refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 167 results
Sort by

Filters

Technology

Platform

accession-icon SRP094827
RNA-seq of N2 and lin-45(n2018) mutant C.elegans responses to osmotic stress
  • organism-icon Caenorhabditis elegans
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We profiled how animals RNA expression changes in response to osmotic stress, how lin-45 mutants have an altered response to osmotic stress, and how maternal preconditioning at 300 mM NaCl modifies progeny response to 500 mM NaCl Overall design: Examination of total RNAseq at 50 mM NaCl, 500 mM NaCl, and 500 mM NaCl from maternally preconditioned animals

Publication Title

Insulin-like signalling to the maternal germline controls progeny response to osmotic stress.

Sample Metadata Fields

Subject, Time

View Samples
accession-icon GSE26297
CYTOKININ HYPERSENSITIVE1 (CKH1) and CKH2 affect to cytokinin responses in tissue culture
  • organism-icon Arabidopsis thaliana
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Analysis of calli derived from the wild type (Ler), the ckh1 and ckh2 mutants cultured on media in the absence of cytokinin (control), in the presence of low (25 ng/ml kinetin) or high (200 ng/ml kinetin) levels of cytokinin, or in the presence of Trichostatin A (TSA). In these conditions, a constant 2,4-dichlorophenoxyacetic acid (2,4-D) was included as an auxin.

Publication Title

The CKH2/PKL chromatin remodeling factor negatively regulates cytokinin responses in Arabidopsis calli.

Sample Metadata Fields

Disease, Treatment

View Samples
accession-icon GSE4754
MCF10A cells in 3-D culture after treatment with BRCA1-RNAi or CtIP-RNAi
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Removal of BRCA1/CtIP/ZBRK1 repressor complex on ANG1 promoter leads to accelerated mammary tumor growth contributed by prominent vasculature.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE4751
MCF10A cells in 3-D culture for 15 h after treatment with CtIP-RNAi vs Luc-RNAi adenovirus
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

BRCA1 exerts transcriptional repression through interaction with CtIP in the C-terminal BRCT domain and ZBRK1 in the central domain. A dozen of genes including angiopoietin-1 (ANG1), a secreted angiogenic factor, are co-repressed by BRCA1 and CtIP based on microarray analysis of mammary epithelial cells in 3-D culture. BRCA1, CtIP and ZBRK1 form a complex that coordinately represses ANG1 expression via a ZBRK1 recognition site in ANG1 promoter. Impairment of this complex upregulates ANG1, which stabilizes endothelial cells forming capillary-like network structure. Consistently, Brca1-deficient mouse mammary tumors exhibit accelerated growth, pronounced vascularization and overexpressed ANG1. These results suggest, besides its role in maintaining genomic stability, BRCA1 directly regulates the expression of angiogenic factors to modulate the tumor microenvironment.

Publication Title

Removal of BRCA1/CtIP/ZBRK1 repressor complex on ANG1 promoter leads to accelerated mammary tumor growth contributed by prominent vasculature.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE4750
MCF10A cells in 3-D culture for 15 h after treatment with BRCA1-RNAi vs Luc-RNAi adenovirus
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

BRCA1 exerts transcriptional repression through interaction with CtIP in the C-terminal BRCT domain and ZBRK1 in the central domain. A dozen of genes including angiopoietin-1 (ANG1), a secreted angiogenic factor, are co-repressed by BRCA1 and CtIP based on microarray analysis of mammary epithelial cells in 3-D culture. BRCA1, CtIP and ZBRK1 form a complex that coordinately represses ANG1 expression via a ZBRK1 recognition site in ANG1 promoter. Impairment of this complex upregulates ANG1, which stabilizes endothelial cells forming capillary-like network structure. Consistently, Brca1-deficient mouse mammary tumors exhibit accelerated growth, pronounced vascularization and overexpressed ANG1. These results suggest, besides its role in maintaining genomic stability, BRCA1 directly regulates the expression of angiogenic factors to modulate the tumor microenvironment.

Publication Title

Removal of BRCA1/CtIP/ZBRK1 repressor complex on ANG1 promoter leads to accelerated mammary tumor growth contributed by prominent vasculature.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP015845
Next Generation Sequencing Facilitates Quantitative Analysis of Argonaute 2 (Ago2)-immunoprecipitation (IP) after miR-195 or miR-497 overexpression in HepG2
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

To explore functionally crucial tumor-suppressive (TS)-miRNAs in hepatocellular carcinoma (HCC), we performed integrative function- and expression-based screenings of TS-miRNAs in six HCC cell lines. The screenings identified seven miRNAs, which showed growth-suppressive activities through the overexpression of each miRNA and were endogenously downregulated in HCC cell lines. Further expression analyses using a large panel of HCC cell lines and primary tumors demonstrated four miRNAs, miR-101, -195, -378 and -497, as candidate TS-miRNAs frequently silenced in HCCs. Among them, two clustered miRNAs miR-195 and miR-497 showed significant growth-suppressive activity with induction of G1 arrest. Comprehensive exploration of their targets using Argonute2-immunoprecipitation-deep-sequencing (Ago2-IP-seq) and genome-wide expression profiling after their overexpression, successfully identified a set of cell-cycle regulators, including CCNE1, CDC25A, CCND3, CDK4, and BTRC. Our results suggest the molecular pathway regulating cell cycle progression to be integrally altered by downregulation of miR-195 and miR-497 expression, leading to aberrant cell proliferation in hepatocarcinogenesis. Identification of miR-195 and miR-497 target genes by sequencing Ago2-binding mRNAs and total mRNAs of miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell. Overall design: Deep sequencing of RNAs in Ago2-IP fraction and mRNAs extracted from miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell.

Publication Title

The tumor-suppressive miR-497-195 cluster targets multiple cell-cycle regulators in hepatocellular carcinoma.

Sample Metadata Fields

Cell line, Treatment, Subject, Time

View Samples
accession-icon SRP135818
Layer-specific molecular expression in neocortical astrocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Protoplasmic astrocytes in layers II to VI of the mammalian neocortex have historically been thought to comprise a homogeneous population. Given that layer-specific neuronal subtypes play essential roles in cortical circuitry, astrocytes might also be expected to support and modify this circuitry in a layer-specific manner. In order to investigate whether protoplasmic astrocytes exhibit layer-specific heterogeneity, we compared the gene expression profiles of astrocytes between upper layers (layers II to IV) and deep layers (layers V and VI). Although most genes known to be preferentially expressed in astrocytes (astrocyte-enriched genes) were equally expressed between upper-layer astrocytes and deep-layer astrocytes, some such genes (astrocyte-enriched genes or genes with known function in astrocytes) were significantly enriched in upper-layer astrocytes or deep-layer astrocytes. Overall design: With the use of fluorescence-activated cell sorting (FACS), we prepared upper-layer astrocytes and deep-layer astrocytes from the corresponding dissected layers of the somatosensory cortex of Aldh1l1-eGFP mice, in which all astrocytes are expected to be labeled with GFP. The meninges, layer I, and the corpus callosum were removed from upper- and deep-layer tissue samples. In addition, parts of layers IV and V were lost during separation of these layers in such a way as to prevent cross-contamination between the upper- and deep-layer samples. Total RNA from upper-layer astrocytes and deep-layer astrocytes (n = 3 brains from 4-week-old male mice) was isolated from sorted cells with TRIzol (Invitrogen) or RNAiso Plus (Takara) and was then subjected to reverse transcription with the use of a SMART-Seq v4 Ultra Low Input RNA Kit for Sequencing (Clontech). Bar-coded libraries were prepared with a Nextera XT DNA Library Preparation Kit (Illumina), and single-end 36-bp sequencing was performed with a HiSeq 2500 instrument (Illumina).

Publication Title

Layer-specific morphological and molecular differences in neocortical astrocytes and their dependence on neuronal layers.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE41260
Expression Profiles of E11.5 Mouse Optic Fissure
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mice that are mutant for both Fgfr1 and Fgfr2 specifically in the developing retina develop coloboma. To analyze the transcripts that are affected by defective FGF signaling, we micro-dissected the optic fissure region from the control and FGFR condtional mutant mice and did microarray analysis.

Publication Title

Defective FGF signaling causes coloboma formation and disrupts retinal neurogenesis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE55222
Targets of ALTERED PHLOEM DEVELOPMENT (APL)
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

We profiled transcripts from sorted phloem cells of wild-type and apl mutants to identify the genes regulated by APL in phloem.

Publication Title

Plant development. Arabidopsis NAC45/86 direct sieve element morphogenesis culminating in enucleation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE31210
Gene expression data for pathological stage I-II lung adenocarcinomas
  • organism-icon Homo sapiens
  • sample-icon 230 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Identification of genes up-regulated in ALK-positive and EGFR/KRAS/ALK-negative lung adenocarcinomas.

Publication Title

Identification of genes upregulated in ALK-positive and EGFR/KRAS/ALK-negative lung adenocarcinomas.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact