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accession-icon GSE26983
Comparison of salt stress resistance genes in transgenic Arabidopsis thaliana indicates that extent of transcriptomic change may not predict secondary phenotypic or fitness effects
  • organism-icon Arabidopsis thaliana
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Engineered abiotic stress resistance is an important target for increasing agricultural productivity.There are concerns, however, regarding possible ecological impacts of transgenic crops. In contrast to the first wave of transgenic crops, many abiotic stress resistance genes can initiate

Publication Title

Comparison of salt stress resistance genes in transgenic Arabidopsis thaliana indicates that extent of transcriptomic change may not predict secondary phenotypic or fitness effects.

Alternate Accession IDs

E-GEOD-26983

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE38093
Diet-Induced Obesity Exacerbates Inflammatory and Oxidative Stress Responses in Mice Exposed to Cigarette Smoke
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively.

Publication Title

Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.

Alternate Accession IDs

E-GEOD-38093

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE47022
Impaired Transcriptional Response of the Murine Heart To Cigarette Smoke in the Setting of High Fat Diet and Obesity
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively.

Publication Title

Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.

Alternate Accession IDs

E-GEOD-47022

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE38092
Diet-Induced Obesity Reprograms the Inflammatory Response of the Murine Lung to Inhaled Endotoxin
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To identify key biological pathways that define susceptibility factors for pulmonary infection during obesity, diet-induced obese (DIO) and regular weight (RW) C57BL/6 mice were exposed to 0.5 g/L inhaled lipopolysaccharide (LPS) for 1 hr/d for 4 days over a period of 2 weeks.

Publication Title

Diet-induced obesity reprograms the inflammatory response of the murine lung to inhaled endotoxin.

Alternate Accession IDs

E-GEOD-38092

Sample Metadata Fields

Specimen part

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accession-icon GSE63790
Braf inhibitors reverse the unique molecular signature and phenotype of hairy cell leukemia, and exert anti-leukemic activity
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hairy cell leukemia (HCL) shows unique clinico-pathological and biological features. HCL responds well to purine analogues but relapses are frequent and novel therapies are required. BRAF-V600E is the key driver mutation in HCL and distinguishes it from other B-cell lymphomas, including HCL-like leukemias/lymphomas (HCL-variant and splenic marginal zone lymphoma). The kinase-activating BRAF-V600E mutation also represents an ideal therapeutic target in HCL. Here, we investigated the biological and therapeutic importance of the activated BRAF-MEK-ERK pathway in HCL by exposing in vitro primary leukemic cells purified from 26 patients to clinically available BRAF (Vemurafenib; Dabrafenib) or MEK (Trametinib) inhibitors. Results were validated in vivo in samples from Vemurafenib-treated HCL patients within a phase-2 clinical trial. BRAF and MEK inhibitors caused, specifically in HCL (but not HCL-like) cells, marked MEK/ERK dephosphorylation, silencing of the BRAF-MEK-ERK pathway transcriptional output, loss of the HCL-specific gene expression signature, downregulation of the HCL markers CD25, TRAP and cyclin-D1, smoothening of leukemic cells' hairy surface, and, eventually, apoptosis. Apoptosis was partially blunted by co-culture with bone marrow stromal cells antagonizing MEK-ERK dephosphorylation. This protective effect could be counteracted by combined BRAF and MEK inhibition. Our results strongly support and inform the clinical use of BRAF and MEK inhibitors in HCL.

Publication Title

BRAF inhibitors reverse the unique molecular signature and phenotype of hairy cell leukemia and exert potent antileukemic activity.

Alternate Accession IDs

E-GEOD-63790

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE52171
Novel Immunotherapy-Induced Tertiary Lymphoid Aggregates Accumulate as Intratumoral Nodal Structures of Immune Regulation in Pancreatic Cancer
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Immunotherapy provides an alternative approach for cancer treatment. However, in-depth analyses of the effects of immunotherapy on the tumor microenvironment (TME) have not been conducted in non-melanoma tumors. Here we describe changes in the pancreatic ductal adenocarcinoma (PDAC) TME following immunotherapy treatment, and show for the first time that vaccine-based immunotherapy directly alters the TME, inducing neogenesis of tertiary lymphoid structures that convert immunologically quiescent tumors into immunologically active tumors. Alterations in five pathways important for immune modulation and lymphoid structure development (TH17/Treg, NFkB, Ubiquitin-proteasome, Chemokines/chemokine receptors, and Integrins/adhesion molecules) in vaccine-induced intratumoral lymphoid aggregates were associated with improved post-vaccination responses. Additional studies in other cancers and patients treated with other forms of immunotherapy are warranted to further develop signatures defined in intratumoral lymphoid structures into biomarkers that predict effective anti-tumor immune responses. These signatures may also expose therapeutic targets for promoting more robust antitumor immune responses in the TME.

Publication Title

Immunotherapy converts nonimmunogenic pancreatic tumors into immunogenic foci of immune regulation.

Alternate Accession IDs

E-GEOD-52171

Sample Metadata Fields

Specimen part

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accession-icon GSE8030
miRNAs and codon usage regulate striatal gene and protein expression in two mouse models of Parkinsons disease
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The molecular mechanisms underlying the changes in the nigrostriatal pathway in Parkinsons disease (PD) are not completely understood. Here we use microarrays and mass spectrometry to study the transcriptomic and proteomic changes in the striatum of two mouse models of PD induced by distinct neurotoxins, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and methamphetamine (METH). Transcripts and proteins were found with similar abundance changes in both models which may be involved in the pathophysiology of PD. GFAP transcript and protein levels were significantly up-regulated by both neurotoxins, confirming the known astrocytic response to these drugs. Other genes and proteins were idiosyncratic in their responses to the two toxins, suggesting specific toxicological responses. Comparing transcript and protein levels revealed that efficiently translated genes used more commonly occurring codons than inefficiently translated genes. Additionally, a potential role was found for miRNAs in translational control in the striatum. The results constitute one of the largest datasets integrating transcript and protein changes for these two neurotoxin models with many similar endpoint phenotypes but distinct pathologies. Using multiple toxins while examining proteins and transcripts can be an effective method of delineating the molecular pathology of neurodegenerative diseases.

Publication Title

Mitochondrial dysfunction, oxidative stress, and apoptosis revealed by proteomic and transcriptomic analyses of the striata in two mouse models of Parkinson's disease.

Alternate Accession IDs

E-GEOD-8030

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE34860
Gene expression profiling in acute myeloid leukemia with mutated NPM
  • organism-icon Homo sapiens
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Approximately one third of acute myeloid leukemias (AMLs) are characterized by aberrant cytoplasmic localization of Nucleophosmin (NPMc+ AML), consequent to mutations in the NPM putative nucleolar localization signal. These events are mutually exclusive with the major AML-associated chromosomal rearrangements, and are frequently associated with normal karyotype, Fms-like tyrosine kinase (FLT3) mutations and multilineage involvement. We report the gene expression profiles of 78 de novo AMLs (72 with normal karyotype; 6 with non-major chromosomal abnormalities) that were characterized for the subcellular localization and mutation status of NPM. Unsupervised clustering clearly separated NPMc+ from NPMc- AMLs, regardless of the presence of FLT3 mutations or non-major chromosomal rearrangements, supporting the concept that NPMc+ AML represents a distinct entity. The molecular signature of NPMc+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem cell phenotype, suggesting that NPMc+ AML may derive from a multipotent hematopoietic progenitor.

Publication Title

Acute myeloid leukemia bearing cytoplasmic nucleophosmin (NPMc+ AML) shows a distinct gene expression profile characterized by up-regulation of genes involved in stem-cell maintenance.

Alternate Accession IDs

E-GEOD-34860

Sample Metadata Fields

Specimen part

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accession-icon SRP096656
Crizotinib v. DMSO in SW480 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

SW480 cells were treated with 2uM crizotinib for 72h (versus DMSO) Overall design: Examination of differential up- or down-regulated genes after crizotinib treatment

Publication Title

Global survey of the immunomodulatory potential of common drugs.

Alternate Accession IDs

GSE93124

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP069721
Psh1-mediated Proteolysis Prevents the Budding Yeast Centromeric Histone Variant from Mislocalizing to Promoter Nucleosomes [RNA-seq]
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Precise localization of the histone H3 variant CENP-A(Cse4) to centromeres is essential for accurate chromosome segregation. In budding yeast, CENP-A(Cse4) is regulated by ubiquitin-mediated proteolysis to ensure its exclusive localization to the centromere. Overexpression of CENP-A(Cse4) is lethal when the CENP-A(Cse4) E3 ubiquitin ligase, Psh1, is deleted. CENP-A(Cse4) mislocalizes to promoters in this condition, so we investigated if there was an effect on gene expression of downstream genes using RNA-seq. Overall design: RNA-seq from two or three biological replicates each, at t0 and t2 hours after adding galactose for each of 6 experimental genotypes.

Publication Title

Regulation of Budding Yeast CENP-A levels Prevents Misincorporation at Promoter Nucleosomes and Transcriptional Defects.

Alternate Accession IDs

GSE77596

Sample Metadata Fields

Subject, Time

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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