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accession-icon GSE34066
Expression data from mesodermal Tbx1-knockout ears, otic vesicles, and periotic mesenchyme
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE55811
Colon Tumor Cell Macrophage Interactions
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE27873
Wild-type vs. PU.1 Q202L mutant mouse ST_HSC (lin- Sca-1+ c-kit+ CD150- CD48+) and GMP (lin- Sca-1+ c-kit- FcgRII/IIIhi CD34+)
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Identification of differentially regulated genes in the PU.1 Q202L point mutant that disrupts association with c-Jun. The goal was to identify PU.1 target genes that depend on the co-activation of PU.1 by c-Jun. Mice have normal ST-HSC but lack normal GMP, so a population of GMP-like cells (lin- Sca-1+ c-kit- FcgRII/IIIhi CD34intermediate) was used in the mutant.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE55809
Cell autonomous and non-autonomous interactions of a western-style diet and the vitamin D receptor in intestinal homeostasis and tumorigenesis
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

These data suggest that co-culture with macrophages increases expression of NDRG-1 in epithelial cell lines. The finding is confirmed in 2 human epithelial cell lines, and in tissue derived from mice genetically and dietetically altered to increase macrophage infiltration of the small and large intestinal epithelium. NDRG1 is identified as a potential mediator of macrophage effects on tumorigenesis in the large and small intestine.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE34065
Expression data from mesodermal Tbx1-knockout otic vesicles and periotic mesenchyme at E11.5
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

The T-box transcription factor Tbx1 is expressed in the otic vesicle and surrounding periotic mesenchyme during inner ear development. Mesenchymal Tbx1 is essential for inner ear development, with conditional mutants displaying defects in both auditory and vestibular systems. We have previously identified reduced expression of retinoic acid metabolic genes in the periotic mesenchyme of mesoderm conditional Tbx1 mutants, using the T-Cre mouse line, implicating retinoic acid in mesenchymal-epithelial signaling downstream of Tbx1 in the periotic mesenchyme.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE18446
BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

The biology of chronic myeloid leukemia (CML)-stem cells is still incompletely understood. Therefore, we previously developed an inducible transgenic mouse model in which stem cell targeted induction of BCR-ABL expression leads to chronic phase CML-like disease. Here, we now demonstrate that the disease is transplantable using BCR-ABL positive LSK cells (lin-Sca-1+c-kit+). Interestingly, the phenotype is enhanced when unfractionated bone marrow (BM) cells are transplanted. However, neither progenitor cells (lin-Sca-1-c-kit+) nor mature granulocytes (CD11b+Gr-1+), or potential stem cell niche cells were able to transmit the disease or alter the phenotype. The phenotype was largely independent of BCR ABL priming prior to transplant. However, BCR-ABL abrogated the potential of LSK cells to induce full blown disease in secondary recipients. Subsequently, we found that BCR-ABL increased the fraction of multipotent progenitor cells (MPP) at the expense of long term HSC (LT-HSC) in the BM. Microarray analyses of LSK cells revealed that BCR-ABL alters the expression of genes involved in proliferation, survival, and hematopoietic development. Our results suggest that BCR-ABL induces differentiation of LT-HSC and decreases their self renewal capacity. Furthermore, reversion of BCR-ABL eradicates mature cells while leukemic stem cells persist, giving rise to relapsed CML upon re-induction of BCR-ABL.

Publication Title

BCR-ABL enhances differentiation of long-term repopulating hematopoietic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE34064
Expression data from mesodermal Tbx1-knockout otic vesicles at E11.5
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

The T-box transcription factor Tbx1 is expressed in the otic vesicle and surrounding periotic mesenchyme during inner ear development. Mesenchymal Tbx1 is essential for inner ear development, with conditional mutants displaying defects in both auditory and vestibular systems. We have previously identified reduced expression of retinoic acid metabolic genes in the periotic mesenchyme of mesoderm conditional Tbx1 mutants, using the T-Cre mouse line, implicating retinoic acid in mesenchymal-epithelial signaling downstream of Tbx1 in the periotic mesenchyme.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE14459
NSCLC metastasis: K-ras/p53 mutant and syngeneic mouse models
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Expression signatures of metastatic capacity in a genetic mouse model of lung adenocarcinoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10290
Gene expression analyses of PR action in the mammary gland of ovariectomized mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon

Description

Beyond demonstrating a critical role for progesterone receptor signaling in normal mammary epithelial proliferation, the progesterone receptor knockout mouse disclosed the progesterone receptor along with its effector pathways as key determinants of mammary neoplastic progression. Despite these advances, however, further progress in our mechanistic understanding of progesterones involvement in mammary morphogenesis and tumorigenesis is contingent upon defining the essential effector pathways responsible for transducing the progesterone signal into a mammary proliferative and/or pro-survival response. Toward this goal, a judiciously chosen acute progesterone treatment regimen together with microarray methods was applied to the mammary gland of the normal mouse to uncover new effectors that operate immediately downstream of the progesterone mammary signal. Examination of the resultant progesterone-responsive transcriptome disclosed inhibitor of differentiation or DNA binding 4 (Id4) as a molecular target acutely induced by progesterone in the murine mammary epithelium.

Publication Title

Transcriptional response of the murine mammary gland to acute progesterone exposure.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9914
Expression data from early symptomatic Sca1154Q/2Q and Sca7266Q/5Q knock-in cerebellum
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

Comparative analysis of cerebellar gene expression changes occurring in Sca1154Q/2Q and Sca7266Q/5Q knock-in mice

Publication Title

The insulin-like growth factor pathway is altered in spinocerebellar ataxia type 1 and type 7.

Sample Metadata Fields

Sex, Age

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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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