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accession-icon SRP060707
TET2 Regulates Mast Cell Differentiation and Proliferation through Catalytic and Non-catalytic Activities.
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Dioxygenases of the TET family impact genome functions by converting 5-methylcytosine in DNA to 5-hydroxymethylcytosine, but the individual contribution of the three family members to differentiation and function of myeloid cells is still incompletely understood. Using cells with a deletion in the Tet2 gene, we show that TET2 contributes to the regulation of mast cell differentiation, proliferation and effector functions. The differentiation defect observed in absence of TET2 could be however completely rescued or further exacerbated by modulating TET3 activity, and it was primarily linked to dysregulated expression of the C/EBP family of transcription factors. In contrast, hyper-proliferation induced by the lack of TET2 could not be modified by TET3. Together, our data indicate the existence of both overlapping and unique roles of individual TET proteins in regulating myeloid cell gene expression, proliferation and function. Overall design: Total mRNA of FACS-sorted Kit+ FceRIa+ populations of primary bone marrow-derived mast cells (BMMCs) from Tet2-/- and Tet2+/+ animals was extracted and subjected to multiparallel sequencing.

Publication Title

TET2 Regulates Mast Cell Differentiation and Proliferation through Catalytic and Non-catalytic Activities.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP056216
Transcription of mammalian cis-regulatory elements is restrained by actively enforced early termination [RNA]
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Upon recruitment to active enhancers and promoters, RNA polymerase II (Pol_II) generates short non-coding transcripts of unclear function. The mechanisms that control the length and the amount of ncRNAs generated by cis-regulatory elements are largely unknown. Here, we show that the adapter protein WDR82 and its associated complexes actively limit such non-coding transcription. WDR82 targets the SET1/COMPASS H3K4 methyltransferase and the nuclear Protein Phosphatase 1 (PP1) complexes to the initiating Pol_II. WDR82 and PP1 also interact with components of the transcriptional termination and RNA processing machineries. Depletion of WDR82, SET1 or the PP1 subunit required for its nuclear import caused distinct but overlapping transcription termination defects at highly expressed genes, active enhancers and promoters, thus enabling the increased synthesis of unusually long ncRNAs. These data indicate that transcription initiated from cis-regulatory elements is tightly coordinated with termination mechanisms that impose the synthesis of short RNAs. Overall design: polyA-mRNAs or 4sU-labeled RNAs from BMDMs, either untreated or treated for with lipopolysaccharide (LPS) for the indicated time. Experiments were carried out in cells containing either a short hairpin targeting either of these: 1) Wdr82; 2) Set1a+Set1b; 3) Pnuts; or the empty vector (LMP) or a scrambled as a control. When specified, cells were pre-treated with 5,6-Dichloro-1-ß-D-ribofuranosylbenzimidazole (DRB) in order to prevent RNA polymerase II elongation.

Publication Title

Transcription of Mammalian cis-Regulatory Elements Is Restrained by Actively Enforced Early Termination.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13204
Microarray Innovations in LEukemia (MILE) study
  • organism-icon Homo sapiens
  • sample-icon 1492 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

An international standardization programme towards the application of gene expression profiling in routine leukaemia diagnostics: the Microarray Innovations in LEukemia study prephase.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13159
Microarray Innovations in LEukemia (MILE) study: Stage 1 data
  • organism-icon Homo sapiens
  • sample-icon 357 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

An International Multi-Center Study to Define the Clinical Utility of MicroarrayBased Gene Expression Profiling in the Diagnosis and Sub-classification of Leukemia (MILE Study)

Publication Title

An international standardization programme towards the application of gene expression profiling in routine leukaemia diagnostics: the Microarray Innovations in LEukemia study prephase.

Sample Metadata Fields

Disease

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accession-icon GSE11135
The MILE (Microarray Innovations In LEukemia) study pre-phase
  • organism-icon Homo sapiens
  • sample-icon 204 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

An international standardization program towards the application of gene expression profiling in routine leukaemia diagnostics: The MILE study pre-phase.

Publication Title

An international standardization programme towards the application of gene expression profiling in routine leukaemia diagnostics: the Microarray Innovations in LEukemia study prephase.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP159645
Haploinsufficiency of the intellectual disability-gene SETD5 disturbs developmental gene expression and cognition
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

SETD5 gene mutations have been identified as a frequent cause of idiopathic intellectual disability. Here we show that Setd5 haploinsufficient mice present developmental defects such as abnormal brain to body weight ratio and neural crest defect associated phenotypes. Furthermore, Setd5 mutant mice show impairments in cognitive tasks, enhanced long-term potentiation, delayed ontogenetic profile of ultrasonic vocalisation and behavioural inflexibility. Behavioural issues are accompanied by abnormal expression of postsynaptic density proteins previously associated with cognition. Our data suggest that Setd5 might regulate RNA polymerase II dynamics and gene transcription during development and learning via its interaction with the Hdac3 and Paf1 complexes. Our results emphasize the decisive role of Setd5 in a biological pathway found to be disrupted in intellectual disability and autism spectrum disorder patients. Overall design: RNA-sequencing for wild type and Setd5 heterozygous knockout mice in two settings. First, in whole embryo samples (age E9.5), three biological replicates each. Second, gene expression changes due to contextual fear conditioning (CFC) was studied by comparing baseline transcription in homecage (HC) mice with transcription one hour (CFC_1h) or three hours (CFC_3h) after fear conditioning (4-5 biological replicates per time point and genotype).

Publication Title

Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE15777
Spontaneous regression of chronic lymphocytic leukemia: clinical and biological features of 9 cases
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

We describe 9 CLL patients who underwent a spontaneous clinical regression. CD38 and ZAP-70 were negative in all cases. Immunoglobulin heavy chain variable region (IgVH) genes, mutated in all 7 evaluable patients, were restricted to the VH3 family in 6, with the usage of VH3-30 gene in 2. The light chain variable region genes were mutated in 6/8 cases, with the usage of V4-1 gene in 3. Microarray analysis of CLL cells revealed a distinctive genomic profile. The number of activated T lymphocytes expressing IFN-, TNF- and IL-4 was similar between CLL in spontaneous regression and healthy individuals.

Publication Title

Spontaneous regression of chronic lymphocytic leukemia: clinical and biologic features of 9 cases.

Sample Metadata Fields

Specimen part

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accession-icon GSE3920
EC_interferon
  • organism-icon Homo sapiens
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

IFNs are highly pleiotropic cytokines also endowed with marked anti-angiogenic activity. In this study, the mRNA expression profiles of endothelial cells (EC) exposed in vitro to IFN-alpha, IFN-beta, or

Publication Title

Identification of genes selectively regulated by IFNs in endothelial cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE49697
Increased chronic lymphocytic leukemia proliferation upon IgM stimulation is sustained by the upregulation of miR-132 and miR-212
  • organism-icon Homo sapiens
  • sample-icon 62 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

Increased chronic lymphocytic leukemia proliferation upon IgM stimulation is sustained by the upregulation of miR-132 and miR-212.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE49695
Increased CLL Proliferation upon IgM stimulation is Sustained by the Up-regulation of miR-132 and miR-212: a Combined miRNA and Gene Expression Profiling Analysis and Correlation with Disease Progression [gene expression]
  • organism-icon Homo sapiens
  • sample-icon 62 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In order to investigate a potential involvement of miRNAs in BCR stimulation, in the present work we first evaluated their expression following IgM cross-linking in CLL cells, as well as in healthy B lymphocytes. Next, to infer putative miRNA targeting networks, we combined miRNA profiling results with gene expression and functional analyses

Publication Title

Increased chronic lymphocytic leukemia proliferation upon IgM stimulation is sustained by the upregulation of miR-132 and miR-212.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

View Samples
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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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