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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.

Alternate Accession IDs

E-GEOD-58749

Sample Metadata Fields

Treatment

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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.

Alternate Accession IDs

E-GEOD-67019

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.

Alternate Accession IDs

E-GEOD-76757

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.

Alternate Accession IDs

E-GEOD-85029

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.

Alternate Accession IDs

E-GEOD-85006

Sample Metadata Fields

Specimen part

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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.

Alternate Accession IDs

GSE118555

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP004891
Conserved generation of short products at piRNA loci
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina Genome Analyzer

Description

We analyzed small RNAs from three mammalian species, and found that in all these species piRNA-directed targeting is accompanied by the generation of short sequences that have a very precisely defined length and a specific spatial relationship with the guide piRNAs. Overall design: small RNA-seq of testes lysate (beta-eliminated)

Publication Title

Conserved generation of short products at piRNA loci.

Alternate Accession IDs

GSE26160

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE79184
CCL4 Secretion By Interleukin-15 Dendritic Cells Directs Superior Recruitment Of Cd56+ Cytolytic Lymphocytes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A key requisite for the success of a dendritic cell (DC)-based vaccine in treating malignancies is the capacity of the DCs to attract immune effector cells for further interaction and activation, considering crosstalk with DCs is partially regulated by cell-contact-dependent mechanisms. Although critical for therapeutic efficacy, immune cell recruitment is a largely overlooked aspect regarding optimization of DC therapy. In this paper we examine if the so-called interleukin (IL)-15 DC vaccine provides a favorable chemokine milieu for recruiting T cells, natural killer (NK) cells and gamma delta () T cells, in comparison with the IL-4 DCs used routinely for clinical studies, as well as the underlying mechanisms of immune cell attraction by IL-15 DCs. Chemokine signaling is studied both at the RNA level, using microarray data of mature DCs, and functional level, by means of a transwell chemotaxis assay. Important to note, the classic IL-4 DC vaccine falls short to attract the required immune effector lymphocytes, whereas the IL-15 DCs provide a favorable chemokine milieu for recruiting all cytolytic effector cells. The elevated secretion of the chemokine (C-C motif) ligand 4 (CCL4), also known as macrophage inflammatory protein-1 (MIP-1), by IL-15 DCs underlies the enhanced migratory responsiveness of T cells, NK cells and T cells. Namely, neutralizing its receptor CCR5 resulted in a significant drop in migration of the aforementioned effector cells towards IL-15 DCs. These findings should be kept in mind in the design of future DC-based cancer vaccines.

Publication Title

Desirable cytolytic immune effector cell recruitment by interleukin-15 dendritic cells.

Alternate Accession IDs

E-GEOD-79184

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE70921
Identification and successful negotiation of a metabolic checkpoint in direct neuronal reprogramming
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Despite the widespread interest in direct neuronal reprogramming, the mechanisms underpinning fate conversion remain largely unknown. Our study revealed a critical time point after which cells either successfully convert into neurons or succumb to cell death. Co-transduction with Bcl-2 greatly improved negotiation of this critical point by faster neuronal differentiation. Surprisingly, mutants with reduced or no affinity for Bax demonstrated that Bcl-2 exerts this effect by an apoptosis-independent mechanism. Consistent with a caspase-independent role, ferroptosis inhibitors potently increased neuronal reprogramming by inhibiting lipid peroxidation occurring during fate conversion. Genome-wide expression analysis confirmed that treatments promoting neuronal reprogramming elicit an anti-oxidative stress response. Importantly, coexpression of Bcl-2 and anti-oxidative treatments lead to an unprecedented improvement in glial-to-neuron conversion after traumatic brain injury in vivo, underscoring the relevance of these pathways in cellular reprograming irrespective of cell type, in vitro and in vivo.

Publication Title

Identification and Successful Negotiation of a Metabolic Checkpoint in Direct Neuronal Reprogramming.

Alternate Accession IDs

E-GEOD-70921

Sample Metadata Fields

Sex, Specimen part

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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.

Alternate Accession IDs

E-GEOD-36910

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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