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accession-icon GSE49089
NRASG12V oncogene mediates self-renewal in acute myelogenous leukemia
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE68427
Identification and function of Tbx4 resident fibroblasts as a major source of fibrotic fibroblasts
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
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Description

Progressive tissue fibrosis is a major cause of morbidity, and idiopathic pulmonary fibrosis (IPF) is a terminal illness characterized by unremitting matrix deposition in the lung with very limited choice of therapies. The imcomplete understanding of the mechanisms of progressive fibrosis curbs the progress in therapeutics development. Of which, the origin of fibrotic fibroblasts has been poorly defined during the pathogenesis of tissue fibrosis. Here, we fate-mapped a early embryonic transcription factor T-box gene 4 (Tbx4)-derived mesenchymal progenitors in injured adult lung and found that Tbx4+ lineage cells are the major source of myofibroblasts. The ablation of Tbx4+ cells or disruption of Tbx4 signaling attenuated lung fibrosis in bleomycin injury model in mice in vivo. Furthermore, Tbx4+ fibroblasts are more invasive and the regulation of fibroblast invasiveness by Tbx4 is through mediating hyaluronan synthase 2 (HAS2). This study identified a major mesenchymal transcription factor driving the development of fibrotic fibroblasts during lung fibrosis. Understanding the origin, signaling, and functions of these fibroblasts would prove pivotal in the development of therapeutics for patients with progressive fibrotic diseases.

Publication Title

Transcription factor TBX4 regulates myofibroblast accumulation and lung fibrosis.

Sample Metadata Fields

Specimen part

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accession-icon GSE33106
Expression data from livers in wildtype and Sox17+/-mice at 17dpc
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

The onset of the liver inflamentation in the Sox17+/- embryos.

Publication Title

Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE34093
Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.

Sample Metadata Fields

Specimen part

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accession-icon GSE34091
Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [Mouse430_2 Expression]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

The effect of CTCFL mutation on the transcriptional program in testes

Publication Title

The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.

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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