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accession-icon GSE31049
Circadian temporal profiling of MMH-D3 hepatocytes
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon

Description

The circadian clock generates daily rhythms in mammalian liver processes, such as glucose and lipid homeostasis, xenobiotic metabolism, and regeneration. The mechanisms governing these rhythms are not well understood, particularly the distinct contributions of the cell-autonomous clock and central pacemaker to rhythmic liver physiology. Through microarray expression profiling in MMH-D3 hepatocytes, we identified over 1,000 transcripts that exhibit circadian oscillations, demonstrating that many rhythms can be driven by the cell-autonomous clock and that MMH-D3 is a valid circadian model system. The genes represented by these circadian transcripts displayed both co-phasic and anti-phasic organization within a protein-protein interaction network, suggesting the existence of competition for binding sites or partners by genes of disparate transcriptional phases. Multiple pathways displayed enrichment in MMH-D3 circadian transcripts, including the polyamine synthesis module of the glutathione metabolic pathway. The polyamine synthesis module, which is highly associated with cell proliferation and whose products are required for initiation of liver regeneration, includes enzymes whose transcripts exhibit circadian oscillations, such as ornithine decarboxylase (Odc1) and spermidine synthase (Srm). Metabolic profiling revealed that the enzymatic product of SRM, spermidine, cycles as well. Thus, the cell-autonomous hepatocyte clock can drive a significant amount of transcriptional rhythms and orchestrate physiologically relevant modules such as polyamine synthesis.

Publication Title

Cell-autonomous circadian clock of hepatocytes drives rhythms in transcription and polyamine synthesis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE17297
Mndal, a new interferon-inducible family member, suppresses cell growth and may modify plasmacytoma susceptibility
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
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Description

Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth and may modify plasmacytoma susceptibility.

Publication Title

Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth, and may modify plasmacytoma susceptibility.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE27787
Hematopoietic cells and stem cells
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Forced expression of the histone demethylase Fbxl10 maintains self-renewing hematopoietic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE27785
Gene expression profile of mouse hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Mouse CD34(-)KSL hematopoietic stem cells and CD34(+)KSL multipotent progenitors were purified by cell sorting from bone marrow of 8-week-old C57BL/6 mice, and their gene expression was analyzed.

Publication Title

Forced expression of the histone demethylase Fbxl10 maintains self-renewing hematopoietic stem cells.

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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