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accession-icon GSE81785
Expression data regarding the effect of NPM1 knockdown on TNF-a induced gene expression in HeLa
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

NPM1 was reported to regulate the SOD2 gene expression through regulation of NF-kB. However, the effect of NPM1 on the NF-kB-dependent transcriptome has not been exmained.

Publication Title

Efficient DNA binding of NF-κB requires the chaperone-like function of NPM1.

Sample Metadata Fields

Cell line

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accession-icon GSE50883
Expression data from mouse bone marrow-derived macrophages (BMDMs)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To recruit phagocytes, apoptotic cells characteristically release ATP, which functions as a danger signal. Here, we found that the culture supernatant of apoptotic cells activated the macrophages to express anti-inflammatory genes such as NR4A and Thbs1. A high level of AMP accumulated in the apoptotic cell supernatant in a Pannexin1-dependent manner. A nucleotidase inhibitor and A2a adenosine receptor antagonist inhibited the apoptotic supernatant-induced gene expression, suggesting AMP was metabolized to adenosine by an ecto-5-nucleotidase expressed on macrophages, to activate the macrophage A2a adenosine receptor. Intraperitoneal injection of zymosan into AdoR A2a- or Panx1-deficient mice produced high, sustained levels of inflammatory mediators in the peritoneal lavage. These results indicated that AMP from apoptotic cells suppresses inflammation as a calm down signal.

Publication Title

Immunosuppression via adenosine receptor activation by adenosine monophosphate released from apoptotic cells.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP102431
RNA sequencing analysis of HL-1 cardiomyocytes
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Analysis of murine cardiomyocyte cell line HL-1 treated with Ivermectin or Importazole. Results provide insight into the pathways regulated by the treatments. Overall design: RNA-seq of mouse HL-1 cardiomyocytes treated with vehicle (DMSO), Ivermectin, or Importazole for 24 hours, in triplicate, using Ion Proton System.

Publication Title

Antihypertrophic Effects of Small Molecules that Maintain Mitochondrial ATP Levels Under Hypoxia.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon SRP094618
Mechanism of early light signaling by the carboxy-terminal output module of Arabidopsis phytochrome B
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Phytochromes are evolutionarily conserved photoreceptors in bacteria, fungi, and plants. The prototypical phytochrome comprises an N-terminal photosensory module and a C-terminal histidine kinase signaling-output module. However, the plant phytochrome has been postulated to transduce light signals by interacting with a group of nodal Phytochrome-Interacting transcription Factors (PIFs) and triggering their degradation via the N-terminal photosensory module, while its C-terminal output module, including a Histidine Kinase-Related Domain (HKRD), is thought not to participate directly in signaling. Here, we show that the C-terminal module of Arabidopsis phytochrome B (PHYB) is unexpectedly sufficient to mediate the degradation of PIF3 and to induce a distinct set of PIF-regulated photosynthetic genes. These signaling functions require the HKRD and particularly its dimerization. A D1040V mutation, which disrupts the dimerization of HKRD and the interaction between the C-terminal module and PIF3, abrogates the early light signaling functions of PHYB in nuclear accumulation, photobody biogenesis, and PIF3 degradation. In contrast, disruption of the interaction between PIF3 and PHYB's N-terminal photosensory module has little effect on PIF3 degradation. Together, this study provides novel insight into the central mechanism of early phytochrome signaling that the C-terminal signaling-output module of PHYB interacts with PIF3 in the nucleus to mediate PIF3 degradation by light. Overall design: Whole seedling mRNA profiles of 100h dark-grown phyB-9 mutant and BCY overexpression line were generated by deep sequencing, in triplicate, using Illumina NextSeq 500

Publication Title

Mechanism of early light signaling by the carboxy-terminal output module of Arabidopsis phytochrome B.

Sample Metadata Fields

Subject

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accession-icon GSE47684
Recurrent mutations of multiple components of cohesin complex in myeloid neoplasms
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Recurrent mutations in multiple components of the cohesin complex in myeloid neoplasms.

Sample Metadata Fields

Specimen part, Disease, Cell line

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accession-icon GSE47641
Expression analysis of mock- or RAD21-transduced Kasumi1 cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We recently identified recurrent mutations of cohesin complex in myeloid neoplasms through whole-exome sequencing analysis. RAD21 is one of the main components of the cohesin complex.

Publication Title

Recurrent mutations in multiple components of the cohesin complex in myeloid neoplasms.

Sample Metadata Fields

Cell line

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accession-icon GSE17845
Transcriptional profiling of leaf blades and petioles subjected to shade avoidance syndrome
  • organism-icon Arabidopsis thaliana
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Plants grown under a canopy recognize changes in light quality and modify their growth patterns; this modification is known as shade avoidance syndrome. In leaves, leaf blade expansion is suppressed, whereas petiole elongation is promoted under the shade. However, the mechanisms that control these responses are largely unclear. Here, we demonstrated that both auxin and brassinosteroid (BR) are required for the normal leaf responses to shade. The microarray analysis of leaf blades and petioles treated with end-of-day far-red light (EODFR) revealed that almost half of the genes induced by the treatment in both parts were previously identified as auxin-responsive genes. Likewise, BR-responsive genes were overrepresented in the EODFR-induced genes. Hence, the auxin and BR responses were elevated by EODFR treatment in both leaf blades and petioles, although opposing growth responses were observed in these two parts. The analysis of the auxin-deficient doc1/big mutant and BR-deficient rot3/cyp90c1 mutant further indicates that auxin and BR were equally required for the normal petiole elongation response to the shade stimulus. In addition, the spotlight irradiation experiment revealed that phytochrome in leaf blades but not that in petioles regulated petiole elongation, which was probably mediated through regulation of the auxin/BR responses in petioles. On the basis of these findings, we conclude that auxin and BR cooperatively promote petiole elongation in response to the shade stimulus under the control of phytochrome in the leaf blade.

Publication Title

Involvement of auxin and brassinosteroid in the regulation of petiole elongation under the shade.

Sample Metadata Fields

Specimen part

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accession-icon GSE98147
Global gene expression profiling of SM and the derivatives (DM, D, MYO, SCL, SYN) induced from hiPSCs
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Global gene expression profiling of human iPSC and the iPSC-derived presomitic mesoderm(PSM), somite(SM), and the derivatives, dermomyotome(DM), dermatome(D), myotome(MYO), sclerotome(SCL) and syndetome(SYN).

Publication Title

Modeling human somite development and fibrodysplasia ossificans progressiva with induced pluripotent stem cells.

Sample Metadata Fields

Specimen part, Time

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accession-icon SRP076902
Dysregulated immune system networks in war veterans with PTSD
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: RNA-Seq analysis can help identify large set of differentially expressed genes at a time. We performed RNA-Seq analysis to identify differentially expressed genes in the PBMCs of war veterans suffering from PTSD. Methods: Total RNA from PBMCs from PTSD +ve and -ve individuals were used for RNA-Seq analysis. Results: We obtained, on average, ~60 millions reads per sample. More than 70% of the reads were mapped to human genome. Functional analysis of the differentially expressed genes (362) revealed dysregulation in immune system network. Conclusions: Our present study provides further proof that immune system related genes and pathways are dysregulated in PTSD PBMCs. Overall design: RNA-Seq was performed with RNA from 5 each control and PTSD individuals. PBMCs collected within one hour of blood draw were used for RNA isolation. 1 ug of total RNA was used for library synthesis and sequenced in a HighSeq 2000 illumina instrument at Tufts University.

Publication Title

Decreased AGO2 and DCR1 in PBMCs from War Veterans with PTSD leads to diminished miRNA resulting in elevated inflammation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE70511
Aggressive gene expression signiture of waldenstrom macroglobulinemia with deletion 6q
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Waldenstom macroglobulinemia (WM) with 6q del is still unknown. In the present study, we analyzed gene expression signiture of WM with 6q del.

Publication Title

Gene Expression Profile Signature of Aggressive Waldenström Macroglobulinemia with Chromosome 6q Deletion.

Sample Metadata Fields

Specimen part, Disease

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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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