title: Effect of BRCA1 heterozygous mutation on gene expression

city: Madrid

first: Tereza

last: Vaclova

address: C/ Melchor Fernández Almagro, 3

department: Human Cancer Genetics

institute: CNIO - Spanish National Cancer Research Centre

summary: In order to investigate whether carriers of BRCA1 heterozygous mutation show altered gene expression profiles, we used a whole genome microarray expression profiling of a panel of lymphoblastoid cell lines (LCLs) harboring either mutated or WT BRCA1 (control). We were especially interested whether we find differences in gene expression between carriers of missense versus truncating mutation in BRCA1 gene.

overall_design: We evaluated gene expression of a panel of 21 non-treated lymphoblastoid cell lines (LCLs). Among them, 6 LCLs with WT BRCA1, 5 LCLs carrying missense mutation in BRCA1, and 10 LCLs harboring truncating mutation in BRCA1 were included in this study.

last: Vaclová


title: Deoxynivalenol affects the gene expression of A549 lung epithelial cells

status: Public on Feb 29 2016

city: Obihiro

first: Takahito

last: Toyotome

state: Hokkaido

address: Nishi 2-11, Inada-cho

department: Diagnostic Center for Animal Health and Food Safety

country: Japan

institute: Obihiro University of Agriculture and Veterinary Medicine

summary: Deoxynivalenol (DON) is an important Fusarium toxin of concern for food safety. The inhalation of powder contaminated with deoxynivalenol is possible and may cause lung toxicity. In this study, we investigated the gene expression profile of A549 cells treated with 0.2 microg/mL deoxynivalenol by microarray analysis. In total, 16 genes and 5 noncoding RNAs were significantly affected by deoxynivalenol treatment.

overall_design: 4 samples; 2 samples from nontreated cells and other 2 samples from 0.2 microg/mL DON-treated cells for 24 hours

first: Hiroki

last: Takahashi

first: Katsuhiko

last: Kamei


title: Palmitate-induced gene expression in human gingival fibroblasts (HGF)

status: Public on Dec 31 2015

city: Tokushima

first: Yosuke

last: Shikama

address: 2-50-1 Kuramoto-cho

department: Tokushima University Hospital

institute: Clinical Research Center for Diabetes

summary:
DNA microarray analysis was performed to investigate the expression of genes in HGF stimulated with palmitate
Type 2 diabetes (T2D) is characterized by decreased insulin sensitivity and higher concentrations of free fatty acids (FFAs) in plasma. Among FFAs, saturated fatty acids (SFAs), such as palmitate, have been proposed to promote inflammatory responses. Although many epidemiological studies have shown a link between periodontitis and T2D, little is known about the clinical significance of SFAs in periodontitis. The goal of this study is to demonstrate a potential link between the pathogenesis of periodontitis and SFAs in plasma.

overall_design: HGF were treated with either with 0 (1% Bovine serum albumin) or 100 µM Palmitate for 36 hours (n=2 each).


title: Microarray analysis of high-dose recombinant erythropoietin treatment of unilateral brain injury in neonatal mouse hippocampus

status: Public on Dec 11 2015

city: Seattle

first: James

middle: William

last: MacDonald

state: WA

address: 4225 Roosevelt Way NE

department: Environmental and Occupational Health Sciences

country: USA

institute: University of Washington

summary: Comparison of gene expression in the hippocampus of 10 day old sham-injured and brain-injured BALB-c mice, and examine the effects of high dose Epo on these conditions at 24 hours following injury.

overall_design: Four groups of six mice were treated with epo/no epo, injured/not injured.

first: Theodor

middle: K

last: Bammler

first: Richard

middle: P

last: Beyer

first: Sandra

middle: E

last: Juul


title: Expression data from rat skeletal muscle

status: Public on Dec 03 2015

city: Ann Arbor

first: Yu-yu

last: Ren

state: MI

address: 1241 Catherine St.

department: Human Genetics

institute: University of Michigan

summary:
We used old (~96-102 weeks of age) and young (~28-34 weeks of age) rats from HCR and LCR generations 29 and 32, respectively. The study included eight groups; HCR-Old-Exhausted (H-O-E, n=6), HCR-Old-Rest (H-O-R, n=6), HCR-Young-Exhausted (H-Y-E, n=6), HCR- Young -Rest (H-Y-R, n=6), LCR-Old-Exhausted (L-O-E, n=6), LCR-Old-Rest (L-O-R, n=6), LCR-Young-Exhausted (L-Y-E, n=6), and LCR- Young -Rest (L-Y-R, n=6). For the exhausted rats, dissections were performed within 10 min after the maximal running distance was reached.
We extracted skeletal muscle RNA from a total of 48 female animals (n=6 in each of the 8 group). Skeletal muscle tissue was obtained from the Extensor digitorum longus (EDL). All rats were dissected immediately after sacrificing, and all tissue samples were immediately weighed and snap frozen in liquid nitrogen, and stored at -80 ºC. Total RNA was extracted from frozen tissue with Trizol reagent (Invitrogen, Carlsbad, CA), treated with DNase-free (Invitrogen, Carlsbad, CA) and cleaned up with RNeasy columns (Qiagen, Hilden, Germany)

overall_design: We ran the skeletal muscle RNA on the Affymetrix Rat Gene ST 2.1 array. The microarray hybridizations were performed by the DNA sequencing Core at the University of Michigan according to the manufacturer’s instructions. We used the Affymetrix Expression ConsoleTM software to generate gene expression values from individual probe intensity (CEL) files. The microarray measures a total of 19,607 transcripts based on the Refseq database.

first: Jun

middle: Z

last: Li


title: ADP-ribose derived Nuclear ATP is Required for Chromatin Remodeling and Hormonal Gene Regulation

status: Public on Dec 01 2015

city: Barcelona

first: Roni

last: Wright

address: C/ Doctor Aiguader, 88

country: Spain

institute: CRG-Centre de Regulació Genòmica

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

overall_design: Refer to individual Series


title: Gene expression profiles from human splenic and circulating neutrophils

status: Public on Nov 12 2015

first: Jordi

last: Sintes

address: Dr Aiguader 88

department: B cell Biology

institute: IMIM

summary:
Compared to circulating neutrophils (NC cells), splenic neutrophils (NBH cells) have an activated phenotype and enhanced B cell-helper activity.
The transcriptome analysis of splenic and circulating neutrophils was performed to verify whether the enhanced B cell-helper activity of splenic neutrophils correlated with a specific gene signature.

overall_design: Unstimulated neutrophils were FACS sorted from the peripheral blood and spleen of six adult healthy subjects for RNA isolation and Agilent analysis.

first: Andrea

last: Cerutti

first: Irene

last: Puga

first: Linda

last: Cassis

first: Ramon

last: Garcia-Escudero


title: Effect of PARG or NUDIX5 inhibition on Progesterone Gene Expression Profiling

summary:
T47D cells were starved 0% FCS for 24 hours. Following starvation PARG was inhibited via the use of Tannic Acid (TA) and the gene expression in response to progesterone studied. Cells were stimiulated with R5020 for 1 or 6 hours.
NUDIX5 was reduced in T47D cells 48 hours prior to hormone induction via the use of NUDIX5 specific siRNA. Progesterone response and gene expression changes were analyzed as described above following 6 hours of R5020.

overall_design: T47D cells T0 (Time 0), T6 (6 hours R5020), TA; Tannic Acid

first: Miguel

last: Beato


title: Oncogenic Kras activates a hematopoietic-to-epithelial IL-17 signaling axis in preinvasive pancreatic neoplasia

status: Public on Feb 03 2016

city: Baltimore

first: Florencia

last: McAllister

state: MD

address: 401 N. Broadway

department: Sidney Kimmel Comprehensive Cancer Center

institute: The Johns Hopkins University

summary: Many human cancers are dramatically accelerated in the setting of chronic inflammation. However the specific cellular and molecular elements mediating this effect remain largely unknown. Using a murine model of pancreatic intraepithelial neoplasia (PanIN), we found that KrasG12D induces expression of functional IL-17 receptors on PanIN cells, and stimulates infiltration of the pancreatic stroma by IL-17-producing immune cells.  Both effects are augmented by chronic pancreatitis,  resulting in functional in vivo changes in gene expression among PanIN epithelial cells.  Forced IL-17 overexpression dramatically accelerates PanIN initiation and progression, while inhibition of IL-17 signaling using genetic or pharmacologic techniques effectively prevents PanIN formation.  Together, these studies suggest that a hematopoietic-to-epithelial IL-17 signaling axis is a potent and requisite driver of PanIN formation.

overall_design: In order to assess the functionality of IL-17 receptors on oncogenic pancreatic epithelium, we treated KCiMist1G + CP mice that had already developed mPanIN lesions with a cocktail of monoclonal antibodies directed against the IL-17 Receptor A (IL-17RA) and the cytokines IL-17A and IL-17F.  Beginning at 6 weeks following Kras activation, antibodies were administered by two IP injections during the week prior to sacrifice (Figure 7A). At week 7 mice were sacrificed and GFP+ mPanIN epithelial cells were isolated by FACS.  Microarray-based whole transcriptome expression analysis was performed comparing profiles from GFP+ cells sorted from mice that had received IL-17 neutralizing antibodies versus mice that received IgG isotype control antibodies.

first: Jennifer

middle: M

last: Bailey

first: Janivette

last: Alsina

first: Christopher

middle: J

last: Nirschl

first: Rajni

last: Sharma

first: Hongni

last: Fan

first: Yanique

last: Rattigan

first: Jeffrey

middle: C

last: Roeser

first: Rachana

middle: H

last: Lankapalli

first: Hao

last: Zhang

first: Elizabeth

last: Jaffee

first: Charles

middle: G

last: Drake

first: Franck

last: Housseau

first: Anirban

last: Maitra

first: Jay

last: Kolls

first: Cynthia

middle: L

last: Sears

first: Drew

last: Pardoll

first: Steven

middle: D

last: Leach


title: Opposite phenotypic effects and genetic dosage in mouse models of 16p11.2 deletion and duplication syndromes

status: Public on Nov 18 2015

city: ILLKIRCH

first: Yann

last: HERAULT

address: 1 rue Laurent Fries

country: France

institute: IGBMC/PHENOMIN-ICS

summary:
The 16p11.2 deletion and duplication syndromes have been associated with developmental delay and autism spectrum disorders, and a reciprocal effect on body mass index. Here we explored these links with new engineered mouse models carrying a deletion (Del/+) and duplication (Dup/+) of the whole 16p11.2 homologous Sult1a1-Spn region. On a pure genetic background, compared to wild-types, Del/+ mice carrying the deletion showed weight and adipogenesis deficits, hyperactivity, repetitive behaviors, and recognition memory deficits, whereas Dup/+ mice showed the opposite phenotypes and Del/Dup individuals displayed no changes. Alterations in social interaction were also observed in Del/+ and Dup/+ animals on a mixed genetic background.
Transcriptomic analysis revealed that the majority of genes located on the Sult1a1-Spn were dosage-sensitive and potentially implicated in the opposite phenotypes described above on the neurocognitive aspect. Nevertheless, the outcome of the 16p11 region genetic dosage on metabolism depends on different genetic contributions between human and mouse.

overall_design: We did transcriptomic analysis of animals carrying rearrangements for the 16p11.2 homologous region after behavioral characterisation.

first: Thomas

last: Arbogast

last: Herault


title: Integrin alpha3beta1-dependent gene expression in immortalized keratinocytes

status: Public on Oct 07 2015

city: Rensselaer

first: Sridar

middle: V

last: Chittur

state: NY

address: One Discovery Drive, CRC 342G

department: Center for Functional Genomics

institute: SUNY-University at Albany

summary:
Gene-level analysis of gene expression in immortalized mouse keratinocyte lines that express or lack integrin alpha3beta1
The laminin-332-binding integrin alpha3beta1 is expressed highly in the epidermis, but its roles in regulating gene expression programs that promote normal or pathological skin remodeling have not been underexplored previously.  In order to identify genes that are regulated by alpha3beta1 in keratinocytes, we used microarray approaches to identify alpha3beta1-dependent genes in mouse keratinocytes that were immortalized with SV40 large T antigen (i.e., MK cells).

overall_design: We used the Affymetrix Mouse Exon 1.0 ST platform to analyze biological replicates of MK cell lines that were derived from wild type mice or alpha3-null mice, as well as a variant of the latter in which alpha3 was rescued by transfection with a human alpha3 cDNA.  Array data was processed by Affymetrix Exon Array Computational Tool.

first: C

last: DiPersio

first: Dara

middle: S

last: Missan


title: TrAP expression in Arabidopsis thaliana lead to global reprogramming of endogenous genes

status: Public on Sep 29 2015

city: College Station

first: Claudia

middle: Marcela

last: Castillo-González

state: Texas

department: Biochemistry & Biophysics

institute: Texas A&M University

summary: We examined global expression profiles of 7-days old 35S-TrAP transgenic plants compared to Col-0 wild-type using an Affymetrix ATH1 GeneChip and identified 586 genes that are differentially expressed in the 35S-TrAP transgenic plants (q<0.005). Of these, 295 transcripts were elevated whereas 291 were reduced (Figure 2E). We performed real-time PCR and RNA blot assays to validate the microarray results for the differentially expressed genes (DEGs).

overall_design:
In total 10 samples; 5 Input files (5 different conditions) with the corresponding 5 RIP samples
biological replicate: col-0_seedling_rp2, col-0_seedling_rp3
biological replicate: TA_seedling_rp1, TA_seedling_rp2

first: Xiuren

first: Xiuying

last: Liu

first: Xiu-Jie

last: Wang


title: Cell culture of p63 knock out and wild type bladder epithelial stem cell

status: Public on Oct 01 2015

city: Houston

first: Frank

last: McKeon

state: TX

address: 3455 Cullen Blvd

department: Biology and Biochemistry

institute: University of Houston

summary: Although there are several reports describing a stem cell fraction to form urothelium and lineage tracing studies in urinary bladder, it is still unclear about stem cells in mouse bladder epithelium.  Here, we have established the cloning system of mouse stem cells from wild type and p63 knockout bladder.  We isolated stem/progenitor cells from wild type and p63 knockout epithelium.  From wild type bladder, we have cloned keratin 5-positive stem cells, and from p63 knockout epithelium, which loses basal cell fraction, we have cloned morphologically-distinct keratin 8 and claudin 3 positive stem cells, which may be reminiscent of intestinal metaplasia in bladder.

overall_design: From newborn mice (p63 knockout and wild type), bladder were collected and digested with collagenase for stem cell culture. Epithelial stem cells were cultured on 3T3 feeder cells. Colonies of epithelial stem cells from p63 knockout and wild type bladder were picked up, and total RNA was isolated with Picopure RNA isolation kit.  We used affymetrix mouse exon 1.0 st array to hybridize 2 samples from each of tissues (p63 knockout and wild types).

first: Yue

last: Hong

first: Wa

last: Xian

first: Yusuke

last: Yamamoto

first: Xia


title: Functional characterization of inflammatory bowel disease-associated gut dysbiosis in gnotobiotic mice

status: Public on Oct 10 2015

first: Hiroko

last: Nagao-kitamoto

address: 1150 W Medical Center Dr,

institute: The University of Michigan Medical school

summary:
Gut dysbiosis is closely involved in the pathogenesis of inflammatory bowel disease (IBD). However, it remains unclear whether IBD-associated gut dysbiosis plays a primary role in disease manifestation or is merely secondary to intestinal inflammation. Here, we established a humanized gnotobiotic (hGB) mouse system to assess the functional role of gut dysbiosis associated with two types of IBD - Crohn's disease (CD) and ulcerative colitis (UC).
In order to explore the functional impact of dysbiotic microbiota in IBD patients on host immune responses, we analyzed gene expression profiles in colonic mucosa of hGB mice colonized with healty (HC), CD, and UC microbiota.

overall_design: WT-GF and GB mice (HC, CD, UC) were sacrificed after 2 weeks from human microbiota reconstitution and collected colon tissue for RNA extraction and hybridization on Affymetrix microarrays. WT-GF: n=2, HC-Mb GB mice: n=4, CD-Mb GB mice: n=5, UC-Mb GB mice: n=5.

first: Andrew

middle: B

last: Shreiner

first: Merritt

last: Gillilland

first: Sho

last: Kitamoto

first: Chiharu

last: Ishii

first: Peter

last: Kuffa

first: M

last: El-Zaatar

first: H

last: Gasberge

first: Anna

last: Seekats

first: Jhansi

last: Leslie

last: Higgins

first: Vincent

last: Young

first: Shinji

last: Fukuda

first: John

middle: Y

last: Kao

first: Nobuhiko

last: Kamada


title: Genome-wide analysis of long noncoding RNA expression profile in non-alcoholic fatty liver disease

status: Public on Sep 08 2015

city: Changsha

first: sun

last: chuanzheng

address: tongzhipo

country: China

institute: The Third Xiangya Hospital of Central South Uiversity

type:
Expression profiling by array
Non-coding RNA profiling by array

summary: Non-alcoholic fatty liver disease (NAFLD) is a common liver disorder and affects approximately one third of the general population.Recent studies have shown that long non-coding (lncRNA) plays critical roles in a myriad of biological processes and human diseases,Since the roles of lncRNA in NAFLD remain unknown,they were investigated in the study.Our findings indicate that the expression profiles of lncRNAs has changed in NAFLD as compared with normal liver, and may provide novel insight into the molecular mechanism underlying the disease and potential novel diagnostic or therapeutic targets for NAFLD.

overall_design: Microarray expression profiling of mRNAs and lncRNAs were conducted using RNA extracted from five NAFLD liver tissues and five normal liver samples.

first: Sun

last: Chuanzheng

first: Huang

last: Feizhou

first: Liu

last: Xunyang

first: Yi

last: Zhongjie

first: Xiao

last: Xuefei

first: Yang

last: Mingshi

first: Hu

last: Gui

last: Huaizheng

first: Liao

last: liangkan

first: Yuan

last: Yuan


title: The differential expression of mRNAs and long noncoding RNAs between ectopic and eutopic endometrium of adenomyosis

status: Public on Oct 28 2015

city: Nanjing City

first: Cheng

last: Zhou

address: Hanzhong Road no.140

institute: Nanjing Medical University

summary: Adenomyosis, defined as ectopic endometrial tissue within the myometrium,  can often be misdiagnosed as multiple uterine leiomyomata or endometrial  thickening. We therefore performed a combined mRNA and long noncoding  (lnc)RNA microarray and bioinformatic analysis of eutopic and ectopic  endometrium in women with adenomyosis to better understand its  pathogenesis and help in the development of a semi-invasive diagnostic test.  A total of 586 mRNAs were increased and 305 mRNAs decreased in ectopic  endometrium of adenomyosis compared with eutopic endometrium, while 388  lncRNA transcripts were up-regulated and 188 down-regulated in ectopic  compared with paired eutopic endometrial tissue. Bioinformatic analysis  suggested a series of metabolic and molecular abnormalities in adenomyosis,  which have many similarities with endometriosis. Furthermore, our study  constitutes the first known report of lncRNA expression patterns in human  adenomyosis ectopic and eutopic endometrial tissue.

overall_design: Two-condition experiment, ectopic endometrium vs. eutopic endometrium. 3 samples,self-control

first: Ting

last: Zhang

first: Ji

first: Xiaobei

last: Ni

first: Ran

last: Huo

first: Zhonghua

last: Shi


title: Muscle Hypertrophy Induced by Myostatin Inhibition Accelerates Degeneration in Dysferlinopathy

status: Public on Sep 04 2015

first: Yun-Sil

last: Lee

state: Maryland

address: 725 North Wolfe Street, PCTB 803

department: Molecular Biology and Genetics

institute: Johns Hopkins University School of Medicine

summary: Because myostatin normally limits skeletal muscle growth, there is an extensive effort to develop myostatin inhibitors for clinical use.  One potential concern is that in patients with muscle degenerative diseases, inducing hypertrophy may increase stress on dystrophic fibers.  Here, we show that blocking the myostatin pathway in dysferlin mutant mice results in early improvement in histopathology but ultimately accelerates muscle degeneration.  Hence, benefits of this approach should be weighed against these potential detrimental effects.

overall_design: Affymetrix Mouse Exon 1.0 ST arrays were hybridized in three biologically independent experiments with RNA from quadriceps muscles of wt, Dysf-/-, F66, F66;Dysf-/- mice, and ACVR2B/Fc-injected wt and Dysf-/- mice at the age of 10 weeks (3 duplicates in 6 different groups, 18 samples).

first: C

last: Talbot Jr.

first: Se-Jin


title: Saturated fatty acids regulate retinoic acid signaling and suppress tumorigenesis by targeting fatty acid-binding protein 5

status: Public on Sep 25 2015

city: Cleveland

first: Liraz

last: Levi

state: OH

address: 9500 Euclid Avenue

department: Cellular and Molecular Medicine

institute: Lerner Research Institute; Cleveland Clinic

summary: Long chain fatty acids (LCFA) serve as energy sources, components of cell membranes, and precursors for signalling molecules. Here we show that these important biological compounds also regulate gene expression by controlling the transcriptional activities of the retinoic acid (RA)-activated nuclear receptors RAR and PPARβ/δ. Our data indicates that these activities of LCFA are mediated by FABP5, a protein that delivers ligands from the cytosol to nuclear PPARβ/δ. Both saturated and unsaturated LCFA (SLCFA, ULCFA) tightly bind to FABP5, thereby displacing RA and diverting it to RAR. However, while SLCFA inhibit, ULCFA activate the FABP5/PPARβ/δ pathway. By concomitantly promoting the activation of RAR and inhibiting the activity of PPARβ/δ, SLCFA suppress the growth and oncogenic properties of FABP5-expressing carcinoma cells both in cultured cells and in vivo.

overall_design: Mammary carcinoma line NaF was used to to examine the whole-genome effect of RAR and PPARd ligands on gene expression.

first: Zeneng

last: Wang

first: Mary

last: Doud

first: Stanley

last: Hazen

first: Noa

last: Noy


title: Gene expression profiling reveal different molecular pattern in G-protein coupled receptor protein signaling pathway between early- and late-onset preeclampsia

status: Public on Oct 27 2015

city: Guangzhou

first: Liang

state: Guangdong

address: Xingnan Road 521

department: Translational Medicine Research Center

institute: Guangdong Women and Children Hospital

summary:
Background: Early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE) has been regarded as two different phenotypes with heterogeneous manifestation. The underlying mechanisms remain elusive. Aim to gain insight into the pathogenesis of the two traits, we analyzed the placental gene expression profiles in preeclampsia placentas.

Methods: Whole genome-wide microarray was used to describe the gene expression profiles in the placenta tissues from patients with early-(n=7; <34 weeks), late-onset(n=8; >36 weeks) PE and their controls who delivered preterm (n=5;<34 weeks) or at term(n=5; >36 weeks) Genes were selected as differentially expressed upon a fold-change≥2 and q-value<0.05. qRT-PCR was undertaken to verify the results. Western blot was further performed to verify secreted genes at the protein level.

Results: A total of 627 genes were differentially expressed in early-compared with late-onset PE. Of these, 177 genes were up-regulated and 450 genes down-regulated in early-onset PE. Go analysis showed significant alteration in several biological processes, in addition to the processes which have been found before, such as immune and inflammatory response, cell adhension, female pregnancy and blood vessel development. We also found alteration in G-protein coupled receptor protein signaling pathway, G protein-coupled receptor 124 (GPR124) (P=0.0064) and MAS-related GPR, member F (MRGPRF)(P=0.0155 ) were both down-regulated obviously in early-onset PE.

Conclusion: The different gene expression profiles suggested early- and late-onset PE are separate disease entities. Moreover, G-protein coupled receptor protein signaling pathway may contribute to the mechanism underlying early- and late-onset preeclampsia.

overall_design: Whole genome-wide microarray was used to describe the gene expression profiles in the placenta tissues from patients with early-(n=7; <34 weeks), late-onset (n=8; >36 weeks) PE and their controls who delivered preterm(n=5;<34 weeks) or at term(n=5; >36 weeks). Pooled controls who delivered at term were labled with cy5.

first: Mengmeng

last: Liang

first: Jianmin

last: Niu

first: Hua

last: Deng

first: Jian

last: Ma

first: Weiping

first: Dongmei

last: Duan

first: Yuheng

first: Huikun

last: Xu

first: Longding

last: Chen


title: Expression Data from Memory P14 Tg CD8 T cells after either saline mock-infection, Pichinde Virus Infection (bystander infection) or Pichinde Virus infection with daily treatment with anti-CD122 (clone TM-b1)

status: Public on Sep 01 2015

city: Montreal

first: Martin

last: Richer

state: Quebec

address: 406 Duff Medical Building, 3775 University street

country: Canada

institute: McGill University

summary: Exposure to inflammatory cytokines driven by bystander cytokines can have profound effects on the function of memory CD8 T cells. Here we transferred a 1-5X10^4 of P14 TCR-tg T cells (specific for gp33-41 of LCMV) on day -1 followed by infection with 2X10^5 PFU of LCMV Armstrong ip to generate memory P14 populations. Mice were rested for >50 days before further challenge. Mice containing memory P14 populations were either mock-infected with saline, infected with 2X10^6 Pichinde Virus ip (no cross-reactivity wtih LCMV gp33-41) or infected with 2X10^6 Pichinde Virus ip together with daily injections of 200 micrograms of anti-CD122 antibody (clone TM-b1). On day 4 following indicated treatments P14s were flow sorted and RNA was extracted from 1X10^6 cells using an RNeasy kit (Qiagen). Each group had 3 biological replicates. Transcriptomes were compared by DAVID analysis (p<0.01, Fold-Change > 1.5)

overall_design: 3 biological replicates per group. Groups included P14 from mock-infected mice, P14 from Pichinde virus infected mice and P14 from Pichinde virus and anti-cd122 treated mice.

first: Thomas

last: Bair

first: Gary

last: Hauser

last: Boes

first: John

middle: T

last: Harty


title: Targeting innate immunity for antiviral therapy through small molecule agonists of the RLR pathway

status: Public on Oct 16 2015

city: Minneapolis

first: Michael

last: Gale

state: Minnesota

address: 689 23rd Ave SE

department: Microbiology and Immunology

institute: University of Minnesota

summary:
To better understand the small molecule agonists that can promote IRF3 activation to induce innate immune gene expression could serve as novel antiviral compounds, we used microarray analysis to assess the transcriptional profiles driven by these compounds and to compare them to known activators of the intracellular innate immune response.
We are particularly interested in knowing how the analogs derived by medicinal chemistry (KIN1408 and KIN1409) differ in signaling and gene expression profiles in THP-1 cells as compared to the parent KIN1400 and whether such differences may track with different biological outcomes.

overall_design: THP-1 cells were differentiated in 40nM PMA for 30 hrs and treated with the following controls for 20 hrs in cRPMI supplemented with 0.5% (v/v) DMSO: 0.5% DMSO alone, SeV (25 or 100 HAU/mL),  IFNβ (25 or 100 IU/mL) or LPS (0.25 or 0.025 µg/mL). Alternatively, cells were treated in the same manner with the compounds KIN1400, KIN1408, or KIN1409 at doses of 10 µg/mL, 2.5 µg/mL, and 0.625 µg/mL. As an additional control, another set of cells were transfected with 2 µg/mL HCV pU/UC or XRNA in cRPMI without DMSO.

first: Sowmya

last: Pattabhi

first: Courtney

last: Wilkins

first: Ran

last: Dong

first: Megan

last: Knoll

first: Jeffrey

last: Posakony

first: Shari

last: Kaiser

first: Chad

last: Mire

first: Myra

first: Renee

last: Ireton

middle: W

last: Geisbert

first: Kristin

last: Bedard

first: Shawn

last: Iadonato

first: Yueh-Ming

last: Loo

last: Gale Jr


title: Annexin A2 controls pancreatic cancer invasion and metastasis through a novel axon guidance pathway

status: Public on Sep 03 2015

first: Lei

last: Zheng

address: 1650 Orleans Street, CRB1 Rm 488

summary: The mechanisms involved in promoting metastasis of pancreatic ductal adenocarcinoma have yet to be elucidated. Here, we show that AnnexinA2 regulates the secretion of Semaphorin3D from pancreatic tumor cells allowing it to bind to its receptor PlexinD1 on the surface of the tumor cell, which induces invasion and metastasis. Knockdown of AnnexinA2 or Semaphorin3D decreases the metastatic potential of pancreatic tumor cells, while over expression of AnnexinA2 or Semaphorin3D is sufficient to rescue the invasion capacity of these cells. Clinically, we found that Semaphorin3D expression correlates with poor survival and increased metastatic potential in human PDA patients. This study identified a novel axon guidance pathway downstream of AnnexinA2 that can be targeted in the treatment of metastatic pancreatic cancer.

overall_design: Two primary pancreatic tumor cell lines were analyzed. The first primary line was derived from a KrasG12D/p53172H/Pdx-1Cre mouse, which served as the reference sample. The second primary line was derived from a KrasG12D/p53R172H/Pdx-1Cre/AnxA2-/- mouse.

first: Kelly

last: Foley

first: Qian

last: Xiao

first: Agnieszka

last: Rucki

first: Donger

last: Zhou

first: Elizabeth

last: Jaffee


title: Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice (part 2)

city: Frederick

first: Xiaojun

last: Hu

address: 1050 Boyles St.

department: CSP

institute: SAIC_Frederick, INc

summary: In wild-type mice, expression of chemokines that are ligands for Ccr2, Cxcr3, and Cxcr2 increased at days 32 to 41 post-infection, with a return to baseline by day 75. Concomitant increases were seen in Ccr2 and Cxcr3 but not in Cxcr2 expression. Induction of these same factors also occurred in CD40-ligand and CD40 knockout mice but only at a much later time-point, during uncontrolled Pneumocystis pneumonia (PCP). Expression of CD4 Th1 markers was increased in wild-type mice during clearance of infection. Ccr2 and Cx3cr1 knockout mice cleared Pneumocystis infection with kinetics similar to wild-type mice, and all animals developed anti-Pneumocystis antibodies. Upregulation of Ccr2 and Cxcr3 and their ligands supports an important role for T helper cells and mononuclear phagocytes in the clearance of Pneumocystis infection. However, based on the current and prior studies, no single chemokine receptor appears to be critical to the clearance of Pneumocystis.

overall_design: Gene expression microarrays were from 2 controls (CD40L-KO(+/-)) non exposure compared with 3 controls 5 months exposure and were from 3 CD40L-KO(-/-) non exposure compared with 4 CD40L-KO 5 months exposure

first: Lisa

middle: R

last: Bishop

first: Michail

last: Lionakis

first: Monica

last: Sassi

first: Philip

last: Murphy

first: Da

last: Huang

first: Brad

last: Sherman

first: Jun

last: Yang

first: Richard

middle: A

last: Lempicki

first: Joseph

last: Kovacs


title: Withaferin A (WA) causes cell death in prostate cells.

status: Public on Aug 02 2015

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

institute: Osaka univ.

summary: Withaferin A (WA), a major chemical component of an Indian herb Withania somnifera, induces cell death (apoptosis/necrosis) in a variety of tumor cells, but its molecular mechanism remains elusive. We report that WA induces cell death selectively in high-grade prostate (PC-3 and DU-145) and tongue (SAS) cancer cells but not in normal human fibroblast (TIG-1) and low-grade prostate cancer (LNCaP) cells.

overall_design: To identify genes whose expression levels were up- or down-regulated in prostate cancer cells following WA treatment, we examined the transcriptome profiles of mRNA prepared from TIG-1, LNCaP, PC-3 and DU-145 cells using Agilent’s Whole Human Genome Microarray.

first: Yukihiro

last: Nishikawa

first: Hiroshi

last: Nojima


title: The effect of Vdr gene ablation in the mouse placenta

status: Public on Aug 04 2015

city: Perth

first: Sam

last: Buckberry

address: 35 Stirling Highway, Crawley

country: Australia

institute: The University of Western Australia

summary: Analysis of mouse placenta retrieved at day 18.5pc from vitamin D (1,25-dihydroxyvitamin D3) receptor (Vdr) knockout, heterozygous and wild-type mice. Results provide insight into the molecular mechanisms underlying the effect of vitamin D on placental function.

overall_design: Vdr heterozygous males and females were mated to generate Vdr knockout, heterozygous and wild-type offspring. At day 18.5pc, mouse placentae were collected and RNA was extracted and assayed on Affymetrix MoGene 2.1 ST arrays to measure the effect of Vdr on global gene expression.


title: Expression data from ICR mouse spinal cords - normal or injured spinal cord

city: Changzhou

first: Ding

last: Ya

state: Jiangsu

address: No. 185 Juqian street

department: Department of Orthopedics

institute: The Third Affiliated Hospital of Suzhou University

summary:
LncRNAs played a crucial role in the cell growth, development and some diseases relating to central nerve system.This study suggest that with regulating the LncRNAs expression level we might design novel therapy for spinalcord injury.
In this dataset, we profiled the expression pattern of LncRNAs by microarray method after spinal cord injury (SCI). Through Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis seek LncRNAs potential function in the repair of spinal cord injury.

overall_design: Fifteen samples were analyzed. In these sample, we divided into five groups (sham operation, 1 day post-injured, 3 days post-injured, 1 week post-injued and 3 weeks post-injured) and each group contained three mice.After RNA extraction,RNA form mice in the same group were mixed by equal mass for the preparation of microarray.Compared with spinal cord without injury, the differential expression level of LncRNAs had a few changes at 1day post-injury, reached the peak at 1 week after SCI, and subsequently declined until 3 weeks post-injury. Genes with an FDR≤0.05 and a fold-change ≥2 were selected. Subsequently we analysis the significant differential expression genes.

first: Ya

last: Ding

first: Jinbo

last: Liu


title: Myeloid derived suppressor cells from tumor-bearing L2-Cre;p120f/f mice

status: Public on Aug 31 2015

city: Philadelphia

first: Anil

middle: K.

last: Rustgi

state: PA

address: 421 Curie Boulevard

department: Gastroenterology

institute: University of Pennsylvania

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

overall_design: Refer to individual Series


title: Expression data from CD11b+Gr1+ splenocytes from tumor-bearing L2-Cre;p120f/f mice, compared to controls

summary:
Myeloid derived suppressor cells (MDSCs) are an immunosuppressive population of immature myeloid cells found in advanced stage cancer patients and mouse tumor models.  To identify potential genes playing essential role in MDSC biology, we have conducted microarray analysis of gene expression in MDSCs from esophageal tumor-bearing mice, compared to immature myeloid cells from healthy littermate control mice.
In this dataset, we include the expression data obtained from sorted splenic CD11b+Gr1+ cells from tumor-bearing L2-Cre;p120f/f mice, compared to healthy littermate controls. Using these data, we have identified 964 genes showing differential expression between the two groups. Among these was the Cd38 gene, which was among the genes most upregulated in MDSCs from tumor-bearing mice.

overall_design: 9 total samples were analyzed: 6 sample from experimental tumor-bearing mice and three pooled samples from control mice.  Gene expression difference was determined by univariate test (two-sample t-test) with multivariate permutation test (10,000 random permutations). A cut-off p-value of less than 0.001 and minimum 2-fold expression change were used to identify genes with significant expression differences between the two groups.

first: T

last: Waldron

first: A

middle: K


title: Frequent derepression of the mesenchymal transcription factor gene in acute myeloid leukemia

status: Public on Sep 17 2015

city: Manchester

first: Tim

last: Somervaille

state: Lancashire

address: Wilmslow Road

country: United Kingdom

institute: Cancer Research UK Manchester Institute

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Frequent derepression of the mesenchymal transcription factor gene in acute myeloid leukemia (mouse)

summary: Murine CD45.1+ CD117+ BM cells were co-transduced pairwise with retroviral vectors expressing Hoxa9, Meis1, Foxc1 or a control empty vector. Ninety-six hours later 10^6 drug resistant cells were transplanted into CD45.2+ irradiated congenic recipients. To investigate the consequences of FOXC1 expression on the transcriptome in murine AML, we performed exon array analysis using flow sorted CD117+Gr1+ leukemia cells recovered from sick mice (Hoxa9/control; Moxa9/Meis1; or Hoxa9/FOXC1 leukemias; 3 mice per cohort).

overall_design: Nine exon arrays total; 3 arrays for each cohort (Hoxa9/control; Moxa9/Meis1; or Hoxa9/FOXC1), each from a separate mouse.


title: Expression data from CD38high vs CD38low CD11b+Gr1+ splenocytes from tumor-bearing L2-Cre;p120f/f mice.

summary:
Myeloid derived suppressor cells (MDSCs) are an immunosuppressive population of immature myeloid cells found in advanced stage cancer patients and mouse tumor models.  We have identified Cd38 gene as potentially playing an essential role in MDSC biology. To determine the diffences between CD38high and CD38 low MDSCs from tumor-bearing mice, we have conducted this microarray.
In this dataset, we include the expression data obtained from sorted splenic CD38high CD11b+Gr1+ cells from tumor-bearing L2-Cre;p120f/f mice, compared to CD38low CD11b+Gr1+ cells from the same mice. Using these data, we have detected differential expression of 498 genes . The Nos2 gene was among the genes most upregulated in CD38high MDSCs.

overall_design: 8 total samples were analyzed: 3 pairs of CD38high and CD38 low MDSCs (coming from individual mice), as well a pair of CD38high and CD38low pulled MSDCs (splenocytes from 3 mice were pulled together for sorting to increase yields).  Gene expression difference was determined by univariate test (two-sample t-test) with multivariate permutation test (10,000 random permutations). A cut-off p-value of less than 0.001 and minimum 2-fold expression change were used to identify genes with significant expression differences between the two groups.

middle: J

last: Karakasheva


title: Transcriptomic expression analysis on hippocampus samples

status: Public on Jul 06 2015

city: Durham

first: arbogast

last: thomas

state: NC

address: 300N Duke Street

department: neurosciences

institute: Duke University

summary: Hippocampus transcriptome analysis of Ms5Yah carrying a 7.7Mb deletion on chromosome 16 and wild-type littermates.

overall_design: We analyzed hippocampi from 8 wild-type and 9 Ms5Yah male mice using the Affymetrix Mouse Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool.

first: Arbogast

last: Thomas

first: Yann

last: Herault

first: Doulaye

last: Dembele


title: Microarray analysis of developing mouse cortex reveals regulation of ribosomal protein mRNAs throughout development

status: Public on Jun 26 2015

city: Piscataway

first: Ronald

middle: P.

last: Hart

state: NJ

address: 604 Allison Rd Rm B430

department: Cell Biology & Neuroscience

institute: Rutgers University

summary: Neocortical development is spatiotemporally regulated by exogenous factors, but the mechanism regulating timed specificity of neocortical mRNA translation is unknown. We find that active mRNA translation sites (polysomes) contain ribosomal protein subsets that undergo dynamic spatiotemporal rearrangements during mouse neocortical development.

overall_design: Two samples of cortext total RNA each from four embryonic time points were collected.

middle: P

first: Matthew

last: Kraushar

first: Kevin

last: Thompson

first: Mladen-Roko

last: Rasin


title: Gene expression analysis of Ets1-/- CD4+ CD8+ thymocytes

status: Public on Dec 19 2015

city: Freiburg

first: Pierre

middle: Daniel

last: Cauchy

state: Baden-Württemberg

address: Breisacher Str. 115

department: Zentrum für Translationale Zellforschung

country: Germany

institute: University Medical Center Freiburg

summary: We performed microarray analysis of gene expression in WT and Ets1-/- CD4+ CD8+ DP thymocytes. Overall, we find that Ets1-/- thymocytes display gene expression signatures closer to previous stages of thymocyte development (e.g. DN3-4) than WT DP cells, suggesting that while these cells do become DP thymocytes in the absence of Ets1, that the latter is required for the upregulation of later T-cell genes and that its presence is required for the downregulation of genes corresponding to earlier and alternative stages of development.

first: Joaquin

last: Zacarias-Cabeza

first: Laurent

last: Vanhille

first: Frederic

last: Koch

first: Romain

last: Fenouil

first: Angelica

last: Santana

first: Ahmad

last: Maqbool

first: Aurélien

last: Griffon

first: Jean

last: Imbert

first: Carolina

last: Moraes-Cabé

first: Jean-Christophe

last: Bories

last: Ferrier

first: Salvatore

last: Spicuglia

last: Andrau


title: Genome wide DNA copy number analysis of sarcomatoid renal cell carcinoma.

status: Public on Jun 18 2015

first: Kanishka

last: Sircar

address: 1515 Holcombe Blvd., G1.3623

institute: MD Anderson Cancer Center

summary: The genome wide DNA copy number profiles of the biphasic epithelioid (E-) and sarcomatoid (S-) components of sarcomatoid clear cell renal cell carcinoma were analyzed using SNP arrays.  The E- and S- components showed a similar DNA copy number profile, despite morphologic differences.

overall_design: Total DNA obtained from 10 sarcomatoid renal cell carcinoma samples (9 E- and S- pairs and 1 unpaired S) and 5 normal adjacent kidneys.


title: Host microbiota constantly control maturation and function of microglia in the central nervous system (part 2)

status: Public on May 25 2015

first: Ori

last: Staszewski

address: Breisacher Str. 64

department: Institute of Neuropathology

summary:
As tissue macrophages of the central nervous system (CNS), microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. Here we reveal significant contributions of the host microbiota to microglia homeostasis as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determined that short-chain fatty acids (SCFA), microbiota-derived bacterial fermentation products, regulate microglia homeostasis. Accordingly, mice deficient for the SCFA receptor FFAR2 mirrored microglia defects found under GF conditions. These findings reveal that host bacteria vitally regulate microglia maturation and function, whereas microglia impairment can be restored to some extent by complex microbiota.
We used microarrays to determine the gene expression of microglia after LCMV challenge.

overall_design: Lymphocytic Choriomeningitis Virus (LCMV) strain WE was propagated and titrated as plaque forming units (PFU) on L929 cells as described before (Herz,J. et al. Acid sphingomyelinase is a key regulator of cytotoxic granule secretion by primary T lymphocytes. Nat. Immunol. 10, 761-768 (2009)). PFU were multiplied by the factor 10 to be converted into infectious units (IU). Mice were infected by intracerebral inoculation of 103 IU into the right hemisphere.

first: Daniel

last: Erny

first: Anna

middle: L

last: Hrabě de Angelis

first: Diego

last: Jaitin

first: Peter

last: Wieghofer

first: Eyal

last: David

first: Hadas

last: Keren-Shaul

first: Tanel

last: Mahlakoiv

first: Kristin

last: Jakobshagen

first: Thorsten

last: Buch

first: Vera

last: Schwierzeck

first: Olaf

last: Utermöhlen

first: Eunyoung

last: Chun

first: Wendy

last: Garrett

first: Kathy

last: McCoy

first: Andreas

last: Diefenbach

last: Staeheli

first: Bärbel

last: Stecher

first: Ido

last: Amit

first: Marco

last: Prinz


title: Gene expression signatures in GIST-T1 cells transfected with a miR-34a mimic molecule

city: Sapporo

first: Hiromu

last: Suzuki

state: Hokkaido

address: S1, W17, Chuo-ku

department: Department of Molecular Biology

institute: Sapporo Medical University

summary: To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-34a mimic or a negative control.  We found that 2,621 probe sets (1,933 unique genes) were downregulated (>1.5-fold) by ectopic miR-34a expression, including PDGFRA gene which was previously reported as a miR-34a target gene.

overall_design: GIST-T1 cells were transfected with a mirVana miR-34a mimic  (Ambion) or mirVana miRNA mimic Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.

first: Takeshi

last: Niinuma


title: Expression data from mouse perigonadal white adipose tissue - various mutant conditions [gene-level analysis]

status: Public on Jun 05 2015

city: Paris

first: Pierre

last: de la Grange

address: 29, rue du Faubourg Saint-Jacques

department: Paris Biotech Santé

institute: GenoSplice technology

summary: Progerin-expressing mice (HGPS-like) demonstrated increased energy metabolism and lipodystrophy. Increased mitochondrial biogenesis was found in adipose tissue from HGPS-like mice, whereas lamin C-only mice had fewer mitochondria. Thus we analyse which molecular pathways mediated the changes in adipose tissue caused by lamin C and progerin expression and the roles of these pathways in energy metabolism and aging.

overall_design: 10 cDNAs samples were analysed. We compared the mean fold change of 2 to 4 biological replicates. We performed an unpaired Student’s t-test to compare intensities in the different biological replicates. Genes were considered significantly regulated when the fold change was ≥ 1.5, and the p-value was ≤0.05.

first: J

last: Tazi


title: Expression data from mouse perigonadal white adipose tissue - various mutant conditions


title: Long noncoding RNAs expression patterns associated with chemo response to cisplatin based chemotherapy in lung squamous cell carcinoma patients

status: Public on May 18 2015

city: Hangzhou

first: Xuefeng

last: Fang

address: 86 jiefang road

department: College of Medcine

institute: Zhejiang University

summary: There is large variability among lung squamous cell carcinoma (SCC) patients in response to treatment with cisplatin based chemotherapy. LncRNAs is potentional a new type of predictive marker that can identify subgroups of patients who benefit from chemotherapy and it will have great value for treatment guidance.

overall_design: Differentially expressed LncRNAs were identified using microarray profiling of tumors with partial response (PR) vs. with progressive disease (PD) from advanced lung SCC patients treated with cisplatin based chemotherapy and validated by quantitative real-time PCR (qPCR). Results: Compared with the PD samples, 953 lncRNAs were consistently overregulated and 749 lncRNAs

first: Zhibo

last: Hou

first: Chunhua

last: Xu

first: Haiyan

last: Xie

first: Huae

first: Ping

last: Zhan

first: Like

last: Yu


title: Identification of PARD3 signature on PARD3 deficient H157 cell line, reconstituting the expression of PARD3 gene, with a wt and a mutant form.

status: Public on May 19 2015

city: L'Hospitalet de Llobregat

first: Manel

last: Esteller

state: Barcelona

address: Hospital Duran i Reynals Av. Gran Via s/n km, 2.7

department: PEBC

institute: IDIBELL

summary: To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the polarity protein PAR3. Human SCC cell line, NCI-H157 (H157), has a big deletion at PARD3 locus and showed no PAR3 protein expression. This cell line was used as a model in which we restored the expression of PAR3 (wt or mutant form). Afterwards, this model was used to identify PARD3 signature on Human  SCC.

overall_design: There are triplicates of each sample. We compare the effects in gene expression between the different situations: no PARD3 expression in the cell, expression of the  mutant form of PARD3 gene and expression of the PARD3 wt form in the cells.

first: Ester

last: Llort

first: Montse

last: Sánchez-Céspedes


title: Host microbiota constantly control maturation and function of microglia in the central nervous system

first: Ori

last: Staszewski


title: Gene expression signatures in GIST-T1 cells transfected with a miR-335 mimic molecule

summary: To clarify the effect of miRNAs, we carried out a gene expression microarray analysis using GIST-T1 cells transfected with a miR-335 mimic or a negative control.  We found that 1,095 probe sets (853 unique genes) were downregulated (>1.5-fold) by ectopic miR-335 expression.

overall_design: GIST-T1 cells were transfected with a mirVana miR-335 mimic  (Ambion) or a mirVana miRNA mimic Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.


title: Host microbiota constantly control maturation and function of microglia in the central nervous system (part 1)

summary: As tissue macrophages of the central nervous system (CNS), microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. Here we reveal significant contributions of the host microbiota to microglia homeostasis as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determined that short-chain fatty acids (SCFA), microbiota-derived bacterial fermentation products, regulate microglia homeostasis. Accordingly, mice deficient for the SCFA receptor FFAR2 mirrored microglia defects found under GF conditions. These findings reveal that host bacteria vitally regulate microglia maturation and function, whereas microglia impairment can be restored to some extent by complex microbiota.

overall_design: For acute inflammatory challenges, LPS was applied intracranially and 6 hours later, animals were analyzed. Control animals were injected PBS i.c. Transcriptional profiles of FACS-sorted microglia were assessed using Affymetrix® (Santa Clara, USA) GeneChip Arrays (Mouse Gene 2.1 ST Arrays).

first: Daniel

last: Erny

first: Anna

last: Hrabě de Angelis

first: Diego

last: Jaitin

first: Peter

last: Wieghofer

first: Eyal

last: David

first: Hadas

last: Keren-Shaul

first: Tanel

last: Mahlakoiv

first: Kristin

last: Jakobshagen

first: Thorsten

last: Buch

first: Vera

last: Schwierzeck

first: Olaf

last: Utermöhlen

first: Eunyoung

last: Chun

first: Wendy

last: Garrett

first: Kathy

middle: D

last: McCoy

first: Andreas

last: Diefenbach

last: Staeheli

first: Bärbel

last: Stecher

first: Ido


title: Gene expression signatures in GIST-T1 cells transfected with miR-34a and miR-335 mimic molecules

first: Hiromu

last: Suzuki


title: Septic shock in advanced age: Transcriptome analysis reveals altered molecular signatures in neutrophil granulocytes

status: Public on Jun 10 2015

city: São Paulo

first: Eduardo

middle: Moraes

last: Reis

state: SP

address: Av. Prof. Lineu Prestes, 748

department: Biochemistry

country: Brazil

institute: University of São Paulo

summary: Transcriptional profiling of granulocytes from 24 subjects was used to investigate their differences regarding sepsis and aging.

overall_design: Two-colour hybridization design. Aliquots of total RNA isolated from adult or elder individuals with sepsis or healthy controls were labeled with Cy3 and co-hybridized with a common reference RNA pool (Universal Human Reference RNA, Agilent, cat #740000) labeled with Cy5 . Biological replicates:6 per group. No technical replicates.

first: Diogo

middle: V

last: Pellegrina

first: Patrícia

last: Severino

first: Fabiano

last: da Silva

middle: M


title: Differential gene expression after ingenol mebutate (IM) treatment

status: Public on May 03 2015

city: Zurich

first: Sandra

middle: Nicole

last: Freiberger

state: Zurich

address: Gloriastrasse 31

department: Department of Dermatology

country: Switzerland

institute: University Hospital Zurich

summary: We treated primary keratinocytes and SCC cells with IM for 24h to identify differentially expressed genes after treatment compared to DMSO contorl

overall_design: 3x DMSO keratinocytes, 3x IM 100 nM IM keratinocytes, 3x 10 uM IM keratinocytes, 3x DMSO SCC cells, 3x 1 nM IM SCC cells, 3x 100 nM IM SCC cells, 3x 10 uM IM SCC cells

first: S

middle: N


title: Analyses of iHC transcriptome profiles

status: Public on Jun 02 2015

city: Edinburgh

first: Aida

last: Santos da Costa

state: Edinburgh

address: Old College, South Bridge

institute: University of Edinburgh

summary:
Mechanosensory hair cells (HCs) are the primary receptors of our senses of hearing and balance. However, very little is known about the transcriptional regulators involved in HC fate determination and differentiation. In this paper, we show that expression of three HC lineage-specific transcription factors: Gfi1, Pou4f3 and Atoh1, can induce a direct commitment towards HC fate during in vitro embryonic stem cell (ESC) differentiation. Induced HCs (iHCs) express numerous HC-specific genes and exhibit polarized membrane protusions reminiscent of stereociliary bundles.
The ability to obtain purified populations of iHCs by virtue of the Myo7:mVenus reporter line (iGPA-Myo7a:mVenus) allowed us to generate highly reproducible gene expression profiles for these cells, at various phases of their development (day 8 and day 12 of cell culture).

overall_design: Embryoid bodies (EBs) derived from the iGPA-Myo7a:mVenus reporter ESC line at day 8 and day 12, treated with Dox alone or with Dox and RA, were used to obtain FACS-purified populations of iHCs. Unsorted EBs from the same reporter line, grown in the same conditions but without Dox or RA treatment, were used as controls. Independent RNA preparations from each of the selected time points and treatments (three biological replicates for Dox or Dox+RA treatments, two for “no treatment”) were processed and hybridized on Affymetrix whole-transcript microarrays (Mouse Genome 2.1 ST Arrays Strip).

last: Costa

first: Domingos

last: Henrique


title: Polysome purified mRNA in control and RACK1 silenced in human hepatocarcinoma cells

status: Public on May 14 2015

city: Strasbourg

first: Catherine

last: Schuster

address: 3 rue Koeberlé

institute: INSERM

summary: Fighting viral infections is hampered by the scarcity of viral targets and their variability resulting in development of resistance. Viruses depend on cellular molecules for their life cycle, which are attractive alternative targets, provided that they are dispensable for normal cell functions. Using the model organism Drosophila melanogaster, we identify the ribosomal protein RACK1 as a cellular factor required for infection by internal ribosome entry site (IRES)-containing viruses. We further show that RACK1 is an essential determinant for hepatitis C virus translation and infection indicating that its function is conserved among distantly related human and fly viruses. Inhibition of RACK1 does not affect Drosophila or human cell viability and proliferation, and RACK1-silenced adult flies are viable, indicating that this protein is not essential for general translation. Our findings demonstrate a specific function for RACK1 in selective mRNA translation and uncover a new target for the development of broad antiviral intervention.

overall_design: 4 Controls 4 RACK1 silenced cells

first: Thomas

last: Baumert


title: Analysis of RNA from liver tumors in SRSF3 hepatocyte knockout mice

status: Public on May 01 2015

city: La Jolla

first: Nick

last: Webster

state: CA

address: 9500 Gilman Drive

department: Medicine

institute: UCSD

summary: RNA from three hepatocellular carcinomas from 24-month-old SRSF3HKO mice compared to RNA from non-tumorous liver from 24-month-old SRSF3HKO mice for changes in exon utilization and gene expression.

overall_design: Liver tumor vs. normal liver, three replicates each.

first: Nicholas

first: Supriya

last: Sen


title: Analysis of RNA from primary hepatocytes from hepatocyte-specific SRSF1 knockout mice vs. WT

summary: RNA from primary hepatocyte cultures from three 3-month-old SRSF1HKO mice compared to RNA from three 3-month-old WT mice for changes in exon utilization and gene expression.

overall_design: SRSF1 KO vs. WT, three replicates each.


title: Aberrant splicing in livers of SRSF KO mice

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

overall_design: Refer to individual Series


title: Gene Expression Profiling of human leukemic B-cells. Two-color Microarray-Based Gene Expression Analysis.

status: Public on Apr 22 2015

city: Łódź

first: Ida

last: Franiak-Pietryga

address: Pomorska 251

department: Clinical Genetics

country: Poland

institute: Medical Univ. of Lódź

summary:
Fresh MEC1 cells (chronic lymphocytic leukemia) (ACC-497, DSMZ) previously untreated and treated in cultures in vitro with glycodendrimers (nanoparticle with maltotriose on the surface). MEC1 cells were centrifuged after incubation with drugs or dendrimers.
Agilent’s Low Input Quick Amp Labeling Kit was used to generate fluorescent cRNA (complimentary RNA) with a sample input 100ng of total RNA for two-color processing. The method uses T7 RNA polymerase, which simultaneously amplifies target material and incorporates cyanine 3- or cyanine 5-labeled CTP. Amplification is typically at least a 100-fold from total RNA to cRNA with the use of this kit. cRNA quantification had been done using NanoDrop ND-1000 UV-VIS Spectrophotometer version 3.2.1. Arrays were placed onto the gaskets and than to the slide chamber in rotisserie in a hybridization oven set.  Hybrydization was carried out at 65-Celsius degrees for 17 hours. Arrays were scanning using Agilent Scanner. Scan resolution was set up for 3μM.

overall_design:
Microarray gene expression profiling. Intensity of gene expression in MEC1 cells before treatment was compared with the gene expression signals in MEC1 cells from the same cell culture after 4 and 48 hours of treatment. MEC1 cells were treated with PPI-G4-OS-Mal-III dendrimer, PPI-G4-DS-Mal-III, Fludarabina.

Sample titles represent;
A = Cy3
B = Cy5
R = reference (48h incubation)
R4 = reference (4h incubation)
1 = PPI-G4-DS-Mal III (1st cell culture flask) (48h incubation)
2 = PPI-G4-DS-Mal III (2nd cell culture flask)(48h incubation)
3 = PPI-G4-OS-Mal III (1st cell culture flask)(48h incubation)
4 = PPI-G4-OS-Mal III (2nd cell culture flask)(48h incubation)
5 = PPI-G4-DS-Mal III (4h incubation)
6 = PPI-G4-OS-Mal III (4h incubation)
7 = FA (4h incubation)
8 = FA (48h incubation)

first: Henryk

last: Maciejewski


title: Gene expression profiling of altered NF-kB p65 ser536 phosphorylation in prostate cancer cells

status: Public on Mar 12 2015

city: Houston

first: Chad

last: Creighton

state: TX

address: One Baylor Plaza, Mail Stop: BCM305

department: Biostatistics, Ducan Cancer Center

institute: Baylor College of Medicine

summary: Aberrant regulation of NF-kB pathway is believed to be a major event contributing to malignant transformation and progression of prostate cancer (PCa). P65 consists of a DNA-binding and dimerization domain (RHD), nuclear localization signal (NLS) and transactivation domains (TA1 and TA2). The c-terminal 30 amino acids (TA1 domain) comprise the most important transactivation domain and NF-kB transactivation may be regulated by multiple phosphorylation in this domain. This p536 is located in TA1 domain and is conserved in human, mouse, chicken. We previously discovered that p536 is present in majority of PCa and associated with ERG expression indicating that ERG can significantly enhance phosphorylation of p65 at Ser536 in vivo. We have successfully generated a dominant negative (DN) p65 which has been mutated (S536A) such that it cannot be phosphorylated at Ser 536 and cannot carry out Ser536 phosphorylation dependent functions. We also generated two mutants S536D and S536E which are the phosphomimetic mutant that resembles phospho-p65 and can be detected by anti-phospho-p65 antibody. We carried out microarray studies and discovered a set of p536 regulated genes compared with wild type p65 regulated gene set.

overall_design: We established PNT1a stable cell lines expressing WT p65, S536E (active p536), S536A (DN p635) or control (pCDH). Groups were profiled for gene expression.

first: Li

last: Zhang

first: Michael

last: Ittmann

first: Jianghua

last: Wang

first: Yiqun


title: Gene expression data from type II pneumocytes from adult mice with and without Trf2

status: Public on Apr 20 2015

city: Baltimore

first: Mary

last: Armanios

state: MD

address: 401 North Broadway

department: School of Medicine

institute: The Johns Hopkins University

summary:
Gas exchange in the mammalian lung occurs in the alveolar sacs lined by epithelial cells that form a barrier allowing effective oxygen diffusion.  Telomere syndromes have their most common manifestation in degenerative disease of the alveoli, both pulmonary fibrosis and emphysema.  We tested the role of telomere dysfunction by inducing deletion of the telomere binding protein Trf2 in type 2 alveolar epithelial cells (AEC2s) that both express the gene encoding surfactant protein C and constitute the regenerative compartment of the alveolar epithelium.  Acquired telomere dysfunction in these cells preferentially induced cellular senescence, and mouse lungs were marked by an inflammatory response even though the telomere dysfunction was restricted to the epithelium.   Senescent AECs had altered gene expression that differentially fell in inflammatory cell signaling pathways.  Bleomycin challenge was uniformly fatal, and Trf2-depleted cells failed to generate clonal alveolar colonies in vitro.  The telomere dysfunction response in AEC2s was in part p53-dependent, and we found evidence of a p53-mediated paracrine survival signal to the mesenchyme.  These data indicate that telomere dysfunction in the alveolar epithelium limits its regenerative capacity and is sufficient to induce inflammation.  It may thus be a primary driving event in telomere-mediated lung disease.  Efforts to restore epithelial regenerative capacity may be an effective approach in a subset of fibrosis and emphysema patients.
We studied the gene expression changes in adult type II pneumocytes 7 days after deleting Trf2.  Mice carried floxed allele of Trf2 and mTmG reporter allele. Type II pneumocytes were collected by FACs sorting GFP+ cells from lungs 7 days after administering tamoxifen.

overall_design: 6 total samples were analysed. Three were from control samples that were heterozygous for Trf2 and three samples had Trf2 deleted.

first: Jonathan

last: Alder


title: FCRL5 delineates functionally impaired memory B cells associated with malaria exposure

status: Public on Apr 27 2015

city: San Francisco

first: Charlie

last: Kim

address: 1001 Potrero Ave

institute: University of California, San Francisco

summary: Classical and atypical memory B cells from Ugandan children were compared in their baseline gene expression patterns.

overall_design: Independent cryopreserved PBMC samples from children were thawed, and classical and atypical memory B cells were double sorted by FACS directly into an RNA lysis buffer. RNA was isolated, amplified using 2 rounds of linear amplification, and hybridized to Agilent-039494 Human 8x60k microarrays as a single color experiment.

first: Charles

middle: C

first: Richard

last: Sullivan

first: Bryan

last: Greenhouse


title: Length-dependent gene misregulation in Rett syndrome (MeCP2)

city: brookline

first: Harrison

middle: Wren

last: Gabel

state: Massachusetts

address: 220 longwood avenue

department: Neurbiology

institute: Harvard Medical School

summary: Disruption of the MECP2 gene leads to Rett syndrome (RTT), a severe neurological disorder with features of autism. MECP2 encodes a methyl-DNA-binding protein that is proposed to function as a transcriptional repressor, but, despite numerous studies examining neuronal gene expression in MeCP2 mutants, no coherent model has emerged for how MeCP2 regulates transcription. Here we identify a genome-wide length-dependent increase in the expression of long genes in neurons lacking MeCP2.  This gene misregulation occurs in human RTT brains and correlates with onset and severity of phenotypes in Mecp2 mutant mice, suggesting that the disruption of long gene expression contributes to RTT pathology. We present evidence that MeCP2 represses long genes by binding to brain-enriched, methylated CA dinucleotides within genes and show that loss of methylated CA in the brain recapitulates gene expression defects observed in MeCP2 mutants. We find that long genes encode proteins with neuronal functions, and overlap substantially with genes that have been implicated in autism and Fragile X syndrome. Reversing the overexpression of long genes in neurons lacking MeCP2 can improve some RTT-associated cellular deficits.  These findings suggest that a function of MeCP2 in the mammalian brain is to temper the expression of genes in a length-dependent manner, and that mutations in MeCP2 and possibly other autism genes may cause neurological dysfunction by disrupting the expression of long genes in the brain.

overall_design: Total RNA was extracted from the cerebellum of 8-10 week old MeCP2 R306C mutant mice and their wild-type controls. Gene expression was analyzed using the Affymetrix Mo_Exon ST 1.0 microarray platform.

middle: W

first: Benyam

middle: Z

last: Kinde

middle: E

last: Greenberg


title: Whole genome expression microarray analysis in quadriceps of wild-type and NF90-NF45 double transgenic mouse

status: Public on Apr 07 2015

city: Nankoku

first: Shuji

last: Sakamoto

state: Kochi

address: Oko-cho, Kohasu

department: Science Research Center

institute: Kochi University

summary: The complex of NF90 and NF45 is known to participate in transcriptional regulation, mRNA stabilization and microRNA biogenesis in vitro. However, the physiological function of the NF90-NF45 complex is still unclear. To elucidate its functions, we generated NF90-NF45 double transgenic (dbTg) mice. Robust expression of NF90 and NF45 was detected in skeletal muscle. As mentioned above, NF90-NF45 complex is involved in regulation of genes via transcription and RNA metabolism. To identify genes regulated by NF90-NF45, we performed comprehensive analyses of mRNA expression in quadriceps of wild-type (WT) and NF90-NF45 dbTg mice.

overall_design: mRNA expression profile in quadriceps comparing WT and NF90-NF45 dbTg mice.


title: Young and elderly fibroblast cells

status: Public on Mar 18 2015

city: Tsukua

first: Osamu

last: Hashizume

state: Ibaraki

address: Ten-noudai 1-1-1

institute: University of Tsukuba

summary: Age-associated accumulation of somatic mutations in mitochondrial DNA (mtDNA) has been proposed to be responsible for the age-associated mitochondrial respiration defects found in elderly human subjects. In contrasts, our previous studies proposed that the age-associated respiration defects found in human fibroblasts are caused not by mtDNA mutations. To addressed these controversial issues, we carried out microarray analysis of two young (TIG3S and TIG121) and two elderly (TIG107 and TIG102) fibroblasts.

overall_design: Young (TIG3S and TIG121) and elderly (TIG107 and TIG102) fibroblasts are analyzed.

first: Jun-Ichi

last: Hayashi


title: Drug resistance-related changes in gene expression profile in multiple myeloma

status: Public on Mar 04 2015

city: Shimotsuke

first: Yusuke

last: Furukawa

state: Tochigi

address: 3311-1 Yakushiji

department: Center for Molecular Medicine

institute: Jichi Medical University

summary:
1) We identified the genes whose expression was up- and down-regulated by the adhesion to bone marrow stromal cells in human multiple myeloma cell line RPMI8226.
2) We identified the genes whose expression was up- and down-regulated by the PI3K inhibitor PF-04691502 in human multiple myeloma cell line RPMI8226.

overall_design: We isolated mRNA from the multiple myeloma cell line RPMI8226 under drug-resistant conditions, and subjected them to gene expression profiling using an Agilent GeneChip Array.

first: Jiro

last: Kikuchi


title: Exon Array analysis of WT1(+KTS) mutant mice

status: Public on Mar 27 2015

city: Nice

first: Andreas

last: Schedl

address: Parc Valrose

department: iBV

institute: University of Nice

summary: This exon array analysis was performed on mice carrying splice specific mutations at the end of exon9 of the Wilms tumor supressor gene that interfere with the production of WT1(+KTS) isoforms (Hammes et al., 2001; Cell 106:309)

overall_design: 4 wildtype and 4 wt1(+KTS) mutant E18.5 mouse embryos were transcardially perfused with magnetic beads, glomeruli isolated and RNA extracted and analyzed for differential expression on Affymetrix Exon Arrays

last: Clarkson

first: Herbert

last: Schulz


title: Length-dependent gene misregulation in Rett syndrome (Dnmt3a)

overall_design: Total RNA was extracted from the cerebellum of 10-11 week old Dnmt3a conditional knockout and control animals. Gene expression was analyzed using the Affymetrix Mo_Exon ST 1.0 microarray platform.

first: Michael


title: TIA-proteins suppress cell and tumor growth via promoting  select p53 gene targets-mediated cell cycle arrest and apoptosis

status: Public on Mar 05 2015

city: Cantoblanco

first: Juan

middle: Carlos

last: Oliveros

state: Madrid

address: Darwin 3

institute: CNB, CSIC

summary: The knock down of T-cell intracellular antigen (TIA) proteins enhances the acquisition of aberrant cellular phenotypes promoting uncontrolled cell and tumor growth. Hereby, we report that inducible expression of either TIA1 or TIAR in human embryonic kidney (HEK293) cells represses cell proliferation. Mechanistically, the sustained expression of either TIA1 or TIAR protein abolishes endogenous TIA1/TIAR protein expression via regulating splicing of their own pre-mRNAs. This event is concomitant with cell cycle arrest and cell death by apoptosis. Based on genome-wide analysis of the transcript expression patterns in HuR-, TIA1- or TIAR-expressing HEK293 cells, we found regulatory links among the up-regulation on a select subset of p53 pathway genes involved in G1/S cell-cycle and apoptosis control. Finally, nude mice injected with TIA1- or TIAR-expressing HEK293 cells decrease, and even abolishing, the growth of tumor xenografts relative to control cells. Collectively, these observations show that TIA proteins can function as tumor suppressor genes.

overall_design: Two independent biological replicates were performed per sample type. Agilent SurePrint G3 Human Gene Expression 8x60K v2 array were used in all cases (single-channel hybridizations)

first: Carmen

last: Sánchez-Jiménez

first: María

last: Ludeña

first: José

last: Izquierdo


title: Expression data from in vitro versus in vivo differentiated Th17 cells

status: Public on Apr 18 2015

city: Ann Arbor

first: Gary

last: Glick

state: MI

address: 2800 Plymouth Road

institute: Lycera

summary: In vitro differentiated Th17 have a distinct expression profile compared to in vivo differentiated Th17

overall_design: Several conditions of Th17 cells were tested, with 2-3 replicates per condition.

first: Luigi

last: Franchi

first: Aditi

last: Kulkarni

first: Ling-Yang

last: Hao


title: Gene expression in Galectin-3 KO vs. WT CD8 T cells

status: Public on Feb 19 2015

first: Theodore

last: Kouo

address: 733 North Broadway

summary:
The goal of this study was to examine differences in gene expression of tumor specific CD8 T cells in an in vivo tumor mouse model after inhibition of galectin-3 protein expression by genetic knockout.  Galectin-3 is thought to modulate CD8 T cell response by cross-linking cell surface glycoproteins
Galectin-3 is a 31 kD carbohydrate-binding lectin that is over-expressed by many human malignancies.  It also modulates T cell responses through a diverse array of mechanisms including induction of apoptosis, TCR cross linking in CD8+ T cells, and T cell receptor (TCR) down regulation in CD4+ T cells.      We found that patients responding to a granulocyte-macrophage colony-stimulating factor (GM-CSF) secreting allogeneic pancreatic tumor vaccine developed post immunization antibody responses to galectin-3 on a proteomic screen.  We used the HER-2/neu (neu-N) transgenic mouse model to study galectin-3 binding on adoptively transferred high avidity neu-specific CD8+ T cells derived from TCR transgenic mice.  Here, we show that galectin-3 binds preferentially to activated antigen-committed CD8+ T cells only in the tumor microenvironment (TME).  Galectin-3 deficient mice exhibit improved CD8+ T cell effector function and increased expression of several inflammatory genes when compared with wild type (WT) mice.  We also show that galectin-3 binds to LAG-3, and LAG-3 expression is necessary for galectin-3 mediated suppression of CD8+ T cells in vitro.  Lastly, galectin-3 deficient mice have significantly elevated levels of circulating plasmacytoid dendritic cells (pDCs), which are superior to conventional dendritic cells (cDCs) in activating CD8+ T cells.    Binding of galectin-3 to cell-surface glycoproteins on immune cells suppresses a pro-inflammatory immune response.  Thus, inhibiting galectin-3 in conjunction with CD8+ T cell directed immunotherapies should enhance the tumor specific immune response.

overall_design: 3 different experimental groups were studied.  Galectin-3 WT CD8 T cells adoptively transferred into Galectin-3 WT mice, galectin-3 WT CD8 T cells transferred into galectin-3 KO mice, and finally galectin-3 KO CD8 T cells transferred into galectin-3 KO mice.  Galectin-3 WT CD8 T cells transferred into Galectin-3 WT mice were used as the reference group.  Four biological replicates were submitted for each group, and adoptively transfered CD8 T cells were isolated 5 days post-adoptive transfer into tumor-bearing mice treated with a whole cell GM-CSF secreting vaccine.  Cells were purified by cell sorting on the Thy1.2 surface marker.

first: Lanqing

last: Huang

first: Alexandra

last: Pucsek

first: Minwei

last: Cao

first: Sara

last: Solt

first: Todd

last: Armstrong

first: Elizabeth

last: Jaffee


title: PlGF-1 and -2 induce hyperplasia and invasiveness of primary rheumatoid synoviocytes

status: Public on Jan 14 2015

city: Daejeon

first: Ji-Hwan

last: Park

address: 125 Gwahak-ro, Yuseong-gu

country: South Korea

institute: Korea Research Institute of Bioscience and Biotechnology (KRIBB)

summary: Inflammation-mediated oncogenesis has been implicated in a variety of cancer types. Rheumatoid synovial tissues can be viewed as a tumor-like mass, consisting of hyperplastic fibroblast-like synoviocytes (FLSs). FLSs of rheumatoid arthritis (RA) patients have pro-migratory and invasive characteristics, which may be caused by chronic exposure to genotoxic stimuli, including hypoxia and growth factors. We tested whether a transformed phenotype of RA-FLSs is associated with placental growth factor (PlGF), a representative angiogenic growth factor induced by hypoxia. Here, we identified PlGF-1 and PlGF-2 as the major PlGF isoforms in RA-FLSs. Global gene expression profiling revealed that cell proliferation, apoptosis, angiogenesis, and cell migration were mainly represented by differentially expressed  genes in RA-FLSs transfected with siRNA for PlGF. Indeed, PlGF-deficient RA-FLSs showed a decrease in cell proliferation, migration, and invasion, but an increase in apoptotic death in vitro. PlGF gene overexpression resulted in the opposite effects. Moreover, exogeneous PlGF-1 and PlGF-2 increased survival, migration, and invasiveness of RA-FLSs by binding their receptors, Flt-1 and NP-1, up-regulating the expression of anti-apoptotic molecules, pErk and Bcl2. Knock-down of PlGF transcripts reduced RA-FLS proliferation in a xeno-transplantation model. Collectively, in addition to their role for neovascularization, PlGF-1 and -2 promote proliferation, survival, migration, and invasion of RA-FLSs in an autocrine and paracrine manner. These results demonstrated how primary cells of mesenchymal origin acquired an aggressive and transformed phenotype. PlGF and its receptors thus offer new targets for anti-FLS therapy.

overall_design: The FLSs were prepared from the synovial tissues of RA patients and incubated in DMEM supplemented with 10% FBS. Cells were cultured in RPMI supplemented with 10% FBS.  There are 4 FLS samples treated with PlGF siRNA, and 4 FLS samples treated with control siRNA.

first: Seung-Ah

last: Yoo

first: Seong-Hye

last: Hwang

first: Sang-Min

last: Oh

first: Saseong

last: Lee

first: Valeria

last: Cicatiello

first: Sangchul

last: Rho

first: Sandro

last: De Falco

first: Daehee

first: Chul-Soo

last: Cho

first: Wan-Uk

last: Kim


title: Identification of LncRNA Expression Signatures for Triple-negative Breast Cancer

status: Public on Dec 01 2014

first: Liuqing

last: Yang

state: Texas

address: 1515 Holcombe Blvd.

department: Molecular and Cellular Oncology

institute: The University of Texas MD Anderson Cancer Center

summary: To identify biologically and clinically novel lncRNAs potentially involved in the progression of breast cancer, we profiled the expression of lncRNAs in two stage III triple-negativebreast cancer tissues and their paired adjacent noncancerous tissues by LncRNA Array 3.0 (ArrayStar). Expression of the mostly upregulated lncRNA (BCAR4) from this signature was quantified in the breast caner tissue microarray by RNA In situ Hybridization and bioinformatic analysis of Oncomine database, confirming its correlation with breast cancer metastasis.

overall_design: LncRNA Expression profiling analysis of the 4 samples including 2 triple-negative breast cancer tissues and their matched adjacent normal breast tissues by Arraystar Human LncRNA Array v3.0.

first: Zhen

last: Xing

first: Aifu

last: Lin

first: Chunlai

last: Li

first: Ke

last: Liang

first: Yang

last: Liu

first: Shouyu

last: Wang

first: Peter

first: Li

last: Qin

first: Yongkun

last: Wei

first: David

last: Hawke

first: Mien-Chie

last: Hung

first: Chunru


title: Expression analysis of superior cervical ganglion from backcrossed TH-MYCN transgenic mice

status: Public on Jan 30 2015

first: William

middle: A.

last: Weiss

address: 1450 3rd Street, HD-220

department: Neurology

summary:
Neuroblastoma susceptibility in TH-MYN mice is heavily influence by mouse strain background.  We have combined linkage analysis of tumor susceptibility with expression QTL analysis of superior cervical ganglia (pure peripheral symptathetic nervous tissue) to identify genes underlying tumor formation
The development of targeted therapeutics for neuroblastoma, the third most common tumor in children, has been limited by a poor understanding of growth signaling mechanisms unique to the peripheral nerve precursors from which tumors arise.  In this study, we combined genetics with gene expression analysis in the peripheral sympathetic nervous system to implicate arginase 1 and GABA signaling in tumor formation in vivo.  In human neuroblastoma cells, activation of GABA-A receptors by a benzodiazepine induced apoptosis and inhibited mitogenic signaling through AKT and MAPK.  These results suggest that GABA influences both neural development and neuroblastoma, and that benzodiazepines in clinical use may have potential for neuroblastoma therapy.

overall_design: 224 backcrossed mice were genotyped at 349 markers to identify susceptibility loci for neuroblastoma.  Gene expression from Superior Cervical Ganglia from 116 of these mice were correlated with genotyping data to identify putative eQTL.

first: Christopher

middle: S

last: Hackett

first: Justin

last: Chen

middle: A

last: Quigley

first: Allan

last: Balmain


title: Expression data from 63 week old mouse hippocampus - comparison between wildtype and transgenic animal

city: Huddinge

first: Jean-Ha

last: Baek

address: 7 Halsovagen

department: Biosciences and Nutrition

country: Sweden

institute: Karolinska Institute

summary:
A number of studies have identified changes in gene expression in cells from HGPS patients and in tissues from animal models for HGPS.
To investigate if the severe nuclear distortions seen in approximately 95% of the neuronal cells of the hippocampus resulted in any changes in gene expression, global genome transcript analysis was performed using the Affymetrix exon arrays on RNA extracted from the hippocampus of 63-week old HGPS and littermate controls.

overall_design: Total of 6 animals were analyzed - 3 wildtype and 3 transgenic animals. Genes with an FDR≤10% and a fold-change ≥2 were selected and analyzed.

first: Maria

last: Eriksson


title: MUNC downregulation decreases muscle differentiation

status: Public on Nov 27 2014

city: Charlottesville

first: Anindya

last: Dutta

state: VA

address: 1300 Jefferson Park Ave

department: Biochemistry & Molecular Genetics

institute: University Of Virginia

summary: Gene expression profiling in differentiating C2C12 cells comparing control cells and MUNC-deprived cells

overall_design: RNA samples were isolated from 4 C2C12 samples: proliferating control (siC) cells, differentiating siC cells, proliferating and differentiating MUNC depleted (siMUNC) cells

first: Adam

last: Mueller

first: Brian

middle: J

last: Reon


title: Coexistent ARID1A-PIK3CA mutations promote ovarian clear cell tumorigenesis through pro-tumorigenic inflammatory cytokine signaling

status: Public on Dec 31 2014

city: Chapel Hill

first: Jonathan

last: Schisler

state: NC

address: MBRB, Rm 2340C

department: McAllister Heart Institute

institute: The University of North Carolina at Chapel Hill

summary: Ovarian clear cell carcinoma (OCCC) is an aggressive form of ovarian cancer with high ARID1A mutation rates.  Here we present a genetically engineered mouse model of OCCC.  We find that ARID1A inactivation is not sufficient for tumor formation, but requires concurrent activation of the phosphoinositide 3-kinase catalytic subunit, PIK3CA.  Remarkably, the mice develop highly penetrant tumors with OCCC-like histopathology, culminating in hemorrhagic ascites and a median survival period of 7.5 weeks.  Therapeutic treatment with the pan-PI3K inhibitor, BKM120, prolonged mouse survival by inhibiting tumor cell growth.  Cross-species gene expression comparisons support a role for IL-6 inflammatory cytokine signaling in OCCC pathogenesis.  We further show that ARID1A-PIK3CA mutations cooperate to promote tumor growth through sustained IL-6 overproduction.  Our findings establish an epistatic relationship between SWI/SNF chromatin remodeling and PI3K pathway mutations in OCCC and demonstrate that these pathways converge on pro-tumorigenic cytokine signaling.  We propose that ARID1A protects against inflammation-driven tumorigenesis.

overall_design: Total RNA was extracted from mouse primary tumor samples or contral ovaries to use on Affymetrix microarrays. As the tumor was induced in only the right ovary, we used the left (control) ovary for a paired analysis in a total of eight mice.

first: Ronald

middle: L

last: Chandler

first: Jeffery

last: Damrauer

first: Terry

last: Magnuson


title: Expression data from Drd1a and Drd2 expressing neurons in striatum and cortex, at 6 weeks and 2 years of age

status: Public on Dec 13 2014

city: Cambridge

first: Myriam

last: Heiman

state: MA

address: 77 Massachusetts Avenue

institute: MIT

summary: We performed a study of gene expression changes that occur during mouse aging in the striatum and cortex in specific neuronal populations.  Using translating ribosome afifnity purificaiton, we captured cell type-specific mRNAs from Drd1a-expressing cortical neurons, Drd1a-expressing striatal neurons, Drd2-expressing cortical neurons, and Drd2-expressing striatal neurons.

overall_design: 31 total samples were anlayzed. We generated the followinf pairwise comparisons: Old (2 years) vs young (6 weeks) Drd1a expressing cortical cells; old (2 years) vs young (6 weeks) Drd2 expressing cortical cells; old (2 years) vs young (6 weeks) Drd1a expressing striatal cells; old (2 years) vs young (6 weeks) Drd2 expressing striatal cells.  We used a restriction of Benjamini-Hochberg FDR  <0.05, and a fold-change restriction of 1.2-fold.

first: M

first: R

last: Shema


title: GTF2IRD1 regulates cone gene expression to maintain the topology and function of retinal cone photoreceptors

first: Don

last: Zack

state: Maryland

address: 400 N Broadway

institute: Johns Hopkins University

summary: The mechanisms that specify cone photoreceptor cell-fate to short-wave-sensitive (S) versus medium-wave-sensitive (M) cones and maintain their nature are not fully understood. Here we report the importance of the GTF2IRD1 transcription factor in maintaining M cone cell identity and function. In the mouse, GTF2IRD1 is expressed in cell-fate determined photoreceptors at postnatal day 10. GTF2IRD1 binds to the enhancer and promoter regions of mouse M and S opsin genes, but regulates their expression differentially, suppressing S opsin expression and, through interaction with the transcription factors CRX and TR2, enhancing M opsin expression. Null mutation of Gtf2ird1 leads to altered topology of cone opsin expression in the retina, with aberrant S opsin over-expression and M opsin under-expression in M cones. Gtf2ird1 null mice also demonstrate abnormal M cone electrophysiological responses. These findings indicate a dual and specific regulatory role of GTF2IRD1 in maintaining normal M cone-specific gene expression and function.

overall_design: Total 16 samples were analyzed for BEN-NULL vs WT. Four biological replicates, two time points (2-week and 4-month) were used.

first: Tomohiro

last: Masuda


title: Role of beclin-1 in breast cancer microenvironment

status: Public on Feb 21 2015

city: Gifu

first: Tamotsu

last: Takeuchi

address: Yanagido

department: Pathology and Translational Research

institute: Gifu University School of Medcine

summary: A comprehensive gene expression analysis was performed on a co-culture of breast cancer cells and mesenchymal stromal cells, the latter of which either expressed beclin-1 or was depleted of beclin-1 by siRNA.

overall_design: To obtain the preliminary data, which was associated with expression genes in beclin-1 expression or siRNA-mediated beclin-1 knockdown of mesenchymal stromal cells, which were co-cultured with breast cancer MCF-7 cells, we used two cRNA samples.

first: Tamostu


title: Long noncoding RNAs profiles of adrenocortical carcinomas, adrenocortical adenomas and normal adrenal cortex

status: Public on Jan 01 2015

city: NSW

first: Anthony

middle: R

last: Glover

state: St Leonards, Sydney

address: Level 9, Kolling Institute of Medical Research, Royal North Shore Hospital

institute: University of Sydney

summary:
Adrenocortical carcinoma (ACC) is an aggressive malignancy with high rates of recurrence following surgical resection.  Long noncoding RNAs (lncRNAs) play an important role in cancer development.  Pathogenesis of adrenal tumours has been characterised by mRNA, microRNA and methylation expression signatures but it is unknown if this extends to lncRNAs. We sought to describe lncRNA expression signatures in adrenocortical carcinoma (ACC), adrenal cortical adenoma (ACA) and normal adrenal cortex (NAC).
RNA was extracted from freshly frozen tissue with confirmation of diagnosis by histopathology.  Focused lncRNA and mRNA transcriptome analysis was performed using the ArrayStar Human LncRNA V3.0 microarray.  Differentially expressed lncRNAs were validated using qRT-PCR.

overall_design: 21 samples were used in total, 15 cases were included (10 ACCs and 5 ACAs) and compared to 6 controls (NAC). Differentially expressed lncRNAs were selected if they had a minimum fold change of 2.0 up or down regulated and a P-value corrected by the false discovery rate of equal to or less than 0.05.

first: Stan

middle: B

last: Sidhu


title: Expression and Prognostic impact of LncRNAs in AML

status: Public on Nov 26 2014

city: Columbus

first: Ramiro

last: Garzon

address: 460 12th street

institute: Ohio State University

summary: Long noncoding RNAs (lncRNAs) are transcripts longer than 200 nucleotides located within the intergenic stretches or overlapping antisense transcripts of protein coding genes. LncRNAs are involved in numerous biological roles including imprinting, epigenetic regulation, apoptosis and cell-cycle. To determine whether lncRNAs are associated with clinical features and recurrent mutations in older patients (aged ≥60 years) with cytogenetically normal (CN) acute myeloid leukemia (AML), we evaluated lncRNA expression in 148 untreated older CN-AML cases using a custom microarray platform.

overall_design: We analyzed 148 older cytogenetically normal(CN)-AML patients samples using a custom microarray platform and describe the expression of lncRNAs among the AML samples.

first: Stefano

last: Volinia

first: Dimitrios

last: Papaioannou

first: Deedra

last: Nicolet

first: Jessica

last: Kohlschmidt

first: Pearlly

last: Yan

first: Krzysztof

last: Mrózek

first: Donna

last: Bucci

first: Andrew

last: Carroll

first: Maria

last: Baer

first: Meir

last: Wetzler

first: Thomas

middle: H

last: Carter

first: Bayard

last: Powell

last: Kolitz

first: Joseph

middle: O

last: Moore

first: Ann-Kathrin

last: Eisfeld

first: James

last: Blachly

first: William

last: Blum

first: Michael

last: Caligiuri

first: Richard

last: Stone

first: Guido

last: Marcucci

first: Carlo

last: M. Croce

first: John

last: Byrd

first: Clara

middle: D

last: Bloomfield


title: Development of lncRNA and Mrna expression signatures for pancreatic ductal adenocarcinoma

status: Public on Nov 18 2014

city: Shanghai

first: yong

middle: wei

last: sun

state: Shanghai

address: Road pujian 200

department: Department of General Surgery

institute: Shanghai Jiao-Tong University School of Medicine, Renji Hospital

summary: To further development of our lncRNA and mRNA expression  approach to pancreatic ductal adenocarcinoma(PDAC), we have employed lncRNA and mRNA microarray expression     profiling as a discovery platform to identify lncRNA and mRNA expression in pancreatic ductal adenocarcinoma.Human pancreatic ductal adenocarcinoma tissues and normal     pancreatic  tissues from PDAC  donors and other duodenum diseases donors.

overall_design: analyze mRNA and lncRNA expression in pancreatic ductal adenocarcinoma (PDAC) by microarray platform

first: Jiao

last: Li

first: Yongwei

last: Sun


title: shRNA Off-Target Effects In Vivo: Impaired Endogenous siRNA Expression and Spermatogenic Defects

status: Public on Dec 19 2014

city: La Jolla

first: Miles

last: Wilkinson

address: 9500 Gilman Dr. MC 0695

department: Reproductive Medicine

institute: UCSD

summary: RNA interference (RNAi) is widely used to determine the function of genes.  We chose this approach to assess the collective function of the highly related reproductive homeobox 3 (Rhox3) gene paralogs.  Using a Rhox3 short hairpin (sh) RNA with 100% complementarity to all 8 Rhox3 paralogs, expressed from a CRE-regulated transgene, we successfully knocked down Rhox3 expression in male germ cells in vivo.  These Rhox3-shRNA transgenic mice had dramatic defects in spermatogenesis, primarily in spermatocytes and round spermatids.  To determine whether this phenotype was caused by reduced Rhox3 expression, we generated mice expressing the Rhox3-shRNA but lacking the intended target of the shRNA – Rhox3.  These double-mutant mice had a phenotype indistinguishable from Rhox3-shRNA-expressing mice that was different from mice lacking the Rhox3 paralogs, indicating that the Rhox3 shRNA disrupts spermatogenesis independently of Rhox3.  Rhox3-shRNA transgenic mice displayed few alterations in the expression of protein-coding genes, but instead exhibited reduced levels of all endogenous siRNAs we tested.  This supported a model in which the Rhox3 shRNA causes spermatogenic defects by sequestering one or more components of the endogenous small RNA biogenesis machinery.  Our study serves as a warning for those using shRNA approaches to investigate gene functions in vivo.

overall_design: Comparison of total RNA from post-natal day 15 testis extracted from three wild-type mice and three transgenic mice genetically engineered to express siRNA designed to knock-down Rhox3.  RNA hybridised to Affymetrix mouse all exon arrays.

first: Hye-Won

last: Song

first: Anilkumar

last: Bettegowda

first: Daniel

last: Oliver

first: Wei

last: Yan

first: Mimi

last: Phan

first: Mark

last: Corbett

first: Dirk

middle: G

last: de Rooij

middle: F


title: Bromodomain dependence of BRD4-dependent gene expression in mouse fibroblasts

status: Public on Nov 10 2014

city: Bethesda

first: Tomohiko

last: Kanno

address: Bldg.10/Room 11B15, NIH

department: NIAID

institute: NIH

summary: To study the role of the bromodomain (BD) in BRD4-dependent gene expression, we compared the function of wild type BRD4 and a mutant BRD4-mBD, which carries a point mutation in each of the two BDs. We first knocked down endogenous BRD4 by shRNA (shBRD4) and then stably reconstituted the cells with shBRD4-resistant YFP-BRD4 (wild type or mBD mutant). Following BRD4 reconstitution, the degree of recovery in gene expression was analyzed by Affymetrix Mouse Exon 1.0 ST array. Wild-type BRD4 restored gene expression significantly and far more efficiently than the mBD mutant.

overall_design: NIH3T3 cells were sequentially infected with shRNA retrovirus (pSRneo-shCont or pSRneo-shBRD4) and YFP-BRD4 expressing retrovirus (pMSCVpuro-YFP, pMSCVpuro-YFP-BRD4, pMSCVpuro-YFP-BRD4-mBD). shBRD4 contains an oligonucleotide encoding an shRNA sequence against mouse BRD4 and shCont contains a scrambled oligonucleotide. The transduced cells were selected with G418 and puromycin. Two independent sets of cell lines (line B set and line D set) were produced from different laboratory stocks of NIH3T3 cells. Each set contained: YFP_shCONT, YFP_shBRD4, BRD4WT_shBRD4, and RD4mBD_shBRD4. The Affymetrix Mouse Exon 1.0 ST platform was used. No technical replicate was performed.

first: Yuka

first: Keiko

last: Ozato

last: O'Shea


title: Nuclear actin activates human transcription factor genes including the OCT4 gene

city: Sendai

first: Masahiko

last: Harata

address: 468-1 Aramaki Aza Aoba, Aoba-ku

department: Graduate School of Agricultural Science

institute: Tohoku University

summary: RNA microarray analyses revealed that nuclear actin activated many human transcription factor genes including OCT4, which is required for gene reprogramming. OCT4 is known to be activated by nuclear actin in Xenopus oocytes. Our findings imply that this process of OCT4 activation is conserved in vertebrates and among cell types, and could be used for gene reprogramming of human cells.

overall_design: HeLa cells expressed EYFP-actin or EYFP-NLS-actin were cultured at 48 hour.  Total RNAs were extracted and subjected to microarray analysis.

first: Shota

last: Yamazaki

first: Koji

last: Yamamoto

first: Makio

last: Tokunaga

first: Kumiko

last: Sakata-Sogawa