Gene expression profiling was performed on CNS tissue from neonatal mice carrying the T9H translocation and maternal or paternal duplication of proximal Chromosomes 7 and 15. Our analysis revealed the presence of two novel paternally expressed intergenic transcripts at the PWS/AS locus. The transcripts were termed Pec2 and Pec3 for paternally expressed in the CNS.Our analysis also revealed imprinting of Magel2, Mkrn3, Ndn,Ube3a and Usp29, as well as Pec2 and Pec3 in embryonic brain, 15.5 dpc, and provided a survery of biallelically expressed genes on proximal Chromosomes 7 and 15 in embryonic and neonatal CNS.
Novel paternally expressed intergenic transcripts at the mouse Prader-Willi/Angelman Syndrome locus.
No sample metadata fields
View SamplesGene expression profiling was performed on CNS tissue from neonatal mice carrying the T9H translocation and maternal or paternal duplication of proximal Chromosomes 7 and 15. Our analysis revealed the presence of two novel paternally expressed intergenic transcripts at the PWS/AS locus. The transcripts were termed Pec2 and Pec3 for paternally expressed in the CNS.Our analysis also revealed imprinting of Magel2, Mkrn3, Ndn,Ube3a and Usp29, as well as Pec2 and Pec3 in embryonic brain, 15.5 dpc, and provided a survery of biallelically expressed genes on proximal Chromosomes 7 and 15 in embryonic and neonatal CNS.
Novel paternally expressed intergenic transcripts at the mouse Prader-Willi/Angelman Syndrome locus.
No sample metadata fields
View SamplesGene expression profiling was performed on CNS tissue from neonatal mice carrying the T9H translocation and maternal or paternal duplication of proximal Chromosomes 7 and 15. Our analysis revealed the presence of two novel paternally expressed intergenic transcripts at the PWS/AS locus. The transcripts were termed Pec2 and Pec3 for paternally expressed in the CNS.Our analysis also revealed imprinting of Magel2, Mkrn3, Ndn,Ube3a and Usp29, as well as Pec2 and Pec3 in embryonic brain, 15.5 dpc, and provided a survery of biallelically expressed genes on proximal Chromosomes 7 and 15 in embryonic and neonatal CNS.
Novel paternally expressed intergenic transcripts at the mouse Prader-Willi/Angelman Syndrome locus.
No sample metadata fields
View SamplesStable expression of SNAI1 in MCF10A cells enhanced resistance to cell death and cellular plasticity by regulating signalling pathways involved in apoptotis and stem cell maintenance.
SNAI1-mediated epithelial-mesenchymal transition confers chemoresistance and cellular plasticity by regulating genes involved in cell death and stem cell maintenance.
Specimen part, Cell line
View SamplesKnock-down of LSD1 using siRNA approach induced regulation of several proliferation-associated genes in ER-negative breast cancer cells MDA-MB-231.
Lysine-specific demethylase 1 (LSD1) and histone deacetylase 1 (HDAC1) synergistically repress proinflammatory cytokines and classical complement pathway components.
Cell line
View SamplesPosttranslational modifications on histone tails control gene expresssion levels in an either positive or negative way. Therefore enzymes which modifiy the modifications on the histon tails, like histone demethylases, are able to strictly regulate the transcriptom.
The H3K4me3 histone demethylase Fbxl10 is a regulator of chemokine expression, cellular morphology, and the metabolome of fibroblasts.
Specimen part
View SamplesIdentification of AP-2d target genes in the midbrain of E15 mouse embryos
AP-2δ is a crucial transcriptional regulator of the posterior midbrain.
Specimen part
View SamplesThe aim of this study is to identify the SPIN1 target genes in liposarcoma cells Overall design: Liposarcoma is one of the most common histological subtypes of soft tissue sarcoma and causes high incidence of morbidity and mortality. Since therapeutic options for liposarcoma treatment are insufficient, there is an urgent need to identify novel therapeutic targets. Here, we show that knockdown of SPIN1, a reader of H3K4me3 and H3R8me2a chromatin marks, strongly reduces proliferation and survival of liposarcoma cells in vitro and in xenograft mouse models. Combining genome-wide chromatin binding and transcriptome analyses, we found that SPIN1 in cooperation with the transcription factor MAZ directly enhances expression of GDNF, an activator of the RET signaling pathway. Accordingly, knockdown of SPIN1 results in reduced levels of GDNF and activated RET explaining diminished liposarcoma cell proliferation and survival. In line with these observations, levels of SPIN1, GDNF, and activated RET are highly increased in human liposarcoma compared to lipoma or normal adipose tissue. Importantly, SPIN1-mediated transcriptional control depends on binding to H3K4me3 suggesting that targeting of this interaction with small molecule inhibitors is a novel strategy to treat liposarcoma.
The histone code reader SPIN1 controls RET signaling in liposarcoma.
No sample metadata fields
View SamplesWe performed single-cell RNA sequencing (RNA-seq) during the in vitro transition of mouse ESCs (mESCs) from a naïve pluripotent state into epiblast-like cells (EpiLCs), a primed pluripotent state. We derived pseudotime expression trajectories to investigate transcript dynamics of key metabolic regulators, with the aim to identify metabolic pathways that potentially impact on early embryonic cell state transitions. Overall design: Single-cell RNA-seq during the in vitro differentiation of mouse embryonic stem cells (ESCs) in 2i culture conditions (time point t=0h) into epiblast-like cells (EpiLCs) at time points t=24h and t=48h.
Metabolic regulation of pluripotency and germ cell fate through α-ketoglutarate.
Specimen part, Cell line, Subject
View SamplesDemonstration of reduced biological effects with a prototypic modified risk tobacco product.
A 28-day rat inhalation study with an integrated molecular toxicology endpoint demonstrates reduced exposure effects for a prototypic modified risk tobacco product compared with conventional cigarettes.
Sex, Specimen part, Treatment
View Samples