title: Acinetobacter oleivorans DR1 : WT stationary phase vs. aqsR mutant stationary phase

status: Public on Feb 16 2013

city: Seoul

first: Jisun

last: Kim

address: Anam-Dong, Sungbuk-Gu

department: Environmental Science and Ecological Engineering

country: South Korea

institute: Korea university

summary: Transcriptional profiling of A. oleivorans DR1 cells comparing wild type stationary phase cells with aqsR mutant stationary phase cells.

overall_design: To identify genes regulated QS system in A. oleivorans DR1, the cells were grown to stationary phase (OD600 >0=2.0).

first: Woojun

last: Park


title: Epigenetic analysis of gastric cancer

status: Public on Oct 24 2012

city: Singapore

first: Patrick

last: Tan

address: 8 College Rd.

country: Singapore

institute: Duke-NUS Graduate Medical School

summary: Genome-wide DNA methylation profiling of gastric tumors and matched gastric non-malignant samples. The Illumina HumanMethylation27 BeadChip was used to obtain DNA methylation profiles across 27,578 CpGs in 203 gastric tumors and  94 matched non-malignant gastric samples.

overall_design: Bisulphite-converted DNA from the 203 gastric tumors and 94 matched gastric non-malignant samples was hybridized to the Illumina HumanMethylation27 BeadChip.

first: Hermioni

last: Zouridis


title: Environmentally Induced Epigenetic Transgenerational Inheritance of Somatic Transcriptomes

status: Public on Jul 01 2012

city: Pullman

first: Michael

middle: K

last: Skinner

state: WA

address: Abelson 507

department: SBS

country: USA

institute: WSU

summary:
Environmentally induced epigenetic transgenerational inheritance of adult onset disease involves a variety of phenotypic changes suggesting a general alteration in genome activity.   Investigation of eleven different tissue transcriptomes in male and female F3 generation vinclozolin versus control lineage rats demonstrated all tissues examined had unique transgenerational transcriptomes.  Common cellular pathways and processes were identified among the tissues.  A bionetwork analysis identified gene modules with coordinated gene expression and each had unique gene networks regulating tissue specific gene expression and function.  A large number of statistically significant over-represented clusters of differentially expressed genes were identified and termed “Epigenetic Control Regions”.  Combined observations demonstrate that all tissues derived from the epigenetically altered germ line develop transgenerational transcriptomes unique to the tissue, but common epigenetic control regions in the genome appear to in part coordinately regulate these tissue specific transcriptomes.  This systems biology approach provides insight into the molecular mechanisms involved in the epigenetic transgenerational inheritance of a variety of adult onset disease phenotypes.
We used microarrays to determine genes expressed differentially in rats 11 male or female smatic tissues -male heart, kidney, liver, testis, prostate, seminal vesicles; female heart, kidney, liver, ovary, uterus  -  due to Vinclozolin treatments of their grand-grandmothers.

overall_design: For each of 11 male or female smatic tissues, RNA samples from 2 treatment groups - control (Con) and vinclozolin (Vin) - were compared to each other.  Each treatment groups contained 3 biological replica. RNA for each replica was pooled from 2 individual animals.

first: Mohan

last: Manikkam

first: M

last: Haque

first: Bin

last: Znang

first: Marina

last: Savenkova


title: CGH: FN1.4_v_M92-220

status: Public on Jun 04 2014

city: Saint Paul

first: Robert

middle: M

last: Stupar

state: MN

address: 1991 Upper Buford Circle

department: Agronomy and Plant Genetics

institute: University of Minnesota

summary:
Soybean fast neutron (FN) mutant lines were compared by CGH to catalog structurally variant (e.g. deletion and duplication) regions compared to the parent line (M92-220).
The CGH comparisons reveal reveal putative deletions and duplications among the mutant lines.

overall_design: FN lines were compared through a common reference, M92-220 (this is a sub-line individual isolated from the M92-220 seed stock).  Each FN line was represented by a single individual plant.  The reported values show the log2 ratio of the normalized FN line hybridization signals (Cy3) over the normalized M92-220 hybridization signal (Cy5).

first: Adrian

middle: O

last: Stec

first: Bolon

last: Yung-Tsi

first: Justin

middle: E

last: Anderson


title: High-throughput sequencing of sequentially reprogrammed iPS cells reveals key epigenetic modifications correlated with reduced pluripotency of iPS cells [RNA-seq]

status: Public on Dec 06 2013

city: Beijing

first: Tao

last: Cai

address: No. 7 Science Park Road, Zhongguancun Life Science Park

country: China

institute: National Institute Of Biological Sciences, Beijing (NIBS)

type: Expression profiling by high throughput sequencing

summary: Full pluripotency of induced pluripotent stem (iPS) cells has been determined as viable all-iPS mice can be generated through tetraploid complementation. Subsequently, activation of imprinted Dlk-Dio3 gene cluster has been suggested to correlate with the pluripotency of iPS cells1. However, evidence from recent studies has demonstrated that loss of imprinting at the Dlk-Dio3 locus did not correlate strictly with the reduced pluripotency of iPS cells. Therefore, it becomes indispensable to exploit other reliable molecular markers for evaluating the quality of iPS cells accurately. In the present study, we successfully utilize the sequential reprogramming approach and produce all-iPS mice to six generations using iPS cell lines derived from different cell lineages which contain the same proviral integration in the genome. By comparing the global gene expression and epigenetic modifications of both "tetra-on" and corresponding "tetra-off" iPS cell lines established from either mesenchymal or hematopoietic lineages through deep sequencing analysis of mRNA expression, small RNA profiling, histone modifications (H3K4m2, H3K4me3 and H3K27me3) and DNA methylation, very few differences are detected among all the iPS cell lines investigated. However, we find that two imprinted genes, disruption of which correlate with the reduced pluripotency of iPS cells. Therefore, our data not only provide the first demonstration that producing of all-iPS mice to six generations is feasible, but reveal that two imprinted regions can be served as pluripotency markers of iPS cells.

overall_design: Examination of the mRNA expression in 13 cell types

first: Gang

last: Chang

first: Shuai

last: Gao

first: Jianhui

last: Tian

first: Shaorong


title: Systematical identification of GATA-1, EKLF, and NF-E2 regulated miRNAs by ChIP-on chip and microRNA microarray in K562 cells into erythroid differentiation

status: Public on Dec 31 2011

city: Bei Jing

first: Jia

last: Yu

address: Dong Dan San Tiao #5

department: Biochemistry

institute: Peking Union Medical College

type: Genome binding/occupancy profiling by array

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

overall_design: Refer to individual Series


title: Expression profiling of lung cancer cell lines (UTSW Lung Panel V2)

status: Public on Oct 25 2012

city: Dallas

first: Luc

last: Girard

state: TX

address: 5323 Harry Hines Blvd

department: Hamon Center for Therapeutic Oncology Research

institute: UT Southwestern Medical Center

summary: Epithelial/mesenchymal transition (EMT) is associated with loss of cell adhesion molecules, such as E-cadherin, and increased invasion, migration, and proliferation in epithelial cancers. In non-small cell lung cancer (NSCLC), EMT is associated with greater resistance to EGFR inhibitors. However, its potential to predict response to other targeted drugs or chemotherapy has not been well characterized. The goal of this study was to develop a robust, platform-independent EMT gene expression signature and to investigate the association of EMT and drug response in NSCLC.  A 76-gene EMT signature was derived in 54 DNA-fingerprinted NSCLC cell lines and tested in an independent set of cell lines and in NSCLC patients from the BATTLE clinical trial.  The signature classified cell lines as epithelial or mesenchymal independent of the microarray platform and correlated strongly with E-cadherin protein levels, as measured by reverse phase protein array.  Higher protein expression of Rab25 (in epithelial lines) and Axl (in mesenchymal lines), two signature genes associated with in EMT in other cancer types, was also confirmed. Mesenchymal cell lines demonstrated significantly greater resistance to EGFR inhibition, independent of EGFR mutation status and were more resistant to drugs targeting the PI3K/Akt pathway. We observed no association between EMT and response to cytotoxic chemotherapies, including cisplatin, pemetrexed, and docetaxel monotherapy and/or doublets (p-values ?0.2).  In NSCLC patients, the EMT signature predicted 8-week disease control in the erlotinib arm, but not in other treatment arms.  In conclusion, we have developed a robust EMT signature that predicts resistance to EGFR inhibitors and PI3K/Akt pathway inhibitors.

overall_design:
To develop gene expression signatures for in vitro drug response and other phenotypes.
Profiling was done on 68 NSCLC cell lines and 2 HBEC-KT cell lines (normal lung cells immortalized with CDK4 and hTERT).

first: John

middle: D

last: Minna


title: High-throughput sequencing of sequentially reprogrammed iPS cells reveals key epigenetic modifications correlated with reduced pluripotency of iPS cells [sRNA-seq]

type: Non-coding RNA profiling by high throughput sequencing

summary: Full pluripotency of induced pluripotent stem (iPS) cells has been determined as viable all-iPS mice can be generated through tetraploid complementation. Subsequently, activation of imprinted Dlk-Dio3 gene cluster has been suggested to correlate with the pluripotency of iPS cells1. However, evidence from recent studies has demonstrated that loss of imprinting at the Dlk-Dio3 locus did not correlate strictly with the reduced pluripotency of iPS cells. Therefore, it becomes indispensable to exploit other reliable molecular markers for evaluating the quality of iPS cells accurately. In the present study, we successfully utilize the sequential reprogramming approach and produce all-iPS mice to six generations using iPS cell lines derived from different cell lineages which contain the same proviral integration in the genome. By comparing the global gene expression and epigenetic modifications of both “tetra-on” and corresponding “tetra-off” iPS cell lines established from either mesenchymal or hematopoietic lineages through deep sequencing analysis of mRNA expression, small RNA profiling, histone modifications (H3K4m2, H3K4me3 and H3K27me3) and DNA methylation, very few differences are detected among all the iPS cell lines investigated. However, we find that two imprinted genes, disruption of which correlate with the reduced pluripotency of iPS cells. Therefore, our data not only provide the first demonstration that producing of all-iPS mice to six generations is feasible, but reveal that two imprinted regions can be served as pluripotency markers of iPS cells

overall_design: Examination of the expression small RNA in 13 cell types


title: Predective Value of Prognosis-Related Gene Expression Study in Primary Bladder Cancer

status: Public on May 06 2010

city: Daejeon

first: Seon-Kyu

last: Kim

address: 125 Gwahak-ro, Yuseong-gu, Daejeon 305-806, Korea

department: Personalized Genomic Medicine Research Center

institute: Korea Research Institutue of Bioscience & Biotechnology

summary:
This study aimed to identify the genetic signatures associated with disease prognosis in bladder cancer. We used 165 primary bladder cancer samples, 23 recurrent non-muscle invasive tumor tissues, 58 normal looking bladder mucosae surrounding cancer and 10 normal bladder mucosae for microarray analysis. Hierarchical clustering was used to stratify the prognosis-related gene classifiers. For validation, real-time reverse-transcriptase polymerase chain reaction (RT-PCR) of top-ranked 14 genes was performed. On unsupervised hierarchical clustering using prognosis related gene-classifier, tumors were divided into 2 groups. The high risk gene signatures had significantly poor prognosis compared to low risk gene signatures (P<0.001 by the log-rank test, respectively). The prognosis-related gene classifiers correlated significantly with recurrence of non-muscle invasive bladder cancer (hazard ratio, 4.09; 95% confidence interval [CI], 1.94 to 8.64; P<0.001), and progression (hazard ratio, 23.68; 95% confidence interval [CI], 4.91 to 114.30; P<0.001), cancer-specific survival (hazard ratio, 29.25; 95% confidence interval [CI], 3.47 to 246.98; P=0.002) and overall survival (hazard ratio, 23.33; 95% confidence interval [CI], 4.97 to 109.50; P<0.001) of muscle invasive bladder cancer (p < 0.001, respectively). No patient with non-muscle invasive bladder cancer experienced cancer progression in low risk gene signature group. Prognosis-related gene classifiers validated by RT- PCR showed identical results. Prognosis related gene-classifiers provided strong predictive value for disease outcome. These gene classifiers could assist in selecting patients who might benefit from more aggressive therapeutic intervention or surveillance.

Keywords: Gene expression, Bladder cancer, Prognosis

overall_design: 165 primary bladder cancer samples and 23 recurrent non-muscle invasive tumor tissues from 14 patients were taken in the Chungbuk National University Hospital. Only histologically verified transitional cell carcinoma samples were selected. Simultaneously 58 normal looking bladder mucosae surrounding cancer were obtained during the operation, which were histologically confirmed normal. Also, 10 normal bladder mucosae were obtained from patients with benign disease. The normal controls were determined to be free of cancer after revealing no malignant cells on urine cytology and no observable bladder cancer on cystoscopic examination during operation for their diseases, and were histologically reconfirmed normal.

first: Sun-Hee

last: Leem

first: In-Sun

last: Chu

first: Yong-June

first: Wun-Jae


title: Pooled macrophage datasets from GEO

status: Public on Jul 16 2019

city: La Jolla

first: Debashis

last: Sahoo

state: California

address: 9500 Gillman Drive

department: Pediatrics

institute: UCSD

summary: This is a collection of diverse publicly available macrophage datasets. The datasets belong to three different platforms and all normalized together using modified CDF files.

relation:
Reanalysis of: GSM249368
Reanalysis of: GSM230352
Reanalysis of: GSM213466
Reanalysis of: GSM300391
Reanalysis of: GSM230360
Reanalysis of: GSM343819
Reanalysis of: GSM343815
Reanalysis of: GSM343831
Reanalysis of: GSM360140
Reanalysis of: GSM183467
Reanalysis of: GSM183209
Reanalysis of: GSM300418
Reanalysis of: GSM300403
Reanalysis of: GSM183465
Reanalysis of: GSM300393
Reanalysis of: GSM300400
Reanalysis of: GSM249378
Reanalysis of: GSM183485
Reanalysis of: GSM183315
Reanalysis of: GSM249418
Reanalysis of: GSM249390
Reanalysis of: GSM249365
Reanalysis of: GSM249370
Reanalysis of: GSM343805
Reanalysis of: GSM300396
Reanalysis of: GSM249374
Reanalysis of: GSM249415
Reanalysis of: GSM183217
Reanalysis of: GSM343826
Reanalysis of: GSM230355
Reanalysis of: GSM300398
Reanalysis of: GSM249401
Reanalysis of: GSM249410
Reanalysis of: GSM183305
Reanalysis of: GSM343803
Reanalysis of: GSM249413
Reanalysis of: GSM213511
Reanalysis of: GSM300413
Reanalysis of: GSM183393
Reanalysis of: GSM249395
Reanalysis of: GSM249417
Reanalysis of: GSM300407
Reanalysis of: GSM343820
Reanalysis of: GSM360142
Reanalysis of: GSM249382
Reanalysis of: GSM300411
Reanalysis of: GSM360221
Reanalysis of: GSM249389
Reanalysis of: GSM249371
Reanalysis of: GSM249398
Reanalysis of: GSM343808
Reanalysis of: GSM343825
Reanalysis of: GSM249416
Reanalysis of: GSM183196
Reanalysis of: GSM230353
Reanalysis of: GSM249375
Reanalysis of: GSM249392
Reanalysis of: GSM343823
Reanalysis of: GSM183487
Reanalysis of: GSM249367
Reanalysis of: GSM360184
Reanalysis of: GSM249369
Reanalysis of: GSM343802
Reanalysis of: GSM249402
Reanalysis of: GSM300390
Reanalysis of: GSM249422
Reanalysis of: GSM343810
Reanalysis of: GSM249387
Reanalysis of: GSM343828
Reanalysis of: GSM249409
Reanalysis of: GSM300389
Reanalysis of: GSM360144
Reanalysis of: GSM360182
Reanalysis of: GSM300420
Reanalysis of: GSM300421
Reanalysis of: GSM249407
Reanalysis of: GSM249381
Reanalysis of: GSM249420
Reanalysis of: GSM360186
Reanalysis of: GSM249384
Reanalysis of: GSM343814
Reanalysis of: GSM300402
Reanalysis of: GSM249403
Reanalysis of: GSM249385
Reanalysis of: GSM230357
Reanalysis of: GSM249397
Reanalysis of: GSM300416
Reanalysis of: GSM360139
Reanalysis of: GSM183483
Reanalysis of: GSM343812
Reanalysis of: GSM300410
Reanalysis of: GSM213465
Reanalysis of: GSM300405
Reanalysis of: GSM183462
Reanalysis of: GSM360145
Reanalysis of: GSM343806
Reanalysis of: GSM183464
Reanalysis of: GSM183193
Reanalysis of: GSM300409
Reanalysis of: GSM300406
Reanalysis of: GSM300412
Reanalysis of: GSM249396
Reanalysis of: GSM183394
Reanalysis of: GSM249405
Reanalysis of: GSM183466
Reanalysis of: GSM213500
Reanalysis of: GSM300392
Reanalysis of: GSM300414
Reanalysis of: GSM183482
Reanalysis of: GSM183165
Reanalysis of: GSM300404
Reanalysis of: GSM249377
Reanalysis of: GSM183484
Reanalysis of: GSM343816
Reanalysis of: GSM300394
Reanalysis of: GSM213512
Reanalysis of: GSM343813
Reanalysis of: GSM249379
Reanalysis of: GSM249400
Reanalysis of: GSM249424
Reanalysis of: GSM230349
Reanalysis of: GSM230351
Reanalysis of: GSM249373
Reanalysis of: GSM230350
Reanalysis of: GSM343821
Reanalysis of: GSM183392
Reanalysis of: GSM249394
Reanalysis of: GSM343818
Reanalysis of: GSM300408
Reanalysis of: GSM249412
Reanalysis of: GSM300415
Reanalysis of: GSM249386
Reanalysis of: GSM249391
Reanalysis of: GSM360185
Reanalysis of: GSM249411
Reanalysis of: GSM249406
Reanalysis of: GSM300397
Reanalysis of: GSM343817
Reanalysis of: GSM300395
Reanalysis of: GSM343804
Reanalysis of: GSM249414
Reanalysis of: GSM343827
Reanalysis of: GSM360141
Reanalysis of: GSM360143
Reanalysis of: GSM213464
Reanalysis of: GSM249376
Reanalysis of: GSM183316
Reanalysis of: GSM249372
Reanalysis of: GSM343824
Reanalysis of: GSM249419
Reanalysis of: GSM249393
Reanalysis of: GSM343830
Reanalysis of: GSM230359
Reanalysis of: GSM343807
Reanalysis of: GSM360146
Reanalysis of: GSM300401
Reanalysis of: GSM343829
Reanalysis of: GSM183306
Reanalysis of: GSM249366
Reanalysis of: GSM360187
Reanalysis of: GSM183463
Reanalysis of: GSM343822
Reanalysis of: GSM249399
Reanalysis of: GSM183486
Reanalysis of: GSM183201
Reanalysis of: GSM249423
Reanalysis of: GSM343809
Reanalysis of: GSM249421
Reanalysis of: GSM249408
Reanalysis of: GSM343811
Reanalysis of: GSM300419
Reanalysis of: GSM360188
Reanalysis of: GSM300399
Reanalysis of: GSM249388
Reanalysis of: GSM230356
Reanalysis of: GSM300417
Reanalysis of: GSM230358
Reanalysis of: GSM249404
Reanalysis of: GSM360183
Reanalysis of: GSM249380
Reanalysis of: GSM249383
Reanalysis of: GSM230354
Reanalysis of: GSM115046
Reanalysis of: GSM115047
Reanalysis of: GSM115048
Reanalysis of: GSM115049
Reanalysis of: GSM115050
Reanalysis of: GSM115051
Reanalysis of: GSM115052
Reanalysis of: GSM115053
Reanalysis of: GSM115054
Reanalysis of: GSM115055
Reanalysis of: GSM115056
Reanalysis of: GSM115057
Reanalysis of: GSM115058
Reanalysis of: GSM115059
Reanalysis of: GSM115060

overall_design: 197 published macrophage samples from seven series assayed on the GPL570, GPL571 and GPL96 platforms were re-analyzed. RMA was used to normalize the CEL files using modified CDF files to analyze the shared probes among the three different platforms.


title: Effects of diet and Acads genotype on transcriptional response in brain and liver

status: Public on Dec 20 2012

city: Baton Rouge

first: Brenda

last: Richards

state: LA

address: 6400 Perkins Rd.

department: Basic Science

institute: Pennington Biomedical Research Center

summary: How signals from fatty acid metabolism are translated into changes in food intake remains unclear.  Previously we reported that mice with a genetic inactivation of Acads (short-chain acyl-CoA dehydrogenase), encoding the enzyme responsible for mitochondrial beta-oxidation of C4-C6 short-chain fatty acids (SCFAs), shift consumption away from fat and toward carbohydrate when offered a choice. This finding demonstrated that the loss of a specific enzyme in fatty acid oxidation alters the choice of diet intake.  To our knowledge, there are no reports of studies on the effects of dietary fat on the brain transcriptome in genetic models of fatty acid oxidation deficiency.  The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. We performed a transcriptional screen for gene expression in brain tissue of Acads-/- and Acads+/+ mice fed either high-fat (HF) or low-fat (LF) diet for 2 d.  Ingenuity Pathway Analysis revealed three top-scoring pathways significantly modified by genotype or diet:  oxidative phosphorylation, mitochondrial dysfunction, and CREB signaling in neurons.  A comparison of statistically significant responses in HF Acads-/- vs. HF Acads+/+ (3917) and Acads+/+ HF vs. LF Acads+/+ (3879) revealed 2551 genes or approximately 65% in common between the two experimental comparisons.  All but one of these genes were expressed in opposite direction with similar magnitude, demonstrating that Acads-deficient mice fed HF diet display transcriptional responses that mimic those of wildtype Acads+/+ mice fed LF diet.  Intriguingly, genes involved in energy sensing and metabolism followed this pattern.  Quantitative RT-PCR in hypothalamus confirmed the dysregulation of several genes in these pathways.  Western blotting showed that the combination of Acads deficiency and HF diet increased hypothalamic AMP-kinase, a key protein in an energy-sensing cascade that responds to depletion of ATP. Our results suggest that the decreased beta oxidation of short-chain fatty acids in Acads-deficient mice fed HF diet produces a state of energy deficiency in the brain and that AMP-kinase is the cellular energy-sensing mechanism linking fatty acid oxidation to feeding behavior in this model.

overall_design: Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from whole brain tissue was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in brain was compared between strains and between diets. Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from liver was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in liver was compared between strains and diets.

first: K

middle: G

last: Kumar


title: Microarray Analysis of the transcriptome of the Subfornical Organ in the rat

status: Public on Oct 01 2008

city: Bristol

first: DAVID

last: MURPHY

state: AVON

address: Whitson Street

department: Medicine and Dentistry

country: United Kingdom

institute: University of Bristol

summary: In these studies we have for the first time described the transcriptome of the rat SFO, and have in addition identified genes the expression of which is significantly modified by either water or food deprivation.

overall_design: For each condition (food deprivation, water deprivation, untreated), 25 animals were denied food for 48 hours prior to sacrifice. The Subfornical organ was removed under a dissecting microscope from a 1mm slice of brain removed from an ice cold brain matrix. SFO's from 5 animals were pooled for each sample prior to RNA extraction to give n=5.

first: Charles

middle: C

last: Hindmarch

first: Mark

last: Fry

first: Song

last: Yao

first: Pauline

last: Smith

first: Alastair

middle: V

last: Ferguson


title: Transcriptional profiling of a  wound healing process in skin and oral mucosa

status: Public on Jul 20 2010

city: Chicago

first: Zarema

middle: H

last: Arbieva

state: IL

address: 835 S. Wolcott A301

department: RRC

institute: UIC

summary: When compared to skin, oral mucosal wounds heal rapidly and with reduced scar formation. This study used an Affymetrix microarray platform to compare the transcriptomes of oral mucosa and skin wounds in order to identify critical differences in the healing response at these two sites.

overall_design: Using microarrays, we explored the differences in gene expression in skin and oral mucosal wound healing in a murine model of paired equivalent-sized wounds. Samples were examined from day 0 to day 10 and spanned all stages of the wound healing process. Unwounded matched tissue was used as a control. Tissue samples collected at each post-wounding time point, as well as control samples, were represented by 3 biological replicates.


title: Analysis of lung cancer cell lines

status: Public on May 16 2006

first: Luc

summary:
These arrays are used for various projects
Keywords: cell type comparison

overall_design: HG-U133A and HG-U133B data are combined and analyzed together with other U133A & B or with HG-U133plus2 samples. No replicates were performed. Controls are human bronchial epithelial cells (HBECs)


title: Expression data from human pancreatic islets

status: Public on Jul 05 2012

city: Malmö

first: Joao

last: Fadista

address: Jan Waldenströms gata 35

country: Sweden

institute: Lund University Diabetes Centre

summary:
Close to 50 genetic loci have been associated with type 2 diabetes (T2D), but they explain only 15% of the heritability.
In an attempt to identify additional T2D genes, we analyzed global gene expression in human islets from 63 donors.

overall_design: Islets from cadaver donors (54 non-diabetic and 9 diabetic) were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChip® Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.

first: João

first: Jalal

last: Taneera


title: NF-kB suppresses genomic instability in non-Hodgkin lymphomas

status: Public on Sep 10 2010

city: Atlanta

first: Xiangxue

last: Guo

state: GA

address: 1365 Clifton Rd, Bld-C, 3rd, B25

institute: Emory University

summary: Oci-Ly3 and Daudi cell lines expressing p100-, p105- and luciferase-siRNA were used to identify genes that are regulated by p100 or p105 in each cell line.

overall_design: p100- (n=3) and p105- (n=3) expressing cells were compared to Luciferase siRNA, using linear models and signficant genes were identified using FDR of 0.001. Then the results for Daudi and OCI-LY3 cell lines were compared and only genes commonly regulated in both cell lines by p100 or p105 were  selected for furhter studies.

first: Leon

last: Bernal-Mizrachi

first: Sampath

last: Ramachandiran


title: Expression profile of hemin induced erythroid differentiation, over-expressing and knocking-down GATA-1, EKLF and NF-E2 in K562s

first: Jia

last: Yu

summary: we profiled miRNA gene expression with the Illumina hybridization system in K562 cells induced by hemin and K562 cells with over-expressing or knocking-down GATA-1, EKLF or NF-E2 treatments.

overall_design: To find differential expression miRNAs, we profiled miRNA gene expression with the Illumina hybridization system in untreated, hemin-treated 48h and 72h K562 cells. To define GATA-1, EKLF or NF-E2 directly targeted miRNA genes, a comprehensive analysis of TF induced miRNA gene expression changes was performed using over-expressing or knocking-down TFs in K562 cells and illumina miRNA profiling Beadchip system.

first: Fang

last: Wang

first: Yong

last: Zhu

first: Rui

last: Su