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accession-icon GSE74680
Expression data from the spinal cord of wild-type C57Bl/6 mice
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The spinal cords of mice submitted to aortic cross-clamping for 7.5 minutes present with gray matter damage and central cord edema. 60% of mice subsequently experience hindlimb and tail paralysis.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-74680

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE25825
Expression data from MxCre;E2F1-/-2-/-3f/f Cd11B myeloid cells
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

To understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.

Publication Title

E2f1-3 are critical for myeloid development.

Alternate Accession IDs

E-GEOD-25825

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE32355
E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells
  • organism-icon Mus musculus
  • sample-icon 101 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Canonical and atypical E2Fs regulate the mammalian endocycle.

Alternate Accession IDs

E-GEOD-32355

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE56009
E2f and Myc transcriptional programs and chromatin binding landscapes in the small intestines
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.

Alternate Accession IDs

E-GEOD-56009

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE32354
Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix)
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon

Description

To understand the underlying cause and mechanisms of changes in hepatocyte ploidy upon Albumin-Cre mediated deletion of E2f7&8 and Mx1-Cre mediated deletion of E2f1,2&3, we analysed global gene expression of 6 weeks and 2 months liver tissues.

Publication Title

Canonical and atypical E2Fs regulate the mammalian endocycle.

Alternate Accession IDs

E-GEOD-32354

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE56007
Expression data from control, Rb KO and Rb/Myc DKO tissues (villi and crypts)
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon

Description

Loss of Myc corrects abrrant transcription in Rb KO villi, while these genetic manipulation does not lead to major gene expression changes in crypts.

Publication Title

No associated publication

Alternate Accession IDs

E-GEOD-56007

Sample Metadata Fields

Specimen part

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accession-icon GSE16454
Gene expression data from small intestines
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon

Description

Rb and E2F are thought to play antagonistic roles in celll proliferation. However, this model is based mostly from in vitro cell culture systems. We used small intestines to test this model in vivo.

Publication Title

E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells.

Alternate Accession IDs

E-GEOD-16454

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE64303
Expression Data from Pten mutant epithelial cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

PTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor roles are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation

Publication Title

Noncatalytic PTEN missense mutation predisposes to organ-selective cancer development in vivo.

Alternate Accession IDs

E-GEOD-64303

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE30248
Expression analysis of eu-miR-155 transgenic mice B-cells.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

miR-155 transgenic mice develop pre-B cell leukemia/lymphoma. Though some targets of miR-155 are known, understanding of the mechanism by which miR-155 overexpression drives malignant transformation is not known. MicroRNAs regulate multiple genes.

Publication Title

miR-155 targets histone deacetylase 4 (HDAC4) and impairs transcriptional activity of B-cell lymphoma 6 (BCL6) in the Eμ-miR-155 transgenic mouse model.

Alternate Accession IDs

E-GEOD-30248

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE25100
Expression data from CD19-positive splenic B cells isolated from 1-month old ID4+/-TCL1-tg and ID4+/+TCL1-tg mice
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The function of ID4 in CLL development was studied in vivo using TCL1 transgenic mouse model that develop leukemia similar to human CLL. TCL1 mice with ID4 single knockout gene have accelerated CLL progression.

Publication Title

Silencing of the inhibitor of DNA binding protein 4 (ID4) contributes to the pathogenesis of mouse and human CLL.

Alternate Accession IDs

E-GEOD-25100

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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