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accession-icon SRP094432
RNA-SEQ of mutants B cell for IgH 3''RR and Emu
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

RNA-SEQ of mutants B cell for IgH 3''RR and Emu Overall design: CD43- splenic B-cells from wt, Eµ-deficient or 3''RR deficient mice, non stimulated (NS) or stimulated (S) with 5mg/ml LPS.

Publication Title

E<sub>μ</sub> and 3'RR IgH enhancers show hierarchic unilateral dependence in mature B-cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP067834
Deciphering the importance of the palindromic architecture of the immunoglobulin heavy chain 3' regulatory region.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The IgH 3' regulatory region (3'RR) controls class switch recombination (CSR) and somatic hypermutation (SHM) in B cells. The mouse 3'RR contains four enhancer elements with hs1,2 flanked by inverted repeated sequences and the center of a 25-kb palindrome bounded by two hs3 enhancer inverted copies (hs3a and hs3b). hs4 lies downstream of the palindrome. Evolution maintained in mammals this unique palindromic arrangement suggesting that it is functionally significant. We report that deconstructing the palindromic IgH 3'RR strongly impacts its function even when enhancers are preserved. CSR and IgH transcription appear poorly dependent from the 3'RR architecture and are more or less preserved provided 3'RR enhancers are present. By contrast, an “architectural effect” significantly lowers VH germline transcription, AID recruitment and SHM. In conclusion, this work indicates that the IgH 3'RR does not simply pile up enhancer units but also optimally expose them into a functional architecture of crucial importance. Overall design: RNAseq analysis of B-cell splenocytes with (S=stimulated) or without (R=resting) LPS activation from wt, delta2leftPAL, and deltaIRIS mice.

Publication Title

Deciphering the importance of the palindromic architecture of the immunoglobulin heavy-chain 3' regulatory region.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP067646
RNA-SEQ on resting (R) and stimulated (S) B cells from several IgH 3''RR mutant models
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We evaluated by RNA-seq obveral transcripts in B cells (resting and activated for 2 days with LPS) sorted from several KO mice models devoid of portion or all the IgH 3'' Regulatory Region Overall design: One RNA-seq point was realized per condition (resting or stimulated) and per genotype. Each point corresponds to a pool of equivalent number of B cells sorted from 4 animals

Publication Title

Sequential activation and distinct functions for distal and proximal modules within the IgH 3' regulatory region.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE25282
HP1gamma Knock Down in Human cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Study of HP1 Knock Down on gene expression and splicing regulation in Human HeLa cells

Publication Title

Histone H3 lysine 9 trimethylation and HP1γ favor inclusion of alternative exons.

Sample Metadata Fields

Cell line

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accession-icon GSE68546
Targets of Pax3 and Zic1 in neural crest and cranial placode progenitors
  • organism-icon Xenopus laevis
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

The transcription factors Pax3 and Zic1 are among the earliest genes activated at the neural plate border. Pax3 and Zic1 in combination promote neural crest fate, while Zic1 alone regulate cranial placode progenitor formation. We used microarrays to identify the global repertoire of genes activated by these facors individually or in combination to gain insights into the molecular mechanisms underlying cell fate decision at the neural plate border.

Publication Title

Identification of Pax3 and Zic1 targets in the developing neural crest.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE98216
Expression data from IMR90 cells expressing either E7-ca-STAT5A-shNTC vs E7-ca-STAT5a-shSOCS1 at 7 days post infection
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

SOCS1 plays a role in cellular senescence. Knocking down SOCS1 in senescence induced by the STAT5 oncogene results in senescence bypass by preventing p53 activation

Publication Title

SOCS1 regulates senescence and ferroptosis by modulating the expression of p53 target genes.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE49422
Expression data from H1299 human non-small cell lung carcinoma cell lines stably expressing CHES1 compared with H1299 infected with an empty vector
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

The expression of the forkhead transcription factor CHES1, also known as FOXN3, is reduced in many types of cancers. In vitro, CHES1 expression suppresses cell proliferation in tumor cell lines but not in normal cells. Conversely shRNA-mediated depletion of CHES1 increases tumor cell proliferation.

Publication Title

CHES1/FOXN3 regulates cell proliferation by repressing PIM2 and protein biosynthesis.

Sample Metadata Fields

Cell line

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accession-icon GSE30074
Expression data from 30 medulloblastomas
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Pediatric medulloblastoma is considered a highly heterogeneous disease, and a new strategy of risk stratification to optimize therapeutic outcomes is required. We aimed to investigate a new risk-stratification approach based on expression profiles of medulloblastoma cohorts. We analyzed gene expression profiles of 30 primary medulloblastomas and detected strong evidence that poor survival outcome was significantly associated with mRNA expression profiles of 17p loss. However, it was not supported in independent cohorts from previously published data (n=100). We speculated that this controversy might come from complex conditions of two important prognostic determinants, loss of tumor suppressors (chromosome 17p) and high expression of oncogenes, c-myc (MYC) or N-myc (MYCN). Simultaneous consideration of these two factors led to a new subgrouping of patients, exhibiting obviously different survival expectancies between the subgroups. Patients with up-regulated WNT signalings were always pre-defined as an independent subgroup, which ultimately removed confounding effect arising from contradictory outcome, favorable prognosis of WNT medulloblastomas despite their high MYC/MYCN expression level. We also found that age is a significant prognostic marker after adjusting for 17p and MYC/MYCN status. Diminished survival in age <3 years was more substantial in groups with high expression of MYC/MYCN or 17p loss, indicating survival outcome might be coordinately affected by these three factors. We suggest a more tailored and easily applicable subgrouping system based on expression profiles of chromosome 17p and MYC/MYCN, while separating WNT medulloblastoma as an independent subgroup, which could provide the basis for a novel risk-stratification strategy in pediatric medulloblastoma.

Publication Title

Prognostic classification of pediatric medulloblastoma based on chromosome 17p loss, expression of MYCC and MYCN, and Wnt pathway activation.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE26549
Gene Expression Profiling Predicts the Development of Oral Cancer
  • organism-icon Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Patients with oral preneoplastic lesion (OPL) have high risk of developing oral cancer. Although certain risk factors such as smoking status and histology are known, our ability to predict oral cancer risk remains poor. The study objective was to determine the value of gene expression profiling in predicting oral cancer development. Gene expression profile was measured in 86 of 162 OPL patients who were enrolled in a clinical chemoprevention trial that used the incidence of oral cancer development as a prespecified endpoint. The median follow-up time was 6.08 years and 35 of the 86 patients developed oral cancer over the course. Gene expression profiles were associated with oral cancer-free survival and used to develope multivariate predictive models for oral cancer prediction.

Publication Title

Gene expression profiling predicts the development of oral cancer.

Sample Metadata Fields

Sex, Age, Race

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accession-icon GSE30767
Vascular endothelial growth factor (VEGF) isoform regulation of early forebrain development
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This work was designed to determine the role of the vascular endothelial growth factor A (VEGF) isoforms during early neuroepithelial development in the mammalian central nervous system (CNS), specifically in the forebrain. An emerging model of interdependence between neural and vascular systems includes VEGF, with its dual roles as a potent angiogenesis factor and neural regulator. Although a number of studies have implicated VEGF in CNS development, little is known about the role that the different VEGF isoforms play in early neurogenesis. We used a mouse model of disrupted VEGF isoform expression that eliminates the predominant brain isoform, VEGF164, and expresses only the diffusible form, VEGF120. We tested the hypothesis that VEGF164 plays a key role in controlling neural precursor populations in developing cortex. We used microarray analysis to compare gene expression differences between wild type and VEGF120 mice at E9.5, the primitive stem cell stage of the neuroepithelium. We quantified changes in PHH3-positive nuclei, neural stem cell markers (Pax6 and nestin) and the Tbr2-positive intermediate progenitors at E11.5 when the neural precursor population is expanding rapidly. Absence of VEGF164 (and VEGF188) leads to reduced proliferation without an apparent effect on the number of Tbr2-positive cells. There is a corresponding reduction in the number of mitotic spindles that are oriented parallel to the ventricular surface relative to those with a vertical or oblique angle. These results support a role for the VEGF isoforms in supporting the neural precursor population of the early neuroepithelium.

Publication Title

Vascular endothelial growth factor (VEGF) isoform regulation of early forebrain development.

Sample Metadata Fields

Specimen part

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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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