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Homo sapiens
13 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
UV Irradiation Induces a Non-coding RNA that Functionally Opposes the Protein Encoded by the Same Gene.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 1 Downloadable Sample
- Illumina HumanHT-12 V4.0 expression beadchip
Description
The transcription-related DNA damage response was analyzed on a genome-wide scale with great spatial and temporal resolution. Upon UV irradiation, a slowdown of transcript elongation and restriction of gene activity to the promoter-proximal ~25 kilobases is observed. This is associated with a shift from expression of long mRNAs to shorter isoforms, incorporating alternative last exons (ALEs) that are more proximal to the transcription start site. Notably, this includes a shift from a protein-coding ASCC3 mRNA to a shorter transcript isoform of which the RNA, rather than an encoded protein, is critical for the eventual recovery of transcription. The protein-coding ASCC3 isoform counteracts the function of the non-coding isoform, indicating crosstalk between them. Thus, the ASCC3 gene expresses both coding and noncoding transcript isoforms with opposite effects on transcription recovery after UV-induced DNA damage
Publication Title
UV Irradiation Induces a Non-coding RNA that Functionally Opposes the Protein Encoded by the Same Gene.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
The transcription-related DNA damage response was analyzed on a genome-wide scale with great spatial and temporal resolution. Upon UV irradiation, a slowdown of transcript elongation and restriction of gene activity to the promoter-proximal ~25 kilobases is observed. This is associated with a shift from expression of long mRNAs to shorter isoforms, incorporating alternative last exons (ALEs) that are more proximal to the transcription start site. Notably, this includes a shift from a protein-coding ASCC3 mRNA to a shorter transcript isoform of which the RNA, rather than an encoded protein, is critical for the eventual recovery of transcription. The protein-coding ASCC3 isoform counteracts the function of the non-coding isoform, indicating crosstalk between them. Thus, the ASCC3 gene expresses both coding and noncoding transcript isoforms with opposite effects on transcription recovery after UV-induced DNA damage
Publication Title
UV Irradiation Induces a Non-coding RNA that Functionally Opposes the Protein Encoded by the Same Gene.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples
SRP094802- Homo sapiens
- 6 Downloadable Samples
Illumina HiSeq 2000
Description
The transcription-related DNA damage response was analyzed on a genome-wide scale with great spatial and temporal resolution. Upon UV irradiation, a slowdown of transcript elongation and restriction of gene activity to the promoter-proximal ~25 kilobases is observed. This is associated with a shift from expression of long mRNAs to shorter isoforms, incorporating alternative last exons (ALEs) that are more proximal to the transcription start site. Notably, this includes a shift from a protein-coding ASCC3 mRNA to a shorter transcript isoform of which the RNA, rather than an encoded protein, is critical for the eventual recovery of transcription. The protein-coding ASCC3 isoform counteracts the function of the non-coding isoform, indicating crosstalk between them. Thus, the ASCC3 gene expresses both coding and noncoding transcript isoforms with opposite effects on transcription recovery after UV-induced DNA damage. Overall design: Cells were treated with DRB (100 µM, 3.5 hrs), followed by UVC irradiation (15 J/m2) or left untreated. Cells were washed with PBS to remove DRB immediately after UV irradiation and incubated for 10, 25 or 40 minutes, followed by cell lysis and nuclei isolation. Nuclei were processed for GRO-Seq.
Publication Title
UV Irradiation Induces a Non-coding RNA that Functionally Opposes the Protein Encoded by the Same Gene.
Sample Metadata Fields
Cell line, Treatment, Subject, Time
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
The experiment was design to address the intrinsic differences between metastatic cancer stem cells in the primary tumour and during metastatic colonization in the mouse mammary gland tumour model MMTV-pyMT.
Publication Title
Mesenchymal Cancer Cell-Stroma Crosstalk Promotes Niche Activation, Epithelial Reversion, and Metastatic Colonization.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2500
Description
We studied the effects of acute activation of the melanoma oncogene RAC1 P29S using a tamoxifen-inducible ER-fusion protein system in mouse melanocytes Overall design: An ER-RAC1 P29S fusion protein was stably expressed in the spontaneously immortalized mouse melanocyte cell line melan-a. The fusion protein was activated by treatment with 500 nM 4OH-tamoxifen. RNA was isolated and sequenced at 0 h, 4 h and 40 h post-treatment. The gene expression profiles at 4 h and 40 h were compared to the 0 h time-point. To control for effects induced by 4OH-tamoxifen independent from ER-RAC1 P29S, we performed the same experiment in melan-a cells transduced with an empty vector.
Publication Title
RAC1<sup>P29S</sup> Induces a Mesenchymal Phenotypic Switch via Serum Response Factor to Promote Melanoma Development and Therapy Resistance.
Sample Metadata Fields
Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 4000
Description
We studied the effects of endogenous expression of the melanoma oncogene RAC1 P29S in BRAF V600E;PTEN hemizygous mouse melanomas. Overall design: Transgenic mice with a conditional knock-in of the P29S mutation in the endogenous Rac1 locus were generated and crossed onto C57BL/6J, Tyr-CreER;BrafCA/wt;Ptenfl/wt mice. Melanomas were induced by topical 4OH-tamoxifen. We compared the gene expression profile in whole tumour lysates from Tyr-CreER+/-;Ptenfl/wt;BrafCA/wt;Rac1LSL-P29S/wt mice versus Tyr-CreER+/-;Ptenfl/wt;BrafCA/wt;Rac1wt/wt mice (n = 6 tumours from 5-6 animals per group).
Publication Title
RAC1<sup>P29S</sup> Induces a Mesenchymal Phenotypic Switch via Serum Response Factor to Promote Melanoma Development and Therapy Resistance.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Microvascular endothelial cells (EC) display a high degree of phenotypic and functional heterogeneity among different organs. Organ-specific EC control their tissue microenvironment by angiocrine factors in health and disease. Liver sinusoidal EC (LSEC) are uniquely differentiated to fulfil important organ-specific functions in development, under homeostatic conditions, and in regeneration and liver pathology. Recently, Bmp2 has been identified by us as an organ-specific angiokine derived from LSEC. To study angiocrine Bmp2 signaling in the liver, we conditionally deleted Bmp2 in LSEC using EC subtype-specific Stab2-Cre mice. Genetic inactivation of hepatic angiocrine Bmp2 signaling in Stab2-Cre;Bmp2fl/fl (Bmp2LSECKO) mice caused massive iron overload in the liver, and increased serum iron levels and iron deposition in several organs similar to classic hereditary hemochromatosis. Iron overload was mediated by decreased hepatic expression of hepcidin, a key regulator of iron homeostasis. Thus, angiocrine Bmp2 signaling within the hepatic vascular niche represents a constitutive pathway indispensable for iron homeostasis in vivo that is non-redundant with Bmp6. Notably, we demonstrate that organ-specific angiocrine signaling is essential not only for the homeostasis of the respective organ, but also for the homeostasis of the whole organism.
Publication Title
Angiocrine Bmp2 signaling in murine liver controls normal iron homeostasis.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 4000
Description
Lgr6-positive cells have been shown to label stem/progenitors cells in several tissues including tongue and skin. However their role in mammary gland has never been investigated. Here we used Lgr6-eGFP-IRES-CreER2 mice to isolate and characterize Lgr6-positive population in mammary gland of 5-week old female mice. Overall design: Examination of transcriptional differences between Lgr6 positive and negative cells
Publication Title
Lgr6 labels a rare population of mammary gland progenitor cells that are able to originate luminal mammary tumours.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Homo sapiens
- 78 Downloadable Samples
- NextSeq 500
Description
Slow-cycling subpopulations exist in bacteria, yeast, and mammalian systems. In the case of cancer, slow-cycling subpopulations have been proposed to give rise to drug resistance. However, the origin of slow-cycling human cells is poorly studied, in large part due to lack of markers to identify these rare cells. Slow-cycling cells pass through a non-cycling period marked by low CDK2 activity and high p21 levels. Here, we use this knowledge to isolate these naturally slow-cycling cells from a heterogeneous population and perform RNA-sequencing to delineate the transcriptome underlying the slow-cycling state. We show that cellular stress responses – the p53 transcriptional response and the integrated stress response – are the most salient causes of spontaneous entry into the slow-cycling state. Overall design: mRNA profiling of spontaneously quiescent human cells and cells forced into quiescence by four different methods
Publication Title
Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways.
Sample Metadata Fields
Cell line, Subject
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