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accession-icon GSE53006
Athero-susceptibility of inbred mouse strains
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE52818
Expression data from the aorta of DBA, B6 and 129 mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a DBA/2J genetic background (DBA-apoE) and C57BL/6 (B6-apoe) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE).

Publication Title

Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE52473
Expression data from thioglycollate-elicited peritoneal macrophages from 129S6/SvEvTac and DBA2/J mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a DBA/2J genetic background (DBA-apoE) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE).

Publication Title

Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE52816
Expression data from thioglycollate-elicited peritoneal macrophages from 129S6/SvEvTac and C57BL/6 mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Strain differences influence susceptibility to atherosclerosis. Apolipoprotein E-null mice on a C57BL/6 genetic background (B6-apoE) are highly susceptible to atherosclerosis in the aortic root area compared with those on a 129S6/SvEvTac background (129-apoE).

Publication Title

Quantitative trait loci affecting atherosclerosis at the aortic root identified in an intercross between DBA2J and 129S6 apolipoprotein E-null mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP074343
Silencing of KDM2B leads to deregulation of apoptosis related genes in GBM
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anti-cancer protein that can specifically kill tumor cells while sparing healthy ones. Emerging evidences suggest that TRAIL resistance in cancers is associated with aberrant expression of the key components of the apoptotic program. However, how these components are regulated at the epigenetic level is not understood. In this study, we aimed to identify novel epigenetic mechanisms regulating TRAIL response in Glioblastoma Multiforme (GBM) by a short-hairpin RNA (shRNA) screen. We employed an shRNA-mediated loss of function approach to interrogate the role of 48 genes in DNA and histone modification pathways. From this we identified KDM2B, an H3K36-specific demethylase, as a novel regulator of TRAIL response. Accordingly, silencing of KDM2B significantly enhanced TRAIL sensitivity, the activation of Caspase-8, Caspase-3, Caspase-7, and cleavage of PARP. KDM2B knockdown also accelerated the apoptosis process, as revealed by live cell imaging experiments. Moreover, simultaneous knockdown of the methyltransferases responsible for generating the histone marks removed by KDM2B significantly recovered the cell death phenotype observed with KDM2B inhibition. To decipher the downstream molecular pathways regulated by KDM2B, levels of apoptosis-related genes were examined by RNA-sequencing and quantitative PCR upon KDM2B loss, which revealed de-repression of pro-apoptotic genes HRK, caspase-7, and DR4 and repression of anti-apoptotic gene Mcl-1. The apoptosis phenotype was dependent on HRK upregulation, as HRK knockdown significantly abrogated the sensitization. In vivo, KDM2B-silenced tumors exhibited slower growth and reduced angiogenic capacity compared to controls. Taken together, our findings suggest a novel mechanism regulating apoptotic response, where the key apoptosis components are under epigenetic control of KDM2B in GBM cells. Overall design: mRNA profiles of U87MG GBM cells transduced either by control shRNA or shRNA targeting KDM2B were generated by RNA-seq (Illumina HiSeq 2500). 2 biological replicates of shControl and shKDM2B total RNAs were barcoded individually and deep sequenced as 3 technical replicates each in 3 lanes.

Publication Title

KDM2B, an H3K36-specific demethylase, regulates apoptotic response of GBM cells to TRAIL.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP075283
Development and differentiation of early innate lymphoid progenitors
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Early innate lymphoid progenitors (EILP) have recently been identified in the mouse adult bone marrow as a multipotential progenitor population committed to ILC lineages, but their relationship with other described ILC progenitors is still unclear. In this study, we examine the progenitor-successor relationships between EILP, IL-7R+ common lymphoid progenitors (ALP), and ILC precursors (ILCp). Bioinformatic, phenotypical, functional, and genetic approaches collectively establish EILP as an intermediate progenitor between ALP and ILCp. Our work additionally provides new candidate regulators of ILC development and clearly defines the stage of requirement of transcription factors key for early ILC development. Overall design: transcriptional profiling of early ILC progenitors (EILP, ILCp), and common lymphoid progenitors (ALP) was performed by RNA sequencing

Publication Title

Development and differentiation of early innate lymphoid progenitors.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE107246
Identification of INSL4-regulated gene program in non-small cell lung cancer cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Gene expression profiling was performed to identify INSL4-regulated gene program in non-small cell lung cancer A549 cells. We compared gene expression profiles of A549 cells transduced with lentiviruses expressing scrambled shRNA control or INSL4 shRNA. Our analysis revealed INSL4-regulated gene program that are involved in the regulation of cell cycle, growth and survival.

Publication Title

Role of INSL4 Signaling in Sustaining the Growth and Viability of LKB1-Inactivated Lung Cancer.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE81960
Identification of LINC00473-regulated transcriptional program in human mucoepidermoid carcinoma
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Gene expression profiling was performed on control and long intergenic non-protein coding RNA 473 (LINC00473)-depleted human mucoepidermoid carcinoma H3118 cells, and differentially expressed genes after LINC00473 depletion were identified.

Publication Title

CRTC1-MAML2 fusion-induced lncRNA LINC00473 expression maintains the growth and survival of human mucoepidermoid carcinoma cells.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE48853
Expression data of PGR isoforms, PRA and PRB, regulated genes in differentiating human endometrial stromal cells
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

gene expression at 6h of differentiation of Human endometrial stromal cell expressing either or both of PRA and PRB

Publication Title

Roles of progesterone receptor A and B isoforms during human endometrial decidualization.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE73550
Expression data of differentially regulated genes in ESR1 depleted human endometrial stromal cells during differentiation.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Estrogen and progesterone are important regulators of human endometrial differentiation. These steroid hormones act, at least in part, through their nucelar receptors. Role of estrogen receptor alpha (ESR1) during human endometrial differentiation is still unclear.

Publication Title

Roles of Estrogen Receptor-α and the Coactivator MED1 During Human Endometrial Decidualization.

Sample Metadata Fields

Specimen part

View Samples
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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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