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accession-icon GSE42327
Genome-wide gene expression analysis in Thoc5- and CFIm68-depleted HeLa cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We found that CFIm68, a mRNA cleavage and polyadenylation factor implicated for alternative polyadenylation site choice, was co-purified with Thoc5, a component of human THO/TREX. Microarray analysis using human HeLa cells reveals knockdown of Thoc5 affects the expression of a subset of non-heat shock genes. Notably, depletion of Thoc5 attenuated the expression of the mRNAs polyadenylated at distal, but not proximal, polyadenylation sites, which phenocopied the depletion of CFIm68.

Publication Title

Human TREX component Thoc5 affects alternative polyadenylation site choice by recruiting mammalian cleavage factor I.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP075525
A comprehensive analysis of gene expression patterns in wild-type and Batf2-/- bone marrow-derived macrophages (BMMf)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We previously identified TLR-independent expression of 4933430F08Rik, encoding Batf2, in T. cruzi-infected bone marrow-derived dendritic cells (BMDCs) (Kayama et al., 2009). To determine the functions of Batf2 in innate immune responses, we performed a comprehensive gene expression analysis in wild-type and Batf2-/- bone marrow-derived macrophages (BMMf). RNA-seq analysis showed that 98 genes are upregulated in Batf2-/- BMMf stimulated with LPS following IFN-? treatment, when compared with that in wild-type cells. Among these genes, we focused on Il23a, encoding IL-23p19, because IL-23 is able to promote expression of Il17a in Th17 cells. Overall design: mRNA of wild-type and Batf2-/- BMMf were subjected to deep sequencing profiling using Illumina HiSeq 2000.

Publication Title

BATF2 inhibits immunopathological Th17 responses by suppressing <i>Il23a</i> expression during <i>Trypanosoma cruzi</i> infection.

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

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accession-icon GSE100806
Spi-C expression in intestinal or bone marrow macrophages
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Heme ameliorates dextran sodium sulfate-induced colitis through providing intestinal macrophages with noninflammatory profiles.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE100804
Expression of Spi-C in intestinal CX3CR1high macrophages
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

In murine large intestinal lamina propria, CX3CR1high resident Mfs possess anti-inflammatory properties and thereby support intestinal homeostasis. Unlike other tissue-resident Ms, transcription factors that regulate differentiation and function of CX3CR1high Ms in the large intestine are poorly understood. Thus, to identify transcription factors specifically expressed in CX3CR1high Ms among large intestinal lamina propria innate myeloid cells, we comprehensively analyzed the genes expression profiles in CX3CR1high Ms, CX3CR1- CD11b+ CD11c+ cells, CD11b- CD11chigh DCs, and CD11b+CD11c- cells.

Publication Title

Heme ameliorates dextran sodium sulfate-induced colitis through providing intestinal macrophages with noninflammatory profiles.

Sample Metadata Fields

Specimen part

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accession-icon SRP111111
Decreased expression of a subset of TLR-dependent genes by heme-inducible Spi-C
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To determine the functions of Spi-C in innate immune responses, we investigated the overall gene expression patterns in M-CSF-BMDMFs prepared from Spicflox/flox and Lyz2-cre; Spicflox/flox mice. M-CSF-BMDMFs were stimulated with or without LPS following heme treatment and used for RNA-seq analysis. Overall design: Control and Spic–/– BMDMF pretreated with 40 µM hemin for 18 h were stimulated with (designated 'CNT_4' and 'cKO_4', respectively) or without (designated 'CNT_0' and 'cKO_0', respectively) 100 ng/ml LPS for 4 h.

Publication Title

Heme ameliorates dextran sodium sulfate-induced colitis through providing intestinal macrophages with noninflammatory profiles.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP151069
Fibroblasts in cholesteatoma activate osteoclasts.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Cholesteatoma arises from a tympanic membrane and expands in the middle ear. It erodes the surrounding bone and leads to hearing loss or brain abscess which is lethal complication. Currently, the only effective treatment is the complete surgical removal of cholesteatoma. However, possibility of recurrence is not satisfactory, other clinical treatment is desired. A mechanism of bone erosion in rheumatoid arthritis, which is one of the bone destructive disease, is progressing to be clarified. Receptor activator of NF-?B ligand (RANKL) secreted by synovial fibroblasts, T cells, and B cells lead to differentiation and activation of osteoclast precursor in rheumatoid arthritis. In contrast it has been still unclear why cholesteatoma erodes bone. In the current study we studied that osteoclasts statistically increased in cholesteatoma, and that fibroblasts in the prematrix of cholesteatoma express RANKL. In this study we studied that osteoclasts statistically increased in cholesteatoma, and that fibroblasts in the prematrix of cholesteatoma express RANKL. We investigated upstream of RANKL from RNA sequence results by Ingenuity Pathways Analysis, which is data base of abundance information about molecular biology. Overall design: To generate the transcriptome profiles of the permatrix of cholesteatoma and dermis cut by laser micro dissection from cholesteatoma, three pairs of both sample from the same patients were adapted to RNA sequencing.

Publication Title

Osteoclasts Modulate Bone Erosion in Cholesteatoma via RANKL Signaling.

Sample Metadata Fields

Disease, Subject

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accession-icon SRP194138
CXCR4 is a host factor that regulates Plasmodium development in hepatocytes
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The liver stage of the etiological agent of malaria, Plasmodium, is obligatory for successful infection of its various mammalian hosts. Differentiation of the rod-shaped sporozoites of Plasmodium into spherical exoerythrocytic forms (EEFs) via bulbous expansion is essential for parasite development in the liver. However, little is known about the host factors regulating the morphological transformation of Plasmodium sporozoites in this organ. Here, we show that sporozoite differentiation into EEFs in the liver involves protein kinase C?-mediated NF-?B activation, which robustly induces the expression of C-X-C chemokine receptor type 4 (CXCR4) in hepatocytes and subsequently elevates intracellular Ca2+ levels, thereby triggering sporozoite transformation into EEFs. Blocking CXCR4 expression by genetic or pharmacological intervention profoundly inhibited the liver stage development of the P. berghei rodent malaria parasite and the human P. falciparum parasite also. Collectively, our experiments show that CXCR4 is a key host factor for Plasmodium development in the liver, and CXCR4 warrants further investigation for malaria prophylaxis. Overall design: To explore the molecular mechanisms by which the HGF/MET/PKC?/NF-?B pathway regulates P. berghei sporozoite development in hepatocytes, we compared the gene expression patterns in wild-type and PKC?-KO Huh7 cells treated or not treated with HGF. We also analyzed the gene expression profiles in wild type and PKC?-KO Huh7 cells uninfected or infected with P. berghei sporozoites.

Publication Title

CXCR4 regulates <i>Plasmodium</i> development in mouse and human hepatocytes.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP107301
Sema6D reverse signaling controls lipid metabolism for macrophage polarization linking mTOR to PPAR?
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this study is to compare downstream genes of Sema6D signaling in both M1 and M2 macrophages. Overall design: Bone marrow derived macrophage mRNA profiles of 7 weeks of wild type (WT) and Sema6D-/- mice were stimulated by IL-4 for 24 hrs.

Publication Title

Semaphorin 6D reverse signaling controls macrophage lipid metabolism and anti-inflammatory polarization.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP107300
Sema6D reverse signaling controls lipid metabolism for macrophage polarization linking mTOR to PPAR?
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: The goal of this study is to compare downstream genes of Sema6D signaling in LPS plus IFNg stimulated macrophages. Methods: Bone marrow derived macrophage mRNA profiles of 7 weeks of wild type (WT) and Sema6D-/- mice were stimulated by LPS for 4 hrs. Results: According to this comparison, we found that 550 genes were downregulated in Sema6D-/- macrophages than WT macrophages in response to LPS. Conclusions: Our study represents 62 genes were supressed in both M1 and M2 Sema6D-/- macrophage than WT macrophages, suggesting of Sema6D reverse sigaling genes. Overall design: Bone marrow derived macrophage mRNA profiles of 7 weeks of wild type (WT) and Sema6D-/- mice were stimulated by LPS for 4 hrs, then isolated total RNA by RNeasy kit.

Publication Title

Semaphorin 6D reverse signaling controls macrophage lipid metabolism and anti-inflammatory polarization.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP099008
Transcriptome analysis of SATB1- and SATB1+ Hematopoietic stem cells.
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Hematopoietic stem cells (HSCs) are now recognized as a heterogeneous population in self-renewing and differentiation capabilities. However, fundamental mechanisms governing the heterogeneity remain uncertain. We here show that special AT-rich sequence-binding protein 1 (SATB1), a global chromatin organizer, is involved in the mechanisms. Analyzing hematological lineage-restricted SATB1 knock out mice proved that SATB1 is indispensable for both self-renewal and normal differentiation of adult HSCs. Using SATB1/Tomato knock-in mice, we subdivided HSCs according to SATB1 intensity. Culture experiments and RNA-sequencing revealed essential differences between SATB1- and SATB1+ HSCs regarding lineage potential. Overall design: Total RNAs isolated from SATB1- and SATB1+ CD150+ Flt3- LSK cells were applied for RNA-sequencing, and then amount of change of each genetic expression in SATB1+ HSCs compared with SATB1- HSCs were calculated.

Publication Title

Variable SATB1 Levels Regulate Hematopoietic Stem Cell Heterogeneity with Distinct Lineage Fate.

Sample Metadata Fields

Specimen part, Subject

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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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