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accession-icon GSE1294
Expression profile of genes in normal and Down syndrome mouse brains
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74B Version 2 Array (mgu74bv2), Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Analyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.

Publication Title

Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE1281
Expression profile of genes in normal and Down syndrome mouse brains MGU74A
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Analyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.

Publication Title

Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE1282
Expression profile of genes in normal and Down syndrome mouse brains MGU74B
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74B Version 2 Array (mgu74bv2), Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Analyses of six Ts1Cje (Down syndrome) and six normal littermate (2N) mouse brains at postnatal day 0.

Publication Title

Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE62210
Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntingtons model mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Huntingtons disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, a process by which aggregated proteins are degraded, and it is associated with several neurodegenerative disorders including HD. Here we investigated the effect of p62 depletion in three HD model mice: R6/2, HD190QG and HD120QG mice. We found that loss of p62 in these models led to longer lifespans and reduced nuclear inclusions, although cytoplasmic inclusions increased with polyglutamine length. In mouse embryonic fibroblasts (MEFs) with or without p62, mutant htt with a nuclear localization signal (NLS) showed no difference in nuclear inclusion between the two MEF types. In the case of mutant htt without NLS, however, p62 depletion increased cytoplasmic inclusions. Furthermore, to examine the effect of impaired autophagy in HD model mice, we crossed R6/2 mice with Atg5 conditional knockout mice. These mice also showed decreased nuclear inclusions and increased cytoplasmic inclusions, similar to HD mice lacking p62. These data suggest that the genetic ablation of p62 in HD model mice enhances cytoplasmic inclusion formation by interrupting autophagic clearance of polyQ inclusions. This reduces polyQ nuclear influx and paradoxically ameliorates disease phenotypes by decreasing toxic nuclear inclusions.

Publication Title

Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE87638
Comprehensive DNA Microarray Analysis for the Gene Sets Involved in Allergic Reaction by Allergic Effector Cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Mast cells, basophils, and eosinophils play an important role in allergic disorders as effector cells. These cells secrete abundant serine proteases as well as chemical mediators and cytokines. Various serine proteases including SLPI are also important for to regulate an allergic response in these effector cells, although the expression profiles and functions of these proteases still remain unclear.

Publication Title

Identification of Secretory Leukoprotease Inhibitor As an Endogenous Negative Regulator in Allergic Effector Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE99316
Gene repression and ChIP-seq in Human Small Cell Lung Cancer
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PRC2 overexpression and PRC2-target gene repression relating to poorer prognosis in small cell lung cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE43346
Gene repression with H3K27me3 modification in human small cell lung cancer
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Small cell lung cancer (SCLC) is a subtype of lung cancer with poor prognosis due to early dissemination and rapid growth. We here analyze gene expression profile of 23 clinical SCLC samples. EZH2 was found to be highly expressed in SCLC samples compared to 42 normal tissues including the normal lung, and other PRC2 members, SUZ12 and EED, were also highly expressed in SCLC. To obtain target genes of PRC2 in SCLC, H3K27me3 mark was mapped in three SCLC cell lines, Lu130, H209 and DMS53, and compared to normal small airway epithelial cells (SAEC). Whereas H3K27me3(+) genes in SAEC were significantly overlapped with PRC-target genes in ES cells (P=1.7x10-31), genes with H3K27me3 in SCLC cell lines but not in SAEC were not significantly overlapped with PRC-target genes in ES cells (P=0.64). These genes with H3K27me3 specifically in SCLC cell lines but not in SAEC showed decreased expression, not only in SCLC cell lines but also in clinical SCLCs, and showed enrichment of GO-terms such as plasma membrane (P=8.1x10-21) and cell adhesion (P=1.7x10-8). Introduction of JUB, a gene showing specific H3K27me3 modification and the strongest repression in the three SCLC cell lines, resulted in repression of cellular growth in DMS53. In clinical SCLC cases, lower JUB level correlated to shorter survival (P=0.002), or a set of PRC target genes (JUB, EPHB4) and marker genes of classic type SCLC (GRP, ASCL1) correlated to shorter survival (P=0.0001) and classified SCLC into two groups with distinct prognosis. Growth of SCLC cell lines was repressed when treated with 3-Deazaneplanocin A, an inhibitor against PRC2. It is suggested that high expression of PRC2 in SCLC contributed to repression of genes including non-PRC-target genes in ES cells, and that the gene repression may play a role in genesis of SCLC.

Publication Title

PRC2 overexpression and PRC2-target gene repression relating to poorer prognosis in small cell lung cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP057118
RNA sequencing of heart samples of myotonic dystrophic (DM1) patients
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of alternative splicing in heart (left ventricles) samples of 3 adult DM1 patients versus 3 adult controls Overall design: PolyA RNA from left ventricles (heart) of 3 controls and 3 DM1 patients were analysed by massive parrallel sequencing

Publication Title

Splicing misregulation of SCN5A contributes to cardiac-conduction delay and heart arrhythmia in myotonic dystrophy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE67067
Exon array of heart samples of myotonic dystrophic patients
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Analysis of alternative splicing of left ventricles heart samples of 3 DM1 adult versus 3 adult controls

Publication Title

Splicing misregulation of SCN5A contributes to cardiac-conduction delay and heart arrhythmia in myotonic dystrophy.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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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