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accession-icon GSE12363
H3K79 methylation profiles define murine and human MLL-AF4 leukemias
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Promoter 1.0R Array (hsprompr), Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Immunophenotypic and gene expression analysis of the ALL cells demonstrated bone marrow replacement with B-precursor cells which express a gene expression profile that has significant overlap with profiles in human MLL-rearranged ALL.

Publication Title

H3K79 methylation profiles define murine and human MLL-AF4 leukemias.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE12310
Expression profiling of normal murine lymphoid progenitors and MLL-AF4 leukemic lymphoblasts
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2), Affymetrix Human Promoter 1.0R Array (hsprompr)

Description

We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Immunophenotypic and gene expression analysis of the ALL cells demonstrated bone marrow replacement with B-precursor cells which express a gene expression profile that has significant overlap with profiles in human MLL-rearranged ALL.

Publication Title

H3K79 methylation profiles define murine and human MLL-AF4 leukemias.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE12313
Expression profiling of activated or control 5-FU bone marrow from MLL-AF4stop knockin mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Immunophenotypic and gene expression analysis of the ALL cells demonstrated bone marrow replacement with B-precursor cells which express a gene expression profile that has significant overlap with profiles in human MLL-rearranged ALL.

Publication Title

H3K79 methylation profiles define murine and human MLL-AF4 leukemias.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE26408
Signatures of murine B-cell development implicate Yy1 as a regulator of the germinal center-specific program
  • organism-icon Mus musculus
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Heirarchical development of B-cells involves the induction and supression of large sets of genes that provide the basis for differentiation and, ultimately, antibody production.

Publication Title

Signatures of murine B-cell development implicate Yy1 as a regulator of the germinal center-specific program.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE43510
Gene expression profiling of five diffuse large B-cell lymphoma (DLBCL) cell lines, DHL4, DHL6, LY7, HBL1 and U2932, treated with the SYK inhibitor, R406
  • organism-icon Homo sapiens
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The five DLBCL cell lines were treated with R406 to assess the signature of SYK inhibition. In previous studies, R406 decreased the proliferation and induced apoptosis of these surface Ig+ cell lines. In the previous studies, R406 inhibited the autophosphorylation of SYK 525/526 and SYK-dependent phosphorylation of BCR signaling components such as BLNK.

Publication Title

SYK inhibition modulates distinct PI3K/AKT- dependent survival pathways and cholesterol biosynthesis in diffuse large B cell lymphomas.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Time

View Samples
accession-icon GSE34176
Gene expression profiling of two diffuse large B-cell lymphoma (DLBCL) cell lines, DHL4 and DHL6, treated with the SYK inhibitor, R406
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

The two DLBCL cell lines were treated with R406 to assess the signature of SYK inhibition. In previous studies, R406 decreased the proliferation and induced apoptosis of these surface Ig+ cell lines. In the previous studies, R406 inhibited the autophosphorylation of SYK 525/526 and SYK-dependent phosphorylation of BCR signaling components such as BLNK.

Publication Title

SYK inhibition modulates distinct PI3K/AKT- dependent survival pathways and cholesterol biosynthesis in diffuse large B cell lymphomas.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon SRP078862
Next-generation sequencing and quantitative analysis of wild type and p110gamma -/- tumors and tumor-associated macrophages
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: The goals of this study were to identify quantitative gene expression differences between whole tumor and tumor-associated macrophages (TAMs) derived from Lewis lung carcinoma (LLC) tumors grown in wild type and PI3Kinase-gamma-null mice. Methods: mRNA profiles of whole tumor or tumor-associated macrophages (CD11b+Gr1- cells) from wild type (WT) or PI3Kinase-gamma-knockout (p110g-/-) mice were generated by single deep read sequencing, in triplicate or quadruplicate, using Illumina HiSeq 2000. The sequence reads that passed quality filters were aligned to mouse transcriptome using the bowtie2 aligner. Gene-level summaries were normalized and analyzed for differential expression using DESeq. Overall design: mRNA profiles of whole tumor and tumor-associated macrophages from WT and p110g-/- mice were generated by deep sequencing in triplicate or quadruplicate using Illumina HiSeq 2000.

Publication Title

PI3Kγ is a molecular switch that controls immune suppression.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon SRP043038
Next Generation Sequencing and Quantitative Analysis of Wild Type and p110gamma-/- macrophages
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: The goals of this study were to identify quantitative gene expression differences between macrophages derived from wild type and PI3Kgamma null macrophages Methods: mRNA profiles of MCSF, IL4 and IFNg/LPS stimulated macrophage wild-type (WT) and PI3Kinase gamma knockout (p110g-/-) mice were generated by single read deep sequencing, in triplicate, using Illumina HiSeq2000. The sequence reads that passed quality filters were aligned to mouse transcriptome using the bowtie2 aligner. Gene-level summaries were normalized and analyzed for differential expression using DESeq. qRT–PCR validation was performed using SYBR Green assays. Conclusions: Our study represents the first detailed analysis of the role of p110g in the control of the macrophage immune response, with biological replicates, generated by RNA-seq technology. Overall design: mRNA profiles of wild type (WT) and p110g-/- macrophages were generated by deep sequencing, in triplicate, using Illumina HiSeq2000.

Publication Title

PI3Kγ is a molecular switch that controls immune suppression.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP156760
Combined Experimental and System-Level Analyses Reveal the Complex Regulatory Network of miR-124 during Human Neurogenesis [Timecourse RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 910 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Non-coding RNAs regulate many biological processes including neurogenesis. The brain-enriched miR-124 is assigned as a key player of neuronal differentiation via its complex, but little understood, regulation of thousands of annotated targets. To systematically chart its regulatory functions, we used CRISPR/Cas9 gene editing to disrupt all six miR-124 alleles in human stem cells. Upon neuronal induction, miR-124-depleted cells underwent neurogenesis and became functional neurons, albeit with altered morphology and neurotransmitter specification. By RNA-induced-silencing-complex precipitation, we found that other miRNA species were upregulated in miR-124 depleted neurons. Furthermore, we identified 98 miR-124 targets of which some directly led to decreased viability. We performed advanced transcription-factor-network analysis and revealed indirect miR-124 effects on apoptosis and neuronal subtype differentiation. Our data emphasizes the need for combined experimental- and systems-level analyses to comprehensively disentangle and reveal miRNA functions, including their involvement in the neurogenesis of diverse neuronal cell types found in the human brain. Overall design: RNA profile for timecourse of neuronal Neurogenin-1 and 2-triggered differentiation from human iPSCs (wildtype and ?miR-124).

Publication Title

Combined Experimental and System-Level Analyses Reveal the Complex Regulatory Network of miR-124 during Human Neurogenesis.

Sample Metadata Fields

Subject

View Samples
accession-icon SRP156757
Combined Experimental and System-Level Analyses Reveal the Complex Regulatory Network of miR-124 during Human Neurogenesis [AGO2-RIP-Seq -miRNAs]
  • organism-icon Homo sapiens
  • sample-icon 93 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Non-coding RNAs regulate many biological processes including neurogenesis. The brain-enriched miR-124 is assigned as a key player of neuronal differentiation via its complex, but little understood, regulation of thousands of annotated targets. To systematically chart its regulatory functions, we used CRISPR/Cas9 gene editing to disrupt all six miR-124 alleles in human stem cells. Upon neuronal induction, miR-124-depleted cells underwent neurogenesis and became functional neurons, albeit with altered morphology and neurotransmitter specification. By RNA-induced-silencing-complex precipitation, we found that other miRNA species were upregulated in miR-124 depleted neurons. Furthermore, we identified 98 miR-124 targets of which some directly led to decreased viability. We performed advanced transcription-factor-network analysis and revealed indirect miR-124 effects on apoptosis and neuronal subtype differentiation. Our data emphasizes the need for combined experimental- and systems-level analyses to comprehensively disentangle and reveal miRNA functions, including their involvement in the neurogenesis of diverse neuronal cell types found in the human brain. Overall design: RNA interacting protein immunoprecipitation with AGO2 for miR-124 target enrichment from neuronal Neurogenin-1 and 2-triggered differentiation from human iPSCs (wildtype and ?miR-124) and subsequent sequencing.

Publication Title

Combined Experimental and System-Level Analyses Reveal the Complex Regulatory Network of miR-124 during Human Neurogenesis.

Sample Metadata Fields

Subject

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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