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accession-icon SRP125420
Dynamic EBF1 occupancy directs sequential epigenetic and transcriptional events in B cell programming [RNA-Seq-Cre]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

EBF1 is essential for B cell specification and commitment. To explore the dynamics of EBF1 initiated B cell programming, we performed EBF1 ChIP-seq, ATAC-seq, bisulfite-seq, RNA-seq and several histone ChIP-seq analyses at different stages of the transition from Ebf1-/- pre-pro-B to pro-B triggered by EBF1 restoration. We also performed Pax5 ChIP-seq in Ebf1-/- pre-pro-B cell and EBF1-restored pro-B cell to study the pioneering function of EBF1 that allows other transcription factors to access certain chromatin sites. Overall design: Time series RNA-Seq analysis during the differentiation from Ebf1-deficient pre-pro-B cell to EBF1-restored pro-B cell.

Publication Title

Dynamic EBF1 occupancy directs sequential epigenetic and transcriptional events in B-cell programming.

Sample Metadata Fields

Subject

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accession-icon SRP156344
Co-chaperone Mzb1 is a key effector of Blimp1 in plasma cell differentiation and b1 integrin function
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 3000

Description

Plasma cell differentiation involves coordinated changes in gene expression and functional properties of B cells. Here, we study the role of Mzb1, a Grp94 co-chaperone that is expressed in marginal zone (MZ) B cells and during the terminal differentiation of B cells to antibody-secreting cells (ASCs). By analyzing Mzb1 -/- Prdm1 +/gfp mice, we find that Mzb1 is specifically required for the differentiation and function of ASCs in a T cell-independent immune response. We find that Mzb1-deficiency mimics, in part, the phenotype of Blimp1 deficiency, including the impaired secretion of IgM and the deregulation of Blimp1 target genes. In addition, we find that Mzb1 -/- plasmablasts show a reduced activation of b1 integrin, which contributes to the impaired plasmablast differentiation and migration of ASCs to the bone marrow. Thus, Mzb1 function is required for multiple aspects of plasma cell differentiation. Overall design: Splenic B cells were purified from Mzb1 +/+ Prdm1 +/gfp and Mzb1 -/- Prdm1 +/gfp mice using anti-B220 magnetic beads and cultured in the presence of 25ug/ml LPS. After 4 days, undifferentiated CD138 - Blimp - B cell blasts (Activated B Cells), CD138 - Blimp + (Pre-PB cells), and CD138 + Blimp + (PB cells) were isolated with FACSAria (Becton Dickinson) sort.

Publication Title

Cochaperone Mzb1 is a key effector of Blimp1 in plasma cell differentiation and β1-integrin function.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE46349
Expression data from long-term Ebf1-deficient, CD19+, Bcl2tg cells
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

An assessment of a role of Ebf1 in committed B lineage cells.

Publication Title

Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP057149
Characterization of Type I Interferon pathway during Hepatic Differentiation of Human Pluripotent Stem Cells and hepatitis C virus infection
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Pluripotent stem cells are being actively studied as a cell source for regenerating damaged liver. For long term survival of engrafting cells in the body, not only do the cells have to execute liverspecific function but also withstand the physical strains and invading pathogens. The cellular innate immune system orchestrated by the interferon (IFN) pathway provides the first line of defense against pathogens. The objective of this study is to assess the innate immune function as well as to systematically profile the IFN-induced genes during hepatic differentiation of pluripotent stem cells. To address this objective, we derived endodermal cells (day 5 postdifferentiation), hepatoblast (day 15) and immature hepatocytes (day 21) from human embryonic stem cells (hESC). Day 5, 15 and 21 cells were stimulated with IFN-a and subjected to IFN pathway analysis. Transcriptome analysis was carried out by RNA sequencing. The results showed that the IFN-a treatment activated STAT-JAK pathway in differentiating cells. Transcriptome analysis indicated stage specific expression of classical and non-classical IFNstimulated genes (ISGs). Subsequent validation confirmed the expression of novel ISGs including RASGRP3, CLMP and TRANK1 by differentiated hepatocytes upon IFN treatment. Hepatitis C virus replication in hESC-derived hepatic cells induced the expression of ISGs – LAMP3, ETV7, RASGRP3, and TRANK1. The hESC-derived hepatic cells contain intact innate system and can recognize invading pathogens. Besides assessing the tissue-specific functions for cell therapy applications, it may also be important to test the innate immune function of engrafting cells to ensure adequate defense against infections and improve graft survival. Overall design: 12 samples total, 4 samples in each time point (day 5, day 15, day 21). Each group of 4 within each time point has 2 control and 2 treatment samples in which the cells were stimulated with human interferon-alpha A (R and D Systems) at a concentration of 5000 IU for 6 hours.

Publication Title

Characterization of type I interferon pathway during hepatic differentiation of human pluripotent stem cells and hepatitis C virus infection.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE5202
Expression data from B. melitensis infected mouse macrophages
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Facultative intracellular Brucella infect and survive inside macrophages, and the outcome of macrophage-Brucella interaction is a basis for establishment of a chronic Brucella infection. The majority of Brucella are killed at the early infection stage. A subpopulation of virulent Brucella strains is instead trafficked to an intracellular replicative phagosome, and are resistant to further attack and begin to multiply dramatically. Virulent Brucella also inhibit macrophage apoptosis that in turn favors pathogen survival and replication.

Publication Title

Brucella melitensis triggers time-dependent modulation of apoptosis and down-regulation of mitochondrion-associated gene expression in mouse macrophages.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE61042
Gene expression changes between sensitive and YK-4-279-resistant Ewing's Sarcoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Microarray gene expression analysis conducted from cell lines in each of three cohorts: (1) Resistant ES cell lines, (2) Sensitive parental ES cell lines treated with YK-4-279 for 72 hours, and (3) untreated sensitive parental ES cell lines (Three replicates from TC32 & TC71 original parental cell lines)

Publication Title

An Oral Formulation of YK-4-279: Preclinical Efficacy and Acquired Resistance Patterns in Ewing Sarcoma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP090864
Gene expression profile of Cnot3(+/+) & Cnot3 (?/?) pro-B cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To study the role Cnot3 in early B cells development, RNASeq analysis of pro-B cells (B220+ and CD43+) was performed in tamoxifen treated Cnot3(fl/fl) RERTCre and Cnot3+/+;RERTCre mice. Overall design: Two individual replicates of Cnot3(fl/fl) RERTCre and Cnot3(+/+) RERTCre mice were tamoxifen treated periodically. Ten days after the initial treatment, B220+CD43+ pro-B cells were sorted from the bone marrow and RNASeq analysis was performed.

Publication Title

Interaction of CCR4-NOT with EBF1 regulates gene-specific transcription and mRNA stability in B lymphopoiesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE67904
Transcriptomic analyses of duodenum from wild type and VDR-null mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

As duodenum is an important Vitamin D target organ, transcriptomic analyses were performed in this tissue.

Publication Title

A vitamin D receptor selectively activated by gemini analogs reveals ligand dependent and independent effects.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE73572
The transcriptional coregulator PGC-1 controls mitochondrial function and anti-oxidant defense in skeletal muscles
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Transcriptional microarray analysis was conducted on gastrocnemius muscle of control and PGC-1(i)skm-/- mice one week after the last tamoxifen administration using the Affymetrix Mouse Gene 1.0 ST.

Publication Title

The transcriptional coregulator PGC-1β controls mitochondrial function and anti-oxidant defence in skeletal muscles.

Sample Metadata Fields

Specimen part

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accession-icon GSE67529
In vivo gene expression changes in EW5 Ewing sarcoma xenografts after IGF-1R or mTOR blockade
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Ewing Sarcoma is caused by a pathognomonic genomic translocation that places an N-terminal EWSR1 gene in approximation with one of several ETS genes (typically FLI1). This aberration, in turn, alters the transcriptional regulation of more than five hundred genes and perturbs a number of critical pathways that promote oncogenesis, cell growth, invasion, and metastasis. Among them, translocation-mediated up-regulation of the insulin-like growth factor receptor 1 (IGF-1R) and mammalian target of rapamycin (mTOR) are of particular importance since they work in concert to facilitate IGF-1R expression and ligand-induced activation, respectively, of proven importance in ES transformation. When used as a single agent in Ewing sarcoma therapy, IGF-1R or mTOR inhibition leads to rapid counter-regulatory effects that blunt the intended therapeutic purpose. Therefore, identify new mechanisms of resistance that are used by Ewing sarcoma to evade cell death to single-agent IGF-1R or mTOR inhibition might suggest a number of therapeutic combinations that could improve their clinical activity.

Publication Title

IGF-1R and mTOR Blockade: Novel Resistance Mechanisms and Synergistic Drug Combinations for Ewing Sarcoma.

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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