We decompose the genome-wide expression patterns in 38 embryonic human lung (53-154 days post conception/dpc) into their independent, dominant directions of transcriptomic sample variation in order togain global insight of the developing human lung transcriptome.The characteristic genes and their corresponding bioontologic attribute profile for the latter were identified. We noted the overrepresentation of lung specific attributes (e.g., surfactant proteins) traditionally associated with later developmental stages, and highly ranked attributes (e.g., chemokineimmunologic processes) not previously reported nor immediately apparent in an early lung development context. We defined the 3,223gene union of the characteristic genes of the 3 most dominant sources of variation as the developing lung characteristic subtranscriptome (DLCS). It may be regarded as the minimal gene set describing the essential biology of this process. The developing lung series in this transcriptomic variation perspectiveform a contiguous trajectory with critical time points that both correlate with the 2 traditional morphologic stages overlapping -154 dpc and suggest the existence of 2 novel phases within the pseudoglandular stage. To demonstrate that this characterization is robust, we showed that the model could be used to estimate the gestational age of independent human lung tissue samples with a median absolute error of 5 days, based on the DLCS of their lung profile alone. Repeating this procedure on the homologous transcriptome profiles of developing mouse lung 1419 dpc, we were able to recover their correct developmental chronology.
Transcriptomic analysis of human lung development.
Sex, Disease, Race
View SamplesWhole human fetal lung transcriptome profiles from estimated gestational ages 54 to 137 days post conception. Maternal cigarette smoking status is indicated by cotinine levels measured in the corresponding placenta.
Age, Sexual Dimorphism, and Disease Associations in the Developing Human Fetal Lung Transcriptome.
Sex, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A comparative study of RNA-Seq and microarray data analysis on the two examples of rectal-cancer patients and Burkitt Lymphoma cells.
Cell line, Treatment
View SamplesRNA-Seq profiling of Burkitt Lymphoma cell line (BL2) with B-cell activating factor (BAFF) for 24 hrs . The Burkitt Lymphoma cell line were either only cultured in cell culture medium supplemented with 10 mM HEPES at 1 × 106 cells/ml or additionally incubated with B-cell activating factor (BAFF) for 24 hrs Overall design: Two conditions of BL2 cells each in 3 replicates: 1. non-stimulated control (BL2), 2. Baff stimulated (BL2Baff)
A comparative study of RNA-Seq and microarray data analysis on the two examples of rectal-cancer patients and Burkitt Lymphoma cells.
Treatment, Subject
View SamplesMicroarray profiling of Burkitt Lymphoma cell line (BL2) with B-cell activating factor (BAFF) for 24 hrs .
A comparative study of RNA-Seq and microarray data analysis on the two examples of rectal-cancer patients and Burkitt Lymphoma cells.
Cell line
View SamplesRNA-binding proteins (RBPs) facilitate post-transcriptional control of eukaryotic gene expression at multiple levels. The RBP tristetraprolin (TTP/Zfp36) is a signal-induced phosphorylated anti-inflammatory protein guiding unstable mRNAs of pro-inflammatory proteins for degradation and preventing translation. Using iCLIP, we have identified numerous mRNA targets bound by wild-type TTP and by a non-MK2-phosphorylatable TTP mutant (TTP-AA) in 1h LPS-stimulated macrophages and correlated their interaction with TTP to changes at the level of mRNA abundance and translation in a transcriptome-wide manner. The close similarity of the transcriptome of TTP-deficient and TTP-expressing macrophages upon short LPS stimulation suggested an effective inactivation of TTP by MK2 under these conditions whereas retained RNA-binding capacity of TTP-AA to 3’UTRs caused profound changes in the transcriptome and translatome, altered NF-?B-activation and induced cell death. Increased TTP binding to the 3''UTR of feedback inhibitor mRNAs, such as Ier3, Dusp1 or Tnfaip3, in the absence of MK2-dependent TTP neutralization resulted in a strong reduction of their protein synthesis contributing to the deregulation of the NF-?B-signaling pathway. Taken together, our study uncovers a role for TTP in NF-?B-signaling and highlights the importance of fine-tuned TTP activity-regulation by MK2 in order to control feedback signaling during the inflammatory response. Overall design: Comparison of the transcriptomes of TTP knockout macrophages inducibly expressing GFP, GFP-TTP or GFP-TTP-AA (S52A, S178A) phosphorylation mutant during 1h LPS stimulation. 3 biological replicates per genotype and condition.
The RNA-binding protein TTP is a global post-transcriptional regulator of feedback control in inflammation.
Specimen part, Subject
View SamplesIn order to identify biologically relevant tumor markers, and novel therapeutic target we have compared the tumor gene expression profiles of long (OS>=24 months,n=14) and short (OS <=7months, n=11) survival patients. Then we conducted Kaplan-Meier survival analysis using all the 50 samples listed here. The Affymetrix gene-expression data of these 50 samples were also included in the earlier submission by us as GEO accession number GSE62452.
Endothelial Nitric Oxide Synthase Traffic Inducer (NOSTRIN) is a Negative Regulator of Disease Aggressiveness in Pancreatic Cancer.
Specimen part
View SamplesIn order to identify biologically relevant tumor markers with prognostic significance, we set out to analyze gene expression profiling of tumor and adjacent non-tumor tissues from PDAC cases.
DPEP1 inhibits tumor cell invasiveness, enhances chemosensitivity and predicts clinical outcome in pancreatic ductal adenocarcinoma.
Specimen part
View SamplesIn order to identify biologically relevant tumor markers , we analyzed gene expression profiling of tumor and adjacent non-tumor tissues from PDAC cases. We compared the microarray gene-expression profiles of MIF-high and MIF low expressing tumors as detrmined by qRT-PCR. Affymetrix gene-expression analysis was done in two sets. Affymetrix data from sample number 1-90 were earlier submited by us as GEO accession#: GSE28735. The batch effect between the two sets of data was removed using Partek Genomic Suite and this normalized data was submitted to GEO in this submission. All the analysis was performed using the merged data set.
A Novel MIF Signaling Pathway Drives the Malignant Character of Pancreatic Cancer by Targeting NR3C2.
Specimen part
View Samplesgene expression database and algorithm to define cell expression modules
Identifying gene expression modules that define human cell fates.
Specimen part
View Samples