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accession-icon SRP100088
Transcriptional and accessible chromatin profiles during conversion process of alternatively activated macrophages (RNA-Seq)
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Whether inflammatory macrophages can adopt features of the tissue resident niche and what mechanisms mediate phenotypic conversion remain unclear. In this study, we show by cell surface phenotyping, as well as by RNA-Seq transcriptional profiling and ATAC-Seq open chromatin regions profiling, that inflammatory monocyte can adopt a tissue resident phenotype, which is also accompanied by re-programming of the transcriptional profiles and remodeling of the open chromatin landscape. The conversion process is dependent on Vitamin A, suggesting that Vitamin A deficiency may lead to the failure to resolve inflammation, as inflammatory macrophages accumulate without adopting a tissue residency phenotype. Overall design: Monocyte-derived (N=3), tissue converted (N=3) and tissue resident (N=3) mouse peritoneal macrophages were FACS-sorted for RNASeq and ATACSeq.

Publication Title

Vitamin A mediates conversion of monocyte-derived macrophages into tissue-resident macrophages during alternative activation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE118022
Co-evolution of Met amplification and Hgf overexpression mediate resistance to BRAF inactivation in mouse anaplastic thyroid cancers.
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Affymetric arrays were performed on thyroid samples collected from GEMMs: normal thyroid, TPO-Cre/LSL-Braf (PTC), TPO-Cre/tetO-BRAF/LSL-rtTAiresGFP/p53-flox (ATC) and TPO-Cre/tetO-BRAF/LSL-rtTAiresGFP/p53-flox (recurrent tumors)

Publication Title

Hgf/Met activation mediates resistance to BRAF inhibition in murine anaplastic thyroid cancers.

Sample Metadata Fields

Specimen part

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accession-icon GSE45225
Gene expression of cultured HUVECs submitted to different shear stress in the presence or absence of stent procedure
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Many studies have characterized the results of shear stress changes on cultured endothelial cells in different bioreactor systems. However it is still unclear how an invasive intervention like stent procedure may influence the transcriptional response of endothelium.

Publication Title

Vascular injury post stent implantation: different gene expression modulation in human umbilical vein endothelial cells (HUVECs) model.

Sample Metadata Fields

Specimen part

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accession-icon SRP021085
RNAseq of PRMT4KD in human cord blood derived CD34+ cells
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Defining the role of epigenetic regulators in normal hematopoiesis has become critically important, as recurrent mutations or aberrant expression of these genes has been identified in both myeloid and lymphoid hematological malignancies. We have found that PRMT4, a type I arginine methyltransferase, whose function in normal and malignant hematopoiesis is unknown, is overexpressed in AML patient samples. In support of an oncogenic role for PRMT4, we find that its overexpression blocks the myeloid differentiation of human stem/progenitor cells (HSPCs) while its knockdown (KD) is sufficient to induce myeloid differentiation of HSPCs and multiple AML cell lines. Although classically thought of as a co-activator, we found that PRMT4 functions to repress the expression of miR-223 in HSPCs via the methylation of RUNX1, which triggers the assembly of a multi-protein repressor complex that includes DPF2. As part of a feedback loop, PRMT4 expression is repressed post-transcriptionally by miR-223 during the normal differentiation process. These data reveal an unidentified role of PRMT4 in myeloid differentiation and its unexpected repressive role in transcriptional regulation. Furthermore, depletion of PRMT4 results in the differentiation of myeloid leukemia cells in vitro and their decrease proliferation in vivo. Thus, targeting PRMT4 holds potential as a novel therapy for acute myelogenous leukemia. Overall design: Purified human primary CD34+ cells were transduced with lentiviruses carrying PRMT4KD or scramble control shRNAs. Total RNA was extrated. RNAseq was performed to identify target genes that are regulated by PRMT4. Experiments were performed in triplicate.

Publication Title

PRMT4 blocks myeloid differentiation by assembling a methyl-RUNX1-dependent repressor complex.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE102124
Gene expression profiling of treated and untreated primary prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

In clinical trials assessing neoadjuvant androgen deprivation therapy plus next-generation androgen receptor axis inhibitors, a subset of patients fail to demonstrate a complete pathologic response following treatment and radical prostatectomy. We performed transcriptome analyses on laser capture microdissected foci of residual tumor from these patients.

Publication Title

Neoadjuvant-Intensive Androgen Deprivation Therapy Selects for Prostate Tumor Foci with Diverse Subclonal Oncogenic Alterations.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE28317
Gene expression data from human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETONHR1
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Compare the gene expression profile among human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETONHR1

Publication Title

The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.

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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