This SuperSeries is composed of the SubSeries listed below.
BRAFV600E-Associated Gene Expression Profile: Early Changes in the Transcriptome, Based on a Transgenic Mouse Model of Papillary Thyroid Carcinoma.
Sex, Age
View SamplesBRAFV600E mutation is the most frequent molecular event in papillary thyroid carcinoma. The relation of this genetic alteration with the factors od poor prognosis has been reported as well as its influence on PTC gene signature. However human material disables distinction of cancer causes from its effect.
BRAFV600E-Associated Gene Expression Profile: Early Changes in the Transcriptome, Based on a Transgenic Mouse Model of Papillary Thyroid Carcinoma.
Sex, Age
View SamplesBRAFV600E mutation is the most frequent molecular event in papillary thyroid carcinoma. The relation of this genetic alteration with the factors od poor prognosis has been reported as well as its influence on PTC gene signature. However human material disables distinction of cancer causes from its effect.
BRAFV600E-Associated Gene Expression Profile: Early Changes in the Transcriptome, Based on a Transgenic Mouse Model of Papillary Thyroid Carcinoma.
Sex, Age
View SamplesWe sequenced mRNA from triplicate log-phase cultures of BY4741 (WT) transformed with pRS313-HA3-SSN6 and taf14D transformed with pRS313-HA3-SSN6 (empty vector), full-length pRS313-TAF14-HA3-SSN6, or pRS313-taf14W81A-HA3-SSN6 cultured in synthetic complete media lacking histidine. Overall design: Examination of changes in gene expression when the YEATS domain of Taf14 is mutated so it cannot bind acetyl-H3.
Association of Taf14 with acetylated histone H3 directs gene transcription and the DNA damage response.
Subject
View SamplesWe performed RNA-seq analysis of polA transcripts in IMR-32 cells with shRNA-mediated depletion of CDK12 and CDK13 and GFP as a control Overall design: Expression of polA transcripts in IMR-32 cells with shRNA-mediated depletion of CDK12 and CDK13 using the RNA-seq library kit (QuantSeq 3' mRNA Sequencing REV, Lexogen) using 2 different shRNA constructs for each target in duplicate, for a total of 10 individual samples Please note that processed data files were generated from the merged replicates, as indicated in the corresponding sample description field.
CDK12 loss in cancer cells affects DNA damage response genes through premature cleavage and polyadenylation.
Specimen part, Cell line, Treatment, Subject
View SamplesWe performed RNA-seq analsysis of polA transcripts in Kelly and Kelly E9 resistant (E9R) cells treated with THZ531 for 6h and DMSO as a control Overall design: Expression of polA transcripts in Kelly and Kelly E9R cells treated with THZ531 using the RNA-seq library kit (QuantSeq 3' mRNA Sequencing REV, Lexogen) in duplicate, for a total of 8 indyvidual samples Please note that the bigWig processed data was generated from both replicates and is linked to the corresponding rep1 (*_1) sample records.
CDK12 loss in cancer cells affects DNA damage response genes through premature cleavage and polyadenylation.
Specimen part, Cell line, Treatment, Subject
View SamplesWe performed RNA-seq analsysis of polA transcripts in IMR-32 cells treated with THZ531 for 2 and 6h and DMSO as a control Overall design: Expression of polA transcripts in IMR-32 treated with THZ531 using the RNA-seq library kit (QuantSeq 3' mRNA Sequencing REV, Lexogen) in duplicate, for a total of 6 individual samples
CDK12 loss in cancer cells affects DNA damage response genes through premature cleavage and polyadenylation.
Cell line, Treatment, Subject
View SamplesInduced and activated regulatory CD4+ Foxp3+ cells compared
Connexin 43 signaling enhances the generation of Foxp3+ regulatory T cells.
Specimen part
View SamplesIn vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression.
C. elegans dysferlin homolog fer-1 is expressed in muscle, and fer-1 mutations initiate altered gene expression of muscle enriched genes.
Specimen part
View SamplesHuman ILCs are classically categorized into five subsets; cytotoxic CD127-CD94+ NK cells and non-cytotoxic CD127+CD94-, ILC1s, ILC2s, ILC3s and LTi cells. Here, we identify a novel subset within the CD127+ ILC population, characterized by the expression of the cytotoxic marker CD94. These CD94+ ILCs strongly resemble conventional ILC3s in terms of phenotype, transcriptome and cytokine production, but are highly cytotoxic. IL-15 was unable to induce differentiation of CD94+ ILCs towards mature NK cells. Instead, CD94+ ILCs retained RORγt, CD127 and CD200R expression and produced IL-22 in response to IL-15. Culturing non-cytotoxic CD127+ ILC1s or ILC3s with IL-12 induced upregulation of CD94 and cytotoxic activity, effects that were not observed with IL-15 stimulation. Thus, human helper ILCs can acquire a cytotoxic program without differentiating into NK cells.
Identification of human cytotoxic ILC3s.
Specimen part, Subject
View Samples