In 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 SamplesGene expression profiling in soybean under aluminum stress: genes differentially expressed between Al-tolerant and Al-sensitive genotypes.
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Specimen part, Treatment
View SamplesGene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level.
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Specimen part, Treatment
View SamplesGene expression profiling in soybean under aluminum stress: Transcriptome response to Al stress in roots of Al-tolerant genotype (PI 416937).
Identification of Aluminum Responsive Genes in Al-Tolerant Soybean Line PI 416937.
Specimen part
View SamplesFamilial Dysautonomia is a genetic disease, however patietns with the same genotype present with mild or severe forms of the disease. We used the pluripotent stem cell technology to capture the differences in disease severity in vitro during neurodevelopment as well as during maintanance of the cells, showing developmental and degenerative phenotypes. RNA seq. analysis of the groups confirmed those diffferences. Overall design: Analysis of RNA from PSC-derived neural crest cells from severe FD, mild FD and healthy patients
Capturing the biology of disease severity in a PSC-based model of familial dysautonomia.
No sample metadata fields
View SamplesWe have generated expression profiles of induced pluripotent stem cells (iPSCs) and iPSC-derived neural crest populations from Familial Dysautonomia patients. These profiles were compared to a normal iPSC line that does not harbor the IKBKAP mutation. Overall design: All cell types were differentiated from patient derived iPSCs. Bulk iPSCs were harvested for RNA and the neural crest populations were sorted on day 18 for p75/HNK1 before RNA isolation.
Capturing the biology of disease severity in a PSC-based model of familial dysautonomia.
No sample metadata fields
View SamplesLevels of C/EBP are low in myeloid blast crisis (BC) of chronic myelogenous leukemia (CML) and its expression in p210BCR/ABL-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation and suppresses leukemogenesis. To assess the mechanisms involved in these effects, C/EBP targets were identified by microarray analyses. Upon C/EBP activation, expression of c-Myb and GATA-2 was repressed in 32D-BCR/ABL, K562 and CML-BC primary cells but only c-Myb levels decreased slightly in CD34+ normal progenitors. The role of these two genes for the biological effects of C/EBP was assessed by perturbing their expression in K562 cells. Expression of c-Myb blocked the proliferation inhibition and differentiation-inducing effects of C/EBP while c-Myb siRNA treatment enhanced C/EBP-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic differentiation. GATA-2 expression suppressed the proliferation inhibitory effect of C/EBP but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBP induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBP activation. In summary, the effects of C/EBP in p210BCR/ABL -expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2. Since perturbation of c-Myb and GATA-2 expression has non identical consequences for proliferation and differentiation of K562 cells, the effects of C/EBP appear to involve different transcription-regulated targets.
Transcriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.
No sample metadata fields
View SamplesDetermine the role of interferons in the transcriptional profile of Ad-F7 transduced primary human macrophages using neutralizing antibody for the type I IFN receptor (IFNAR2).
Transcriptional re-programming of primary macrophages reveals distinct apoptotic and anti-tumoral functions of IRF-3 and IRF-7.
No sample metadata fields
View Samples