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accession-icon GSE36437
Expression data from caudal artery of Notch3WT and Notch3KO mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Notch3 is a transmembrane receptor which is critically important for the structure and myogenic response of distal arteries, particularly cerebral arteries. After activation of the receptor, the intracellular domain translocates in the nucleus to activate target genes transcription.

Publication Title

Transcriptome analysis for Notch3 target genes identifies Grip2 as a novel regulator of myogenic response in the cerebrovasculature.

Alternate Accession IDs

E-GEOD-36437

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE37382
Subgroup specific somatic copy number aberrations in the medulloblastoma genome [mRNA]
  • organism-icon Homo sapiens
  • sample-icon 285 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Affymetrix Human Gene 1.1 ST Array profiling of 285 primary medulloblastoma samples.

Publication Title

Subgroup-specific structural variation across 1,000 medulloblastoma genomes.

Alternate Accession IDs

E-GEOD-37382

Sample Metadata Fields

Sex, Age

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accession-icon GSE31637
Tumor Suppressor BRCA1 epigenetically controls oncogenic miRNA-155
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

BRCA1, a well-known breast and ovarian cancer susceptibility gene with multiple interacting partners, is predicted to have diverse biological functions. However, to date its only well-established role is in the repair of damaged DNA and cell cycle regulation. In this regard, the etiopathological study of low penetrant variants of BRCA1 provides an opportunity to uncover its other physiologically important functions. Using this rationale, we studied the R1699Q variant of BRCA1, a potentially moderate risk variant, and found that it does not impair DNA damage repair but abrogates the repression of miR-155, a bona fide oncomir. We further show that in the absence of functional BRCA1, miR-155 is up-regulated in BRCA1-deficient mouse mammary epithelial cells, human and mouse BRCA1-deficienct breast tumor cell lines as well as tumors. Mechanistically, we found that BRCA1 represses miR-155 expression via its association with HDAC2, which deacetylates H2A and H3 on the miR-155 promoter. Finally, we show that over-expression of miR-155 accelerates whereas the knockdown of miR-155 attenuates the growth of tumor cell lines in vivo. Taken together, our findings demonstrate a new mode of tumor suppression by BRCA1 and reveal miR-155 as a potential therapeutic target for BRCA1-deficient tumors.

Publication Title

Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.

Alternate Accession IDs

E-GEOD-31637

Sample Metadata Fields

Specimen part

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accession-icon GSE31611
Expression data from embryoid body with BRCA1 mutation [mRNA]
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon

Description

We examined the functional significance of the R1699Q variant of human BRCA1 gene using a mouse ES cell-based assay.

Publication Title

Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.

Alternate Accession IDs

E-GEOD-31611

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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