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Accession Number: GSE97047 Platform: GPL19057: Illumina NextSeq 500 (Mus musculus) GPL20084: Illumina NextSeq 500 (Rattus norvegicus) Organism: Mus musculus Published on 2018-01-03 Summary: We report whole tissue transcriptomes from rat and mouse wounds, as well as rat inter-follicular epidermis Overall Design: Total RNA was isolated from adult rat and mouse whole tissues. Tissues included rat and mouse wound dermis and wound epidermis collected one day after scab detachment, the time point that coincides with hair follicle regeneration in mice, and vaccum-suction isolated rat inter-follicular epidermis. Contact: Name: Maksim V Plikus Organization: University of California, Irvine Deparment: Developmental and Cell Biology Address: 845 Health Sciences Road Irvine California 92697 USA Email: plikus@uci.edu Phone: 949-824-1260 Organization: GEO Address: USA
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Accession Number: GSE90128 Platform: GPL19168: Illumina MiSeq (Escherichia coli K-12) Organism: Escherichia coli K-12 Published on 2018-01-03 Summary: Recently, we developed an in vivo technology to draw the interacting map of a specific small regulatory RNA (sRNA). We called it MAPS for MS2-affinity purification coupled with RNA sequencing. Using this technology, we already revealed the targetome of RyhB, RybB and DsrA, three well-characterized sRNAs in Escherichia coli. In this study, we performed MAPS with CyaR sRNA. Overall Design: Identification of RNAs co-purified with MS2-CyaR in a rne131 ΔcyaR strain. CyaR (without MS2) was used as control. Contact: Name: Eric Massé Organization: Université de Sherbrooke Laboratory: Eric Massé Lab Deparment: Biochemistry Address: 3201, Jean Mignault Sherbrooke Québec Canada Email: eric.masse@usherbrooke.ca Organization: GEO Address: USA
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Accession Number: GSE95478 Platform: GPL13112: Illumina HiSeq 2000 (Mus musculus) Organism: Mus musculus Published on 2018-01-03 Summary: Activating Kras mutations are the hallmark genetic alterations in pancreatic ductal adenocarcinoma (PDAC) and key drivers of PDAC initiation and progression. Despite increased efforts to develop novel Kras inhibitors, the degree of Kras oncogene addiction in PDAC cells remains unclear. Here, we analyzed the requirement of endogenous Kras for the maintenance of murine PDAC cells using an inducible shRNA-based system that enables temporal control of endogenous Kras expression. Surprisingly, the majority of murine PDAC cells analyzed tolerated acute and sustained Kras knockdown by adapting to a reversible cell state, characterized by differences in cell morphology, proliferative kinetics, and tumor-initiating capacity. While significant mutational or transcriptional changes were not observed in the Kras-inhibited state, global phosphoproteomic profiling revealed alterations in cell signaling, including increased phosphorylation of focal adhesion pathway components. Accordingly, Kras-inhibited cells displayed prominent focal adhesion plaque structures, enhanced adherence properties, and increased dependency on adhesion for viability in vitro. Our analyses highlight the possibility of adaptive non-genetic and non-transcriptional mechanisms of resistance to Kras inhibition. Furthermore, we have identified candidate proteins whose signaling activities are altered in the Kras-inhibited state, providing a basis for the rational design of combination therapeutic strategies with novel Kras inhibitors. Overall Design: 6 DOX-inducible shKras-expressing clones derived from 3 parental pancreatic tumor cell lines (A, B, and D; 2 clones per cell line) were treated with doxycycline (DOX) to induce Kras knockdown. One control DOX-inducible shLuc-expressing line was used as a control. RNA-sequencing was performed on long-term DOX-treated (LT DOX) or untreated (No DOX) cells. Technical replicates for specific samples are noted. Contact: Name: A Bhutkar Organization: MIT Address: 77 Massachusetts Avenue Cambridge MA 02139 USA Organization: GEO Address: USA
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Accession Number: GSE108678 Platform: GPL17021: Illumina HiSeq 2500 (Mus musculus) Organism: Mus musculus Published on 2018-01-03 Summary: RNA-seq of RNA isolated from E10.5 mandibular prominence of 3 control and 3 Tfap2a;Tfap2b;Wnt1CRE mutant mouse embryos. Overall Design: E10.5 mutant and litter-matched control embryos were dissected in ice-cold PBS. Subsequently, the mandibular prominences were carefully dissected from each embryo and stored in RNAlater (Ambion/Life Technologies) until later use. Following genotyping, RNA was extracted, essentially as previously described (Van Otterloo et al., 2016), from paired (i.e. left and right) mandibular prominences (3 control and 3 DCM embryos – 3 biological replicates) using the microRNA Purification Kit (Norgen Biotek Corp., Thorold, ON), following manufacturer's protocol. Following elution, mRNA was further purified using the Qiagen RNeasy Kit (Qiagen, Valencia, CA), according to manufacturer's protocol. Quality of extracted mRNA was assessed using DNA Analysis ScreenTape (Agilent Technologies, Santa Clara, CA) to ensure that it was of sufficient quality for library production. Following validation of extracted mRNA, cDNA libraries were generated using the Illumina TruSeq Stranded mRNA Sample Prep Kit (Illumina, San Diego, CA). Following library generation and subsequent quality control assessment, cDNA was sequenced using the Illumina HiSeq2500 platform and single-end reads (1x150). Contact: Name: Eric Van Otterloo Organization: University of Colorado - Denver Laboratory: Trevor Williams Deparment: Craniofacial Biology Address: 12801 E 17th Ave Aurora Colorado 80045 USA Email: eric.vanotterloo@ucdenver.edu Organization: GEO Address: USA
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Accession Number: GSE94529 Platform: GPL21530: Illumina HiSeq 2000 (Escherichia coli str. K-12 substr. W3110) Organism: Escherichia coli str. K-12 substr. W3110 Published on 2018-01-03 Summary: Peptides have great potential to combat antibiotic resistance. While many platforms can screen peptides for their ability to bind to target cells, there are virtually no platforms that directly assess the functionality of peptides. This limitation is exacerbated when identifying antimicrobial peptides, since the phenotype, death, selects against itself, and has caused a scientific bottleneck confining research to only a few naturally occurring classes of antimicrobial peptides. We have used this seeming dissonance to develop Surface Localized Antimicrobial displaY (SLAY); a platform that allows screening of unlimited numbers of peptides of any length, composition, and structure in a single tube for antimicrobial activity. Using SLAY, we screened ~800,000 random peptide sequences for antimicrobial function and identified thousands of active sequences doubling the number of known antimicrobial sequences. SLAY hits present with different potential mechanisms of peptide action and access to areas of antimicrobial physicochemical space beyond what nature has evolved. Overall Design: An 800,000 random peptide library was genetically encoded into our surface display system.We used high-throughput sequencing (Hi-seq) to identify surface expressed peptides with antimicrobial activity against E. coli. Samples include a non-induced and an induced (4- hours post-induction) in duplicate. Please note that the Miseq run was a much smaller set of peptides than the Hiseq run. Also the miseq run had samplings at 0, 2, 3 and 4 hours rather than just 0 and 4 hours in the Hiseq. Downstream analysis was the same. Contact: Name: Bryan Davies Organization: University of Texas at Austin Address: 2506 Speedway Austin TX 78712 USA Email: bwdavies@utexas.edu Organization: GEO Address: USA
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Accession Number: GSE101829 Platform: GPL13915: 3D-Gene Human Oligo chip 25k V2.1 Organism: Homo sapiens Published on 2018-01-03 Summary: Transcriptional profiling of human bronchial epithelial cell lines and primary cells. Parental normal 16HBE14o- cells were stably transfected with beta/gammaENaC to generate beta/gammaENaC-16HBE14o- cells. NHBE and DHBE-CF were obtained from TaKaRa. Overall Design: Two-condition experiment, 16HBE14o- vs. beta/gammaENaC-16HBE14o- cells and NHBE vs. DHBE-CF cells. Biological replicates: One replicate per array. Contact: Name: Satoshi Kondo Organization: Toray Industries,Inc. Deparment: New Projects Development Division Address: Tebiro 6-10-1 Kamakura Kanagawa Japan Email: Satoshi_Kondou@nts.toray.co.jp Name: Tsuyoshi Shuto
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Accession Number: GSE93069 Platform: GPL20301: Illumina HiSeq 4000 (Homo sapiens) Organism: Homo sapiens Published on 2018-01-03 Summary: The multi-kinase inhibitor drug sorafenib is used as first line treatment for hepatocellular carcinoma and advanced renal cell carcinoma. Sorafenib mainly undergos cytochrome P450 (CYP) 3A4-mediated oxidation and uridine diphosphate glucuronosyl transferase (UGT) 1A9-mediated glucuronidation in liver, but the biotransformation of sorafenib in kidney remains unclear. Therefore, we integrated the mRNA expression data of 36 kidney samples and the corresponding metabolic activities for sorafenib to study the metabolic mechanism of sorafenib in kidney. Overall Design: Kidney mRNA profiles of 36 patients undergoing nephrectomy were generated by deep sequencing, using Illumina HiSeqTM 4000 Contact: Name: Lan Tang Organization: Southern Medical University Laboratory: Biopharmaceutics Deparment: School of Pharmaceutical Science Address: 1838 Guangzhou North Ave, Guangzhou Guangdong China Email: tl405@smu.edu.cn Phone: +86 20 61648596 Organization: GEO Address: USA
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Accession Number: GSE97389 Platform: GPL17021: Illumina HiSeq 2500 (Mus musculus) Organism: Mus musculus Published on 2018-01-03 Summary: Comparison of transcriptome between control and NIK-stabilized leukemia stem cells Overall Design: murine MLL-AF9 acute myeloid leukemia was generated using bone marrow progenitor cells (lin-cKit+) from NIKERT2 mice (crossing Rosa-loxp-STOP-loxp-NIK mice with Rosa-CreERT2 mice). Leukemia stem cells were sorted by FACS from tamoxifen treated (LSPCT group) and untreated (LSPC group) fully developed leukemia mice and used for RNAseq analysis. Contact: Name: Thomas B Bair Organization: University of Iowa Address: 335 EMRB Iowa City IA 52242 USA Email: iihg-bioinformatics@uiowa.edu Organization: GEO Address: USA
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Accession Number: GSE102870 Platform: GPL16791: Illumina HiSeq 2500 (Homo sapiens) Organism: Homo sapiens Published on 2018-01-02 Summary: We discovered a rare missense mutation in NR1H4 (R436H), which encodes the farnesoid X receptor (FXR), associating with lower levels of total cholesterol in the Icelandic population. To explore the effects of R436H we used CRISPR-Cas9 to generate homozygous NR1H4 R436H and NR1H4 knockout human iPSC lines which we differentiated to hepatocytes. Hepatocytes were treated with an FXR agonist for 24 hours and transcript abundance measured by RNA-seq. The global response to FXR activation in NR1H4 R436H cells was very similar to that of wild-type cells showing that it is not a loss-of-function mutation. However, we did observe subtle gene expression differences compatible with an effect on lipids when we compared R436H agonist treated hepatocytes to wild-type agonist treated hepatocytes. Overall Design: RNA-seq was performed on wild-type, NR1H4 knockout and NR1H4 R436H iPSC-derived hepatocytes treated with FXR agonist GW4064. Contact: Name: Aimee Deaton Organization: Amgen Inc Address: 360 Binney St Cambridge MA 02142 USA Email: adeaton@amgen.com Organization: GEO Address: USA
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Accession Number: GSE101290 Platform: GPL13821: Illumina HiSeq 2000 (Saccharomyces cerevisiae) GPL19756: Illumina NextSeq 500 (Saccharomyces cerevisiae) Organism: Saccharomyces cerevisiae Published on 2018-01-02 Summary: We performed RNA-seq across the yeast metabolic cycle (YMC) in wild-type and a strain lacking ARP5, a central component of the INO80 chromatin remodelling complex. We also perform ATAC-seq on the same samples to examine chromatin architecture across the YMC. Overall Design: RNA-seq and ATAC-seq in wild-type and arp5∆ yeast Contact: Name: Graeme Gowans Organization: Stanford University Laboratory: Ashby Morrison Deparment: Biology Address: Gilbert Building, 371 Serra Mall Stanford CA 94305 USA Email: ggowans@stanford.edu Organization: GEO Address: USA
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