We report the global gene expression of mouse pancreatic cells in a pancreas-specific conditional knock-out mouse for Gata6, as compared with age-matched controls. Total RNA was extracted from the pancreas of 6-8 -week old mice of the two genotypes and analyzed. at this age, Gata6P-/- pancreata are histologically normal, but the acinar differentiation programme is already altered. we observe that loss of Gata6 causes the de-repression of ectopic non-pancreatic genes, as well as some genes involved in the mesenchymal programme. Overall design: mRNA extracted from the pancreas of 4 controls and 4 Gata6P-/- mice was sequenced.
The acinar regulator Gata6 suppresses KrasG12V-driven pancreatic tumorigenesis in mice.
Specimen part, Cell line, Subject
View SamplesWe used microarrays to investigate gene expression changes induced by the inhibition of RRAS2 expression using shRNA techniques to stably knockdown the endogenous transcripts of this GTPase in human MDA-MB-231-Luc cells.
Contribution of the R-Ras2 GTP-binding protein to primary breast tumorigenesis and late-stage metastatic disease.
Cell line
View SamplesNANOG is a key pluripotency factor in embryonic stem cells that is frequently expressed in squamous cell carcinomas (SCCs). However, a direct link between NANOG and SCCs remains to be established. Here, we show that inducible overexpression of NANOG in mouse skin epithelia dramatically promotes the formation of carcinomas upon chemical carcinogenesis. Gene expression analyses in pre-malignant skin indicate that NANOG induces a large set of genes associated to stemness and to epithelial-mesenchymal transition (EMT). Overall design: 4 papillomas from different control mice (CTR), and 3 papillomas from different transgenic Nanog overexpressing mice (TG)
The pluripotency factor NANOG promotes the formation of squamous cell carcinomas.
No sample metadata fields
View SamplesmicroRNAs (miRNAs) regulate virtually all biological processes, but little is known of their role in germinal center (GC) B cells. While the GC reaction is crucial to ensure a competent immune response, GC B cells are also the origin of most human lymphomas. Here we report that miR-217 is specifically upregulated in GC B cells. Gain- and loss-of-function mouse models reveal that miR-217 functions as a positive modulator of the GC response through the regulation of a DNA repair gene network. Moreover, we show that miR-217 overexpression promotes mature B cell lymphomagenesis. Therefore miR-217 provides a novel molecular link between the normal GC response and B cell transformation Overall design: 4 samples were analyzed by RNAseq: 1) naïve (CD19+Fas-GL7-) B cells from miR-217TG, 2) GC (CD19+Fas+GL7+) B cells from miR-217TG, 3) naïve (CD19+Fas-GL7-) B cells from littermate controls and 4) GC (CD19+Fas+GL7+) B cells from littermate controls. Samples were isolated by cell sorting from pooled Peyer’s patches (4-6 animals per genotype). Two independent experiments were performed.
miR-217 is an oncogene that enhances the germinal center reaction.
Specimen part, Subject
View SamplesWe have generated “reprogrammable” transgenic mice that ubiquitously express the four Yamanaka factors in an inducible manner. Transitory induction of the transgene results in multiple teratomas emerging from a variety of organs, thus indicating that full reprogramming into iPSCs can occur in vivo. By performing bone marrow transplant experiments, we demonstrate that both hematopoietic cells, as well as non-hematopoietic cells can be reprogrammed in vivo. Remarkably, reprogrammable mice also present circulating iPSCs in the bloodstream (in vivo-iPSCs) with all the expected properties of bona fide iPSCs. Moreover, in contrast to in vitro-iPSCs or embryonic stem cells (ESCs), in vivo-iPSCs have an increased capacity to undergo trophectoderm lineage differentiation, which suggests that in vivo-iPSCs are more plastic or primitive than in vitro-generated iPSCs or ESCs. Overall design: 6 clones of in vivo-generated iPSCs, 5 indendent clones of in vitro-generated iPSCs, and 3 clones of established ESCs
Reprogramming in vivo produces teratomas and iPS cells with totipotency features.
Specimen part, Cell line, Subject
View SamplesWe report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the reporter gene LacZ (located next to the oncogene in the same polycistronic mRNA), by loading CD31-/CD45- pneumocytes with the LacZ-activated fuorogenic molecule FDG prior to FACS sorting. Overall design: Four replicates of each genetic group (Sirt1-WT and Sirt1-Tg) pneumocytes were used for this study. Sirt1-WT were used as reference controls.
Sirt1 protects from K-Ras-driven lung carcinogenesis.
Subject
View SamplesWe report the RNAseq data obtained from 50.000-100.000 CD31-/CD45- pneumocytes isolated by FACS from mice harboring a normal dose or one extra copy of the Sirt1 gene, and a tamoxifen-inducible oncogenic KI alelle of KRasG12V after 4 weeks of tamoxifen treatment plus 2 weeks without tamoxifen. Pneumocytes with the activated form of the inducible KRasG12V oncogene sere selected making use of the fluorescent reporter gene Katushka (located at an independent locus), by detecting Katushka fluorescence. Overall design: Four replicates of each genetic group (Sirt1-WT and Sirt1-Tg) pneumocytes were used for this study. Sirt1-WT were used as reference controls.
Sirt1 protects from K-Ras-driven lung carcinogenesis.
Sex, Subject
View SamplesBET-regulated transcriptome and BRD4, BRD2, BRD3 and Pol II ChIP-seq datasets in human ESCs before and after BET inhibition. Transcription factors and chromatin remodeling complexes are key determinants of embryonic stem cell (ESC) identity. In this study, we investigate the role of BRD4, a member of the bromodomain and extra-terminal domain (BET) family of epigenetic reader proteins, in control of ESC identity. We performed RNA-seq analyiss in the presense of small molecule inhibitors of BET proteins to show that BRD4 positively regulates the ESC transcriptome. We also integrated RNA-seq analysis with ChIP-sequencing datasets s for BRD4 (and for other BRD2 and BRD3) to demonstrate that BRD4 binds SEs and regulates the expression of SE-associated pluripotency genes. We have also conducted ChIP-seq analysis for Pol II binding to demonstrate that SE-associated genes depend on BRD4-dependent Pol II binding at TSS and gene body for their productive transcriptional elongation. Overall design: Total RNA was extracted from samples using the RNeasy Qiagen kit according to the manufacturer’s instructions. Deep sequencing of RNA (1ug) from hESCs FGF- or MS436-treated at day 1 and day 5 was performed as described in (Higgin et al., 2010c). Samples were subjected to PolyA selection using magnetic oligo-dT beads. The resulting RNA samples were then used as input for library construction as described by the manufacturer (Illumina, CA, USA). RNA libraries were then sequenced on the GAIIx system using 50bp single reads. Chromatin for ChIP-sequencing was obtained from FGF-maintained hESCs, vehicle or MS417-treated (at 250nM concentration for 6h) (10 to 20x106 cells/IP). ChIP-Seq libraries were generated using standard Illumina kit and protocol as described in (Ntziachristos et al., 2012). We performed cluster amplification and single read 50 sequencing-method using the Illumina HiSeq 2000, following manufacturer’s protocols.
Control of embryonic stem cell identity by BRD4-dependent transcriptional elongation of super-enhancer-associated pluripotency genes.
No sample metadata fields
View SamplesGene expression analysis in hLECs treated with gain of function or loss of function of MDK in human melanoma cells. Overall design: Biological triplicates of hLEC treated for 3 days with EGM-2 MV conditioned media of melanoma cells. Cell line SK-Mel-147 KD for MDK (shMDK) and its corresponding control (shCtrl (LoF) and WM164 cell line overexpressing MDK (MDK) or an empty vector (NEG) (GoF) were used to produce the conditioned media.
Whole-body imaging of lymphovascular niches identifies pre-metastatic roles of midkine.
Specimen part, Subject
View SamplesExponentially growing cells and type II persister cells from the DS1-(hipQ)-strain
Novel protocol for persister cells isolation.
Specimen part, Disease, Cell line
View Samples