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accession-icon GSE81661
Transcription Factor TLX1 Controls Retinoic Acid Signaling to Ensure Spleen Development
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcription factor TLX1 controls retinoic acid signaling to ensure spleen development.

Sample Metadata Fields

Specimen part

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accession-icon GSE68519
Transcription Factor TLX1 Controls Retinoic Acid Signaling to Ensure Spleen Development [Microarray Expression]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The molecular mechanisms underlying asplenia, a condition often associated with overwhelming infections remain largely unknown. During spleen development, the transcription factor TLX1 controls morphogenesis and organ expansion, and loss of it causes spleen agenesis. However, the downstream signaling pathways that are deregulated in the absence of TLX1 are mostly unknown. Herein, we demonstrate that loss of Tlx1 in the splenic mesenchyme causes increased retinoic acid (RA) signaling. Increased RA activity causes premature differentiation of the splenic mesenchyme and reduced vasculogenesis of the splenic anlage. Moreover, excess or deficiency in RA signaling, as observed in Cyp26b1 or Rdh10 mutants respectively, also results in spleen growth arrest. Genome-wide analysis revealed that TLX1 binds RA-associated genes through the AP-1 site and cooperates with the AP-1 family transcription factors to regulate transcription. Pharmacological inhibition of RA signaling partially rescues the spleen defect. These findings establish the critical role of TLX1 in controlling RA metabolism, and provide novel mechanistic insights into the molecular determinants underlying congenital asplenia.

Publication Title

Transcription factor TLX1 controls retinoic acid signaling to ensure spleen development.

Sample Metadata Fields

Specimen part

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accession-icon GSE67019
Interaction of CDCP1 with HER2 enhances HER2-driven tumorigenesis and promotes trastuzumab resistance in breast cancer
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Our findings demonstrate that CDCP1 is a novel modulator of HER2 signalling, and a biomarker for the stratification of breast cancer patients with poor prognosis

Publication Title

Interaction of CDCP1 with HER2 enhances HER2-driven tumorigenesis and promotes trastuzumab resistance in breast cancer.

Sample Metadata Fields

Cell line

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accession-icon GSE76757
Combination of the MEK inhibitor pimasertib with BTK or PI3K-delta inhibitors is active in pre-clinical models of aggressive lymphomas
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

assess the efficacy of Pimasertib to characterize its mechanism of action

Publication Title

Combination of the MEK inhibitor pimasertib with BTK or PI3K-delta inhibitors is active in preclinical models of aggressive lymphomas.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE85029
Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE85006
Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (Affy)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.

Publication Title

DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE58749
Human proliferating and differentiating keratinocytes treated with retinoic acid or 3,4-didehydroretinoic acid
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Targets of Retinoic Acid (RA) and 3,4-didehydroretinoic acid (ddRA) were identified in primary human epidermal keratinocytes grown in the presence of atRA or ddRA for 4 and 24 hours.

Publication Title

The effect of two endogenous retinoids on the mRNA expression profile in human primary keratinocytes, focusing on genes causing autosomal recessive congenital ichthyosis.

Sample Metadata Fields

Treatment

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accession-icon SRP157943
The single cell RNA seq of PDGFRa-GFP+ cells in mouse lung
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Pdgfra-expressing (Pdgfra+) cells have been implicated as progenitors in many mesenchymal tissues. To further characterize Pdgfra+ cells during alveologensis, we performed single-cell RNA sequencing (scRNA-Seq) analysis using fluorescence-activated cell sorting (FACS) sorted GFP+ cells from Pdgfra-GFP lungs at P7 and P15. Overall design: We perfomed 10X genomics single-cell RNA-seq of Pdgfra-GFP+ cells at P7 and P15

Publication Title

<i>Pdgfra</i> marks a cellular lineage with distinct contributions to myofibroblasts in lung maturation and injury response.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE36910
Gene expression levels in immortalized B cells from 95 unrelated CEPH-Utah individuals treated with 10Gy of ionizing radiation
  • organism-icon Homo sapiens
  • sample-icon 285 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

We used microarrays to examine gene expression levels from 95 unrelated CEPH-Utah individuals 0, 2 or 6 hours after treatment with 10Gy of ionizing radiation.

Publication Title

Stress-induced changes in gene interactions in human cells.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE36911
Gene expression levels in immortalized B cells from 131 unrelated CEPH-Utah grandparents treated under ER stress.
  • organism-icon Homo sapiens
  • sample-icon 258 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to examine gene expression levels from 131 unrelated CEPH-Utah grandparents with either DMSO or tunicamycin.

Publication Title

Stress-induced changes in gene interactions in human cells.

Sample Metadata Fields

Cell line, Treatment, 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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