status: Public on Sep 01 2013

city: Shenzhen

first: Jiahao

last: Chen

state: Guangdong

address: Beishan road, Yantian district

department: Cancer Research Group

institute: Beijing Genomics Institute

summary: Genome-wide gene expression profile using deep sequencing technologies can drive the discovery of cancer biomarkers and therapeutic targets. Such efforts are often limited to profiling the expression signature of either mRNA or microRNA (miRNA) in a single type of cancer.Here we provided an integrated analysis of the genome-wide mRNA and miRNA expression profiles of three different genitourinary cancers: carcinomas of the bladder, kidney and testis.Our results highlight the general or cancer-specific roles of several genes and miRNAs that may serve as candidate oncogenes or suppressors of tumor development. Further comparative analyses at the systems level revealed that significant aberrations of the cell adhesion process, p53 signaling, calcium signaling, the ECM-receptor and cell cycle pathways, the DNA repair and replication processes and the immune and inflammatory response processes were the common hallmarks of human cancers. Gene sets showing testicular cancer-specific deregulation patterns were mainly implicated in processes related to male reproductive function, and general disruptions of multiple metabolic pathways and processes related to cell migration were the characteristic molecular events for renal and bladder cancer, respectively. Furthermore, we also demonstrated that tumors with the same histological origins and genes with similar functions tended to group together in a clustering analysis. By assessing the correlation between the expression of each miRNA and its targets, we determined that deregulation of 'key' miRNAs may result in the global aberration of one or more pathways or processes as a whole.This systematic analysis deciphered the molecular phenotypes of three genitourinary cancers and investigated their variations at the miRNA level simultaneously. Our results provided a valuable source for future studies and highlighted some promising genes, miRNAs, pathways and processes that may be useful for diagnostic or therapeutic applications.

overall_design: Examination of microRNA expression of cancer and matched adjacent tissues from 7 testicular germ cell tumors and 10 transitional cell carcinomas of bladder

first: Zhizhong

last: Li


country: China

type: Expression profiling by high throughput sequencing

overall_design: Examination of mRNA expression of cancer and matched adjacent tissues of 7 testicular germ cell tumors and 10 transitional cell carcinomas of bladder


title: Effects of group III phospholipase A2 deficiency in mast cells on fibroblast-directed maturation of mast cells in vitro

status: Public on Mar 09 2013

city: Tokyo

first: Yoshitaka

last: Taketomi

address: 7-3-1 Hongo, Bunkyo-ku,

department: CDBIM, Graduate School of Medicine,

country: Japan

institute: The University of Tokyo

summary: Microenvironment-based alterations in mast cell phenotypes influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 synthase (L-PGDS) to provide PGD2, which facilitates mast cell maturation via PGD2 receptor (DP1). Mice lacking PLA2G3, L-PGDS or DP1, mast cell-deficient mice reconstituted with PLA2G3- or DP1-null mast cells, or mast cells cocultured with L-PGDS-ablated fibroblasts exhibited impaired mast cell maturation and anaphylaxis. Thus, we describe a lipid-driven PLA2G3-L-PGDS-DP1 loop that drives mast cell maturation.

overall_design: Model, in vitro mast cell maturation; Cells, bone marrow-derived mast cells (BMMCs) cocultured with Swiss 3T3 fibroblasts; Condition, 4 condition experiments: BMMCs cocultured with (mature) versus without (immature) fibroblasts, Pla2g3 knockout (–/–) versus Pla2g3 wild-type (+/+); Samples, 3 replicates of Pla2g3+/+ BMMCs, 4 replicates of Pla2g3–/– BMMCs, 4 replicates of Pla2g3+/+ cocultuzred BMMCs, 3 replicates of Pla2g3–/– cocultured BMMCs

first: Yasumasa

last: Nishito

first: Makoto

last: Murakami


title: Analysis of Pro-Inflammatory Gene Activation and RNA Processing by RNAseq of Nascent Transcripts [supplement]

status: Public on Jul 01 2012

city: Los Angeles

first: Stephen

last: Smale

state: Ca

address: 6-730 MRL 675 Charles E. Young Drive South

department: MIMG

country: USA

institute: University of California Los Angeles

summary: Note: These datasets are in supplement to, but separate from, Geo GSE32916. We examined pro-inflammatory gene activation in activated wildtype and IFNAR-/- murine macrophages by performing RNA-Seq with poly(A) enriched transcripts. This experimental strategy allowed a global, high-resolution analysis of the transcriptional regulation of diverse classes of co-expressed genes and allowed us to identify co-expressed gene classes that may depend on IFN-signaling for its expression. The results provide quantitative insights into the relationship between transcription and distinct promoter and chromatin properties.

overall_design: RNA-seq of poly(A) enriched RNA from five stimulation time-points in wildtype and IFNAR-/- macrophages

middle: T

first: Ann-Jay

last: Tong

first: Dev

middle: M

last: Bhatt


title: Response of peripheral blood mononuclear cells to influenza virus, human cytomegalovirus, and candida albicans derived peptide stimulation.

status: Public on Aug 15 2016

city: Seattle,

first: Stephanie

last: Osmond

state: WA

address: 1201 9th Ave

institute: Benaroya Research Institute

summary: CD4 T cell responses are characterized based on a limited number of molecular markers selected from exisiting knowledge. The goal of the experiment was to assess antigenic-peptide specific T-cell responses in vitro without bias using microarrays.

overall_design: PBMCs were isolated from 1 healthy donor. The cells were stimulated with peptides derived from influenza virus H1 and H5, human cytomegalovirus, and candida albicans for 24 hours. Unstimulated cells were cultured without the peptides for 24 hours.

first: Shinobu

last: Yamamoto

first: Elizabeth

last: Whalen

first: Daisuke

last: Chujo

first: Durgha

last: Nattamai

first: Nicole

last: Baldwin

first: Kimberly

last: O'Brien

first: Quynh-Anh

last: Nguyen

first: Vivan

last: Gersuk

first: Esperanza

last: Anguiano

first: Junbao

last: Yang

first: William

last: Kwok

first: Jacques

last: Banchereau

first: Gerald

last: Nepom

first: Hideki

last: Ueno

first: Damien

last: Chaussabel


title: Comparative mRNA and microRNA expression profiling of three genitourinary cancers reveals common hallmarks and cancer-specific molecular events

first: Jiahao

last: Chen

type: Non-coding RNA profiling by high throughput sequencing

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Radiation responses in peripheral white blood cells of smokers and non-smokers

status: Public on Mar 16 2011

city: New York

first: Sally

last: Amundson

state: NY

department: Center for Radiological Research

institute: Columbia University

summary: Understanding the possible impact of potential confounding factors is necessary for any approach to radiation biodosimetry.  Potential confounding factors have not been fully addressed for gene expression-based biodosimetry approaches, such as we are developing.  To begin addressing this need, we have used an ex vivo irradiated peripheral blood cell model to investigate the potential effect of smoking on the global radiation gene expression response, and looked for genes that respond to radiation differently in smokers and non-smokers, and also in males and females. The results indicate that only a small number of genes may be significantly confounded by either factor, supporting the idea of developing peripheral blood gene expression strategies for radiation biodosimetry.

overall_design: Blood from each of 24 different donors was exposed to four doses of ionizing radiation (0, 0.1, 0.5, or 2 Gy) and analyzed using single-color microarray hybridization.  The donors represented equal numbers of male and female smokers (1 or more packs a day) and non-smokers.  There are 95 data sets in the study as the sample from one of the female smokers exposed to 2 Gy was lost.

middle: A

first: Paul

last: Sunirmal


title: Streptomyces coelicolor M600 BldD ChIP-chip comparison of wild-type with bldD null mutant

status: Public on Aug 04 2010

city: Norwich

first: Chris

last: den Hengst

state: Norfolk

address: Colney

department: Molecular Microbiology

country: United Kingdom

institute: John Innes Centre

type: Genome binding/occupancy profiling by array

summary: BldD is a transcriptional regulator essential for morphological development and antibiotic production in Streptomyces coelicolor. Here we identify the BldD regulon by means of chromatin immunoprecipitation. The BldD regulon encompasses ~167 transcriptional units, of which more than 20 are known to play important roles in development and/or secondary metabolism. Strikingly, 42 BldD target genes (~25% of the regulon) encode regulatory proteins, stressing the central, pleiotropic role of BldD. Almost all BldD-binding sites identified by ChIP-chip are present in the promoters of the target genes. An exception is the tRNA gene bldA, where BldD binds within the region encoding the primary transcript, immediately downstream of the position corresponding to the processed, mature 3′-end of the tRNA. We identified a novel BldD target gene (cdgA) that influences differentiation and antibiotic production. cdgA encodes a GGDEF domain protein, implicating c-di-GMP in the regulation of Streptomyces development.

overall_design: ChIP-chip exp comparing IP with BldD antibody against total DNA control in wild-type strain vs bldD mutant strain. Wild-type strain was analysed in triplicate

first: Ngat

last: Tran

first: Maureen

last: Bibb

first: Govind

last: Chandra

first: Brenda

last: Leskiw

first: Mark

last: Buttner


title: Analysis of Pro-Inflammatory Gene Activation and RNA Processing by RNAseq of Nascent Transcripts I

status: Public on May 03 2012

first: Stephen

last: Smale

summary: We examined pro-inflammatory gene activation in activated murine macrophages by performing RNA-Seq with fractionated chromatin-associated, nucleoplasmic, and cytoplasmic transcripts. This experimental strategy allowed a global, high-resolution analysis of the transcriptional regulation of diverse classes of co-expressed genes, with a direct comparison to transcript processing and the transit of RNA from the chromatin to the nucleoplasm and the cytoplasm. The results provide quantitative insights into the relationship between transcription and distinct promoter and chromatin properties, as well as genome-scale insights into RNA processing and dynamics.

overall_design: RNA-seq of subcelluar fractions from five stimulation time-points

first: Dev

last: Bhatt

first: Ann-Jay

last: Tong


title: Affymetrix Arrays Interrogated with Tumor/Normal Pancreatic Samples

status: Public on Jul 01 2011

city: Houston

first: Nanyue

state: TX

address: 1515 Holcombe Blvd

institute: UT MD Anderson Cancer Center

summary: To identify genes in the chromosome 3p12 pathway to tumorigenesis in pancreatic cancer, we screened two expression platforms and then as a third platform interrogated pancreatic cancer tumor/normal samples for differential expression.  Data from the third expression platform experiments are shown herein.

overall_design: Frozen tumor and adjacent normal tissue were obtained from untreated, retrospective pancreatic adenocarcinoma samples available from the M. D. Anderson Cancer Center tumor bank and our collaborator (MLF). Total RNA from matched tumor/adjacent normal samples (8 paired samples) was utilized to interrogate the GeneChip U133 plus 2.0 array and resultant bioinformatic analysis performed to identify differentially expressed sequences across all three platforms.

first: Ann

last: Killary


title: mid-L3_25dC_25hrs_post-L1_N2_tiling_array

status: Public on Aug 05 2010

city: Toronto

first: DCC

last: modENCODE

state: Ontario

address: MaRS Centre, South Tower, 101 College Street, Suite 800

country: Canada

institute: Ontario Institute for Cancer Research

type: Expression profiling by genome tiling array

summary:
modENCODE_submission_474
This submission comes from a modENCODE project of Robert Waterston. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: Our experiments are designed to detect all C. elegans transcripts by hybridizing RNA to commerically available genome tiling arrays. To maximize the chances of detecting rare transcripts with limited expression in specific cells, we are extracting RNA from selected embryonic cells isolated by FACS and from postembryonic cells by use of the mRNA tagging method.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

Keywords: Transcript tiling array analysis

overall_design: EXPERIMENT TYPE: Transcript tiling array analysis. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: larva mid-L3 25dC 26.75 hrs post-L1; Genotype: wild type; Sex: Hermaphrodite;  NUMBER OF REPLICATES: 3;  EXPERIMENTAL FACTORS: Strain N2; Developmental Stage larva mid-L3 25dC 26.75 hrs post-L1

first: Bob

last: Waterston

first: Valerie

last: Reinke

last: Gerstein

first: Mike

last: Wilson

first: Ashish

last: Argiwal


title: TRIB1 suppression on human hepatocytes transcriptome

status: Public on Apr 13 2015

city: Ottawa

first: Ruth

last: McPherson

address: 40 Ruskin

institute: UOHI

summary: The TRIB1 locus has been associated with lipid dysfunction.  The underlying mechanisms were investigated by examining the transcription landscape in response to TRIB1 suppression in human primary hepatocytes.

overall_design: Primary hepatocytes from 3 distinct donors were exposed for  48 h to an antisense nucleotide targeting TRIB1 or a control nucleotide.  The resulting impacts on the transcription profile were assessed using Human Transcriptome 2.0 microarrays (Affymetrix).

first: Sebastien

last: Soubeyrand


title: Comparisons of the transcriptional profiles between rat aorta and ductus arteriosus

status: Public on Sep 30 2007

city: Setagaya

first: Yoji

last: Sato

state: Tokyo

address: 1-18-1 Kami-yoga

department: Cell. Gene Thpy. Prod.

institute: NIHS

summary:
The transcriptional profiles of the aorta and the ductus arteriosus during development were compared.
Keywords: time course, development, tissue type comparison

overall_design: Total RNA samples were isolated from pooled tissues obtained from Wister rat embryos on embryonic day 19 and 21, and from neonates on the day of birth (n>=120). The RNA was converted to biotin-labeled cRNA, which was hybridized to Affymetrix RG_U34A microarray. The hybridization experiments were performed in duplicate.

first: Utako

last: Yokoyama

first: Seiichi

last: Ishida

first: Junichi

last: Sawada

first: Yasuo

last: Ohno

first: Mari

last: Iwamoto

first: Hideaki

last: Hori

first: Shumpei

last: Yokota

first: Yoshihiro

last: Ishikawa

first: Susumu

last: Minamisawa


title: Expression data from TRIBAL antisense knock-down in Huh7 hepatoma cells

status: Public on Feb 14 2014

summary: Objective - The TRIB1 locus has been linked to hepatic triglyceride metabolism in mice and to plasma triglycerides and coronary artery disease (CAD) in humans. The lipid associated SNPs identified by genome-wide association studies (GWAS) are located ~ 30 kb downstream from TRIB1 suggesting complex regulatory effects on genes or pathways relevant to hepatic triglyceride metabolism. The goal of this study was to investigate the functional relationship between common SNPs at the TRIB1 locus and plasma lipid traits.  Methods & Results - Characterization of the risk locus reveals that it encompasses a gene, TRIB1 associated locus (TRIBAL) comprised of a well conserved promoter region and an alternatively spliced transcript. Bioinformatic analysis and re-sequencing identified a single nucleotide polymorphism (SNP), rs2001844, within the promoter region that associates with increased plasma triglycerides, reduced HDL-C and CAD risk. Furthermore, we show that rs2001844 is an expression trait locus (eQTL) for TRIB1 expression in blood and alters TRIBAL promoter activity in a reporter assay model. The TRIBAL transcript has features typical of long noncoding RNAs (lncRNA), including poor sequence conservation. Modulation of TRIBAL expression had limited impact on either TRIB1 or lipid regulatory genes mRNA levels in human hepatocyte models. In contrast, TRIB1 knockdown markedly increased TRIBAL expression in HepG2 cells and primary human hepatocytes.  Conclusions - These studies demonstrate an interplay between a novel locus,TRIBAL, and TRIB1. TRIBAL is located in the GWAS identified risk locus, responds to altered expression of TRIB1, harbors a risk SNP that is an eQTL for TRIB1 expression and associates with plasma triglyceride concentrations.

overall_design:
Transcriptome changes to TRIBAL downregulation (48 h)
Huh7 were exposed to non-target or TRIBAL-specific antisense oligonucleotides for 48 h in normal (low glucose DMEM, 10% serum, Pen-Strep)

first: A

last: Douvris

first: S