refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 461 results
Sort by

Filters

Technology

Platform

accession-icon GSE21105
Expression profiling of p53 wildtype inducible DLD-1 cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This is an initial experiment which was performed in order to identify novel transcriptional targets of the tumor suppressor p53

Publication Title

p53 activates the PANK1/miRNA-107 gene leading to downregulation of CDK6 and p130 cell cycle proteins.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE87158
Expression of sulfamethoxazole biotransformation pathways in a macaque model of HIV infection
  • organism-icon Macaca mulatta
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Rhesus Gene 1.0 ST Array (rhegene10st)

Description

Potentiated sulfonamide antibiotics such as trimethoprim/sulfamethoxazole (cotrimoxazole or TMP/SMX) remain the drugs of choice for treatment and prevention of Pneumocystis jiroveci pneumonia, toxoplasma encephalitis, and Isospora infections in HIV infection (aidsinfo.nih.gov). However, HIV-infected patients show a markedly increased risk of delayed hypersensitivity (HS) reactions to TMP/SMX (20-57% incidence) when compared to the general population (3% incidence). The typical manifestation is maculopapular rash with or without fever, and TMP/SMX is the most common cause of cutaneous drug reactions in HIV-infected patients TMP/SMX can also lead to thrombocytopenia, hepatotoxicity, and bullous skin eruptions in more severely affected patients. The risk of sulfonamide HS increases with progression to AIDS, with higher risk seen at lower CD4+ counts. This risk has been attributed, at least in part, to acquired alterations in SMX drug disposition in HIV infection. We hypothesized that HIV infection leads to impaired hepatic SMX detoxification or enhanced SMX bioactivation pathways, which may contribute to the increased incidence of sulfonamide HS. We addressed this question using liver tissue from SIVmac239-infected macaques, a well accepted model of HIV infection. The aim of this study was to evaluate differences in the hepatic expression and activity of SMX biotransformation pathways from drug nave SIV-infected macaques compared to sex- and age-matched uninfected controls.

Publication Title

Hepatic expression profiles in retroviral infection: relevance to drug hypersensitivity risk.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE87433
Hyperglycemic Memory New insights into a thought to be known topic
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Hyperglycemic memory is part of the pathogenesis of diabetic retinopathy. We established a novel mouse model of intermediate-term hyperglycemic memory and demonstrated that changes in gene expression and microvascular damage in the neurovascular unit of the diabetic retina persist after euglycemic reentry, indicating memory.

Publication Title

Hyperglycaemic memory affects the neurovascular unit of the retina in a diabetic mouse model.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE15481
Gene expression data from AP-2 silenced MCF-7 cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Overexpression of the AP-2 transcription factor in breast tumours has been identified as an independent predictor of poor outcome and failure of hormone therapy, even in ER positive, ErbB2 negative tumours; markers of a more favourable prognosis. To understand further the role of AP-2 in breast carcinoma, we have used an RNA interference and gene expression profiling strategy using the MCF-7 cell line as a model for ER positive, ErbB2 negative tumours with AP-2 overexpression.

Publication Title

AP-2gamma promotes proliferation in breast tumour cells by direct repression of the CDKN1A gene.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP090905
p53 activity results in DNA replication fork processivity
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

p53 induces cell death upon DNA damage, but this may not confer all of its tumor suppressor activity. We report that p53 activation enhances the processivity of DNA replication, as monitored by multi-label fiber assays, whereas removal of p53 reduces fork progression. This was observed in tumor-derived U2OS cells, but also in murine embryonic fibroblasts with heterozygous or homozygous p53 deletion, and in freshly isolated thymocytes from mice with differential p53 status. Mdm2, a p53-inducible gene product, similarly supported DNA replication even in p53-deficient cells, suggesting that sustained Mdm2-expression is at least one of the mechanisms allowing p53 to prevent replicative stress. Thus, p53 helps to protect the genome during S phase, by preventing the occurrence of stalled or collapsed replication forks. These results expand p53’s tumor-suppressive functions, adding to the ex-post model (elimination of damaged cells) an ex-ante activity, i.e. the prevention of DNA damage during replication. Overall design: Expression profiling by high throughput sequencing

Publication Title

p53 Activity Results in DNA Replication Fork Processivity.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE72954
A jumonji protein with E3 ligase and histone binding activities regulates transposon silencing in Arabidopsis
  • organism-icon Arabidopsis thaliana
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Transposable elements (TEs) make up a large proportion of eukaryotic genomes. As their mobilization creates genetic variation that threatens genome integrity, TEs are epigenetically silenced through several pathways and this may spread to neighboring sequences. JUMONJI (JMJ) proteins can function as anti-silencing factors and prevent silencing of genes next to TEs. Whether TE silencing is counterbalanced by the activity of anti-silencing factors is still unclear. Here, we characterize JMJ24 as a regulator of TE silencing. We show that loss of JMJ24 results in increased silencing of the DNA transposon AtMu1c, while overexpression of JMJ24 reduces silencing. JMJ24 has a JumonjiC (JmjC) domain and two RING domains. JMJ24 auto-ubiquitinates in vitro, demonstrating E3 ligase activity of the RING domain(s). JMJ24-JmjC binds the N-terminal tail of histone H3 and full-length JMJ24 binds histone H3 in vivo. JMJ24 activity is anti-correlated with histone H3 lysine 9 dimethylation (H3K9me2) levels at AtMu1c. Double mutant analyses with epigenetic silencing mutants suggest that JMJ24 antagonizes histone H3K9me2, and requires H3K9 methyltransferases for its activity on AtMu1c. Genome-wide transcriptome analysis indicates that JMJ24 affects silencing at additional TEs. Our results suggest that the JmjC domain of JMJ24 has lost demethylase activity but has been retained as a binding domain for histone H3. This is in line with phylogenetic analyses indicating that JMJ24 [with the mutated JmjC domain] is widely conserved in angiosperms. Taken together, this study assigns a role in TE silencing to a conserved JmjC-domain protein with E3 ligase activity, but no demethylase activity.

Publication Title

A JUMONJI Protein with E3 Ligase and Histone H3 Binding Activities Affects Transposon Silencing in Arabidopsis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP011903
RBFOX1 Splicing and Transcriptional Regulation in Neurons
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We used RNA sequencing to identify the RBFOX1 splicing network at a genome-wide level in primary human neural stem cells during differentiation. We observe that RBFOX1 regulates a large set of alternative splicing events implicated in neurogenesis and cell maintenance. Subsequent alterations in gene expression define an additional transcriptional network regulated by RBFOX1 involved in neurodevelopmental pathways remarkably parallel to those affected by splicing. Overall design: RNA sequencing at a 75bp single-end read scale was performed using polyA-enriched RNA from 5 biological replicates of primary human neural progenitor cell lines generated by lentiviral-mediated knockdown of GFP (control) or RBFOX1 and differentiated for 4 weeks.

Publication Title

RBFOX1 regulates both splicing and transcriptional networks in human neuronal development.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE13273
LSD1 knock down in SY5Y Cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To analyze the functional relevance of LSD1 in neuroblastic tumors, SH-SY5Y cells were transiently transfected with siRNA directed against LSD1 or with a scrambled control siRNA. Microarray analysis revealed changes in expression that were consistent with these observations 72 hours after LSD1 knock-down. At this time, 28 genes were significantly induced at least 1.5-fold and 29 genes were significantly repressed at least 1.5-fold. Among the 28 induced genes, 4 are markers of cytoskeletal remodelling (TNS1, TPM1, DNM2, DNAL4), indicating differentiation, and 3 (TPM1, DNM2 and SHANK2) are functionally linked to neurite dynamics and synaptic trafficking. TaqMan quantitative RT-PCR confirmed the expression changes detected via microarray analysis for LSD1, DNAL4, DNM2, TNS1 and TPM1

Publication Title

Lysine-specific demethylase 1 is strongly expressed in poorly differentiated neuroblastoma: implications for therapy.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP105329
RNA-Seq of SHEP TET21N cells upon Doxorubicin treatment
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

MYCN-high and MYCN-low neuroblastoma cells differ in their responses to Doxorubicin treatment. To explain this difference we compared the global trancriptomes of MYCN-high and MYCN-low cells before, during and after treatment. Overall design: MYCN-high cells without doxycyline and MYCN-low cells with doxycycline were treated with 0.1µg/ml Doxorubicin. Transcriptome was measured for the following time points: in untreated cells, in cells which were treated with Doxorubicin for 72 hours, and in cells collected three, eight and fourteen days after Doxorubin washout. Experiment was performed in biological duplicate.

Publication Title

Cell-Cycle Position of Single MYC-Driven Cancer Cells Dictates Their Susceptibility to a Chemotherapeutic Drug.

Sample Metadata Fields

Treatment, Subject, Time

View Samples
accession-icon GSE36444
LBH589 (Panobinostat) treatment of a gastric cancer cell line
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

LBH589 is a histone deacetylase (HDAC) inhibitor, treatment and changes in acetylated histones alters gene expression

Publication Title

Pan-histone deacetylase inhibitor panobinostat sensitizes gastric cancer cells to anthracyclines via induction of CITED2.

Sample Metadata Fields

Cell line, Treatment

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