overexpression on lECs transcriptome.
Endothelial deficiency of L1 reduces tumor angiogenesis and promotes vessel normalization.
Specimen part
View SamplesPDGF and FGF treatment in E13.5 MEPMs. 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates) Overall design: 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates)
Receptor tyrosine kinases modulate distinct transcriptional programs by differential usage of intracellular pathways.
No sample metadata fields
View SamplesReceptor tyrosine kinase signaling is critical for mammalian craniofacial development, but the key downstream transcriptional effectors remain unknown. We demonstrate that SRF is induced by both PDGF and FGF signaling in mouse embryonic palatal mesenchyme cells, and Srf neural crest conditional mutants exhibit facial clefting accompanied by proliferation and migration defects. Srf and Pdgfra mutants interact genetically in craniofacial development, but Srf and Fgfr1 mutants do not. This signal specificity is recapitulated at the level of cofactor activation: while both PDGF and FGF target gene promoters show enriched genome-wide overlap with SRF ChIP-seq peaks, PDGF selectively activates a network of MRTF-dependent cytoskeletal genes. Collectively, our results identify a novel role for SRF in proliferation and migration during craniofacial development and delineate a mechanism of receptor tyrosine kinase specificity mediated through differential cofactor usage, leading to a unique PDGF-responsive SRF-driven transcriptional program in the midface. Overall design: Serum Starved MEPMs (4 replicates), 1 hr PDGF treated MEPMs (4 replicates), 1 hr FGF treated MEPMs (3 replicates)
Receptor tyrosine kinases modulate distinct transcriptional programs by differential usage of intracellular pathways.
No sample metadata fields
View SamplesIn this study, we initially screened over 1400 natural products for capacity to inhibit the kinetic enzyme activity of nuclear HDACs isolated from SK-MEL-3 cells. From these findings we evaluate whole transcriptome changes that occur at a 24 hour time point in SK-ME-3 cells in the presence of a known HDAC inhibitor (Trichostatin A) (1uM) or a natural product HDAC inhibitor Grapeseed Extract (120ug/ml), both tested at sub-lethal concentrations relative to untreated controls. Microarrays were acquired for mRNAs and long intergenic non-coding RNA transcripts using the GeneChip Human 2.1ST ARRAY by Affymetrix Inc
Whole-transcriptomic Profile of SK-MEL-3 Melanoma Cells Treated with the Histone Deacetylase Inhibitor: Trichostatin A.
Cell line, Treatment
View SamplesThe effects of BSE and 3-OABA on MDA-MB-231 cells were evaluated for effects on the whole transcriptome: including mRNAs and long intergenic non-coding RNA transcripts (lincRNA) using GeneChip Human Gene 2.1 ST Arrays by Affymetrix Inc.
Transcriptomic Profiling of MDA-MB-231 Cells Exposed to <i>Boswellia Serrata</i> and 3-O-Acetyl-B-Boswellic Acid; ER/UPR Mediated Programmed Cell Death.
Specimen part, Cell line, Treatment
View SamplesThe goal is to investigate gene regulation in endometrial stromal cells expressing the Notch ligand Jag1.
Notch ligand-dependent gene expression in human endometrial stromal cells.
Specimen part
View SamplesWe identify sites of combinatorial control by performing high throughput ChIP experiments on p300, CREB-binding protein (CBP), the deacetylase SIRT1 and on multiple DNA-binding transcription factors in three different tissues. We present a quantitative model of transcriptional regulation that reveals the contribution of each binding site to tissue-specific gene expression in several mouse cell types. Binding to both evolutionarily conserved and non-conserved sequences is found to contribute significantly to transcriptional regulation. We demonstrate that binding location strongly predicts the expression level of nearby genes.
A quantitative model of transcriptional regulation reveals the influence of binding location on expression.
Specimen part
View SamplesAnalysis of wig-1 pathways via suppression of Wig-1 by antisense oligonucleotides
Genomic analysis of wig-1 pathways.
Specimen part, Treatment
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