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accession-icon GSE110104
pre-B cells from normal control, preleukemic, fully leukemic and fully leukemic, nilotinib-treated P190 BCR/ABL transgenic mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Precursor B-lineage acute lymphoblastic leukemia (pre-B ALL) can be subdivided into different categories based on genetic abnormalities.

Publication Title

Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.

Sample Metadata Fields

Specimen part

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accession-icon GSE75388
Gene expression profile of E18.5 epidermis from WT and MafB KO mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

MafB is a member of the Maf family of bZip transcription factor and plays important roles in the developmental processes of various tissues, as well as in cell-type specific gene expression. MafB is expressed in differentiating keratinocytes in mice and is transcriptionally up-regulated upon human keratinocyte differentiation in vitro. In MafB-deficient mice, epidermal differentiation is partially impaired and the cornified layer is thinner. To gain insights into more detailed molecular mechanisms of MafB regulation of epidermal development, we performed microarray analysis of mRNAs isolated from dorsal skin epidermis of MafB-/- and wild-type mice at E18.5.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE43396
Comparison of gene expression in NOD versus B6 splenic B cell subsets.
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
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Description

NOD mice are an inbred strain that display enhanced MZ B cell differentiation from an early age. Interestingly, several lines of evidence implicate MZ B cells in this strain as important contributors to the T cell mediated beta cell destruction associated with the development of type 1 diabetes (T1D). In order to develop a better understanding of the underlying causes for augmented MZ B cell production in NOD mice, we obtained the transcriptional profiles of FO and MZ subsets and TR precursors from NOD mice and compared them to those of the B6 strain.

Publication Title

Intrinsic molecular factors cause aberrant expansion of the splenic marginal zone B cell population in nonobese diabetic mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE30356
Expression data from FAK null mouse embryonic fibroblasts treated with endothelin-1
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

Endothelin-1 (ET-1) plays a critical role in connective tissue remodeling by fibroblasts during tissue repair and fibrosis. We investigated the molecular pathways in the transmission of ET-1 signals that lead to features of connective tissue remodeling, in particular the role of FAK (focal adhesion kinase).

Publication Title

Inhibition of focal adhesion kinase prevents experimental lung fibrosis and myofibroblast formation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE10422
Traf2 and Traf3 B cell knockout mice and Baff tg mice - gene expression in lymph node B cells
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon

Description

Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-B2 (NF-B2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family). This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo. We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling. As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells. This analysis should identify genes that are important in B cell survival.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age

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accession-icon GSE69688
Gene expression data from murine myeloid leukemia genomes induced by Sleeping Beauty transposon mutagenesis
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
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Description

Transcriptome analysis of mRNA samples from a cohort of mice with histopathologically diagnosed Undifferentiated Myeloid Leukemia.

Publication Title

Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE51285
Expression and Metabolic Profiles in a Panel of Five Neural Tube Defect Mouse Models
  • organism-icon Mus musculus
  • sample-icon 33 Downloadable Samples
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Description

Neural tube defects (NTDs) are serious birth defects with an estimated worldwide incidence of 1 per 1,000 live births. The multifactorial nature of NTDs in humans has made it difficult to elucidate pathogenesis mechanisms. However, a strong relationship has been established between folate-homocysteine metabolism and NTD risk. Prevention of a substantial proportion of fetal NTDs can be achieved through maternal folic acid (FA) supplementation. However the mechanism by which FA exerts its beneficial effect remains unclear. METHODS: To improve our understanding of the underlying mechanisms of NTD pathogenesis and the ways in which folate exerts its beneficial effect, we analyzed mRNA profiles as well as folate and vitamin B12 levels in five NTD mouse mutants whose response to dietary FA was previously established. RESULTS: Differentially expressed genes representing the effect of each NTD-causing mutation were identified and associated with biologic pathways. Interestingly, the panel of NTD mutants collectively revealed pathways related to two nuclear receptors, retinoid X receptor (RXR) and pregnane X receptor (PXR), suggesting that these pathways may be related to a shared mechanism of NTD development. Moreover, the NTD-causing mutations that were associated with FA responsiveness had expression profiles that were related to folate-homocysteine metabolic pathways. These pathways were not strongly associated with mutants that do not respond to FA supplementation, implying that FA may be beneficial when the NTD mutation affects pathways related to folate-homocysteine metabolism.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE102232
Gene expression analysis of laser-captured epithelium and stroma from FVB mice and HPV16 E6/E7 transgenic mice under estrogen or control treatment regimens.
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon

Description

Affymetrix Mouse Genome 430 2.0 arrays were used to measure genome-wide gene expression levels. The results show that high-risk human papillomavirus oncogenes E6 and E7 reprogram the cervical cancer microenvironment independently of and synergistically with estrogen, a critical co-factor in cervical cancer development and maintenance.

Publication Title

Human papillomavirus oncogenes reprogram the cervical cancer microenvironment independently of and synergistically with estrogen.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE19137
Interferon response genes as immunopathogenic correlates of SARS coronavirus infection in mice (129/S6/SvEv)
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon

Description

To further identify and understand the molecular and immunological correlates of pathology for SARS-CoV infection, we infected 129/S6/SvEv or B129 mice with the TOR2 strain of SARS-CoV. SARS-CoV was detected in the lung and nasal turbinates of infected mice peaking at 1 day post infection (DPI) in both tissues before decreasing rapidly to levels below detection at 7 DPI and 3 DPI, respectively. Pulmonary lesions in virus-infected animals included bronchiolar, peribronchiolar, and perivascular foci of mild to moderate subacute inflammation. Chronic inflammation included inflammatory macrophages, lymphocytes, and plasma cells. Neutralizing antibodies appeared on 5 DPI (IgM); converting to IgG on 7 DPI. Despite the prevailing notion that SARS-CoV interferes with the induction of interferon (IFN) signaling, mice infected with SARS-CoV in vivo demonstrated significantly increased expression of innate antiviral interferon (IFN) response genes (IRGs) in the lungs during the first week of acute infection. By the end of the second week of infection, coordinated expression of MHC class I / II and antigen presentation genes occurred in correlation with declining viral titres. Collectively, the mouse data suggests that robust IFN-driven innate immune responses and a critical shift from innate to adaptive immune responses is necessary for clearance and recovery from SARS-CoV infection.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE18507
Transcriptional Networks in Mouse Trophoblast Stem Cell Self-Renewal
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon

Description

Trophoblast stem cells (TS cells), derived from the trophectoderm (TE) of blastocysts, require transcription factors (TFs) and external signals (Fgf4, Activin/Nodal/Tgfb) for self-renewal. While many reports have focused on TF networks that regulate embryonic stem cell (ES cell) self-renewal and pluripotency, little is know about TF networks that regulate self-renewal in TS cells. To further understand transcriptional networks in TS cells we used chromatin immunopreciptiation and DNA microarray analysis (ChIP-chip) to investigate targets of TFs Ap-2g (Tcfap2c), Eomes, Ets2, and Gata3, and a chromatin remodeling factor, Brg1 (Smarca4). We then evaluated the transcriptional states of target genes using transcriptome analysis and genome-wide analysis of histone H3 acetylation (AcH3). Our results describe previously unknown transcriptional networks in TS cells, including TF occupancy of genes involved in ES cell self-renewal and pluripotency, co-occupancy of multiple TFs at target genes, and transcriptional regulatory circuitry within the 5 factors. Through genome-wide mapping and global expression analysis of 5 TF target genes, our data provide a comprehensive analysis of transcriptional networks that regulate TS cell self-renewal.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Time

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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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