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accession-icon GSE92711
The transcription factor Tcf1 ensures the development and cytotoxic function of NK cells by limiting the expression of Granzymes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The Transcription Factor Tcf1 Contributes to Normal NK Cell Development and Function by Limiting the Expression of Granzymes.

Sample Metadata Fields

Specimen part

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accession-icon GSE53358
Gene expression analysis of Wnt+ and Wnt- effector CD8 T cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Wnt signal transduction during an immune response is involved in the establishment of functional CD8 T cell memory

Publication Title

Differences in the transduction of canonical Wnt signals demarcate effector and memory CD8 T cells with distinct recall proliferation capacity.

Sample Metadata Fields

Specimen part

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accession-icon GSE92709
The transcription factor Tcf1 ensures the development and cytotoxic function of NK cells by limiting the expression of Granzymes [Affymetrix]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The transcription factor Tcf1 plays an essential role for the development of NK cells, however, its precise role for NK cell development, maturation and function is poorly understood. Here we show that distinct domains of Tcf1 direct bone marrow progenitors towards the NK cell lineage and mediate lineage commitment and NK cell expansion, and that Tcf1 downregulation is required for terminal NK cell maturation. Impaired NK cell development in the absence of Tcf1 is explained by increased cell death due to excessive expression of Granzyme family proteins, which results in NK cell self-destruction. In addition, excessive Granzyme B expression leads to target cell induced NK cell death and consequently reduced target cell killing by NK cells lacking Tcf1. Mechanistically, Tcf1 prevents excessive Granzyme B expression by binding to a newly identified enhancer element upstream of the Granzyme B locus. These data identify an unexpected requirement to limit the expression of cytotoxic effector molecules for lymphocyte development.

Publication Title

The Transcription Factor Tcf1 Contributes to Normal NK Cell Development and Function by Limiting the Expression of Granzymes.

Sample Metadata Fields

Specimen part

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accession-icon GSE42299
Expression profiles of C2C12 myotubes in response to PGC-1 (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha) overexpression and/or iron chelation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mitochondria are centers of metabolism and signaling whose content and function must adapt to changing cellular environments. The biological signals that initiate mitochondrial restructuring and the cellular processes that drive this adaptive response are largely obscure. To better define these systems, we performed matched quantitative genomic and proteomic analyses of mouse muscle cells as they performed mitochondrial biogenesis. We find that proteins involved in cellular iron homeostasis are highly coordinated with this process, and that depletion of cellular iron results in a rapid, dose-dependent decrease of select mitochondrial protein levels and oxidative capacity. We further show that this process is universal across a broad range of cell types and fully reversed when iron is reintroduced. Collectively, our work reveals that cellular iron is a key regulator of mitochondrial biogenesis, and provides quantitative datasets that can be leveraged to explore post-transcriptional and post-translational processes that are essential for mitochondrial adaptation.

Publication Title

Complementary RNA and protein profiling identifies iron as a key regulator of mitochondrial biogenesis.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE53462
Molecular classification of non-melanoma skin cancer by gene expression profiling
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Non-melanoma skin cancers (NMSC) including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are more common kinds of skin cancer. Although these tumors share common pathological and clinical features, their similarity and heterogeneity at molecular levels are not fully elaborated yet. Here, by performing comparative analysis of gene expression profiling of BCC, SCC, and normal skin tissues, we could classify the BCC into three subtypes of classical, SCC-like, and normal-like BCCs. Functional enrichment and pathway analyses revealed the molecular characteristics of each subtype.

Publication Title

Molecular classification of basal cell carcinoma of skin by gene expression profiling.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE56032
Comparative transcriptional profiling of developing wheat grains with contrasting levels of minerals
  • organism-icon Triticum aestivum
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

Transcriptional comparison of developing grains between two wheat genotypes with contrasting levels of minerals in grain, using Affymetrix GeneChip Wheat Genome Array.

Publication Title

Comparative transcriptional profiling of two wheat genotypes, with contrasting levels of minerals in grains, shows expression differences during grain filling.

Sample Metadata Fields

Specimen part

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accession-icon GSE99775
MYD88 L265P differential expression analysis
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The wider transcriptional effects of MYD88L265P were explored by analysing the microarray datasets using the limma package. We focussed on evidence for differential expression between Myd88L265P and Card11L232LI transduced B cells because both cell populations were actively proliferating at the time of RNA isolation.

Publication Title

Synergistic cooperation and crosstalk between <i>MYD88<sup>L265P</sup></i> and mutations that dysregulate CD79B and surface IgM.

Sample Metadata Fields

Specimen part

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accession-icon GSE64505
Identification of a mitochondrial defect gene signature reveals NUPR1 as a key regulator of liver cancer progression
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Many cancer cells require more glycolytic adenosine triphosphate production due to a mitochondrial respiratory defect. However, the roles of mitochondrial defects in cancer development and progression remain unclear. To address the role of transcriptomic regulation by mitochondrial defects in liver cancer cells, we performed gene expression profiling for three different cell models of mitochondrial defects: cells with chemical respiratory inhibition (rotenone, thenoyltrifluoroacetone, antimycin A, and oligomycin), cells with mitochondrial DNA depletion (Rho0), and liver cancer cells harboring mitochondrial defects (SNU354 and SNU423). By comparing gene expression in the three models, we identified 10 common mitochondrial defectrelated genes that may be responsible for retrograde signaling from cancer cell mitochondria to the intracellular transcriptome. The concomitant expression of the 10 common mitochondrial defect genes is significantly associated with poor prognostic outcomes in liver cancers, suggesting their functional and clinical relevance. Among the common mitochondrial defect genes, we found that nuclear protein 1 (NUPR1) is one of the key transcription regulators. Knockdown of NUPR1 suppressed liver cancer cell invasion, which was mediated in a Ca2+ signalingdependent manner. In addition, by performing an NUPR1-centric network analysis and promoter binding assay, granulin was identified as a key downstream effector of NUPR1. We also report association of the NUPR1granulin pathway with mitochondrial defectderived glycolytic activation in human liver cancer. Conclusion: Mitochondrial respiratory defects and subsequent retrograde signaling, particularly the NUPR1granulin pathway, play pivotal roles in liver cancer progression.

Publication Title

Identification of a mitochondrial defect gene signature reveals NUPR1 as a key regulator of liver cancer progression.

Sample Metadata Fields

Specimen part

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accession-icon GSE32129
Targeted ErbB3 loss in mammary organoids harvested from ErbB3 DOX-KO mice +/- DOX treatment
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Mammary organoids harvested from ErbB3 DOX-KO mice, which utilize MMTV-Cre transgene expression in the LE to cause genomic recombination at floxed ErbB3 alleles in ErbB3FL/FL were cultured in the presence or absence of doxycycline to induce ErbB3 loss. The gene expression shift following DOX-induced ErbB3 loss in the 3D organoids was examined by microarray.

Publication Title

The receptor tyrosine kinase ErbB3 maintains the balance between luminal and basal breast epithelium.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE54150
Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells
  • organism-icon Mus musculus
  • sample-icon 38 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

Age- and pregnancy-associated DNA methylation changes in mammary epithelial cells.

Sample Metadata Fields

Sex, Age, 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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Developed by the Childhood Cancer Data Lab

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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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