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accession-icon GSE67358
Promotion of pancreatic cancer metastasis by mutant p53
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The TP53 transcription factor is frequently mutated at later stages of epithelial cancers, indicating a possible role in their invasion and metastasis. Importantly, in most cases rather than a simple loss of function p53 mutation, point mutations of p53 accumulate at the protein level and may have dominant negative functions. This study analyses gene expression differences between mice harbouring p53 mutation who do and do not develop metastasis.

Publication Title

Targeting the LOX/hypoxia axis reverses many of the features that make pancreatic cancer deadly: inhibition of LOX abrogates metastasis and enhances drug efficacy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE108456
Gene expression analyses of CWR22Res Nsi (non-silencing) control and with stable knockdown of Sprouty2 (SPRY2)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Effects of SPRY2 deficiency in gene expression of CWR22Res prostate cancer cells.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE38448
Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Independence of repressive histone marks and chromatin compaction during senescent heterochromatic layer formation.

Sample Metadata Fields

Sex, Cell line, Treatment

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accession-icon GSE13035
Mitochondrial dysfunction by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Cellular stress responses can be activated following functional defects in organelles such as mitochondria and the endoplasmic reticulum. Mitochondrial dysfunction caused by loss of the serine protease HtrA2 leads to a progressive movement disorder in mice and has been linked to parkinsonian neurodegeneration in humans. Here we demonstrate that loss of HtrA2 results in transcriptional up-regulation of nuclear genes characteristic of the integrated stress response, including the transcription factor CHOP, selectively in the brain. We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death. CHOP expression is also significantly increased in Parkinsons disease patients brain tissue. We therefore propose that this brain-specific transcriptional response to stress may be important in the advance of neurodegenerative diseases.

Publication Title

Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13034
Differentially regulated genes in HtrA2 knockout MEFs upon rotenone treatment
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Cellular stress responses can be activated following functional defects in organelles such as mitochondria and the endoplasmic reticulum. Mitochondrial dysfunction caused by loss of the serine protease HtrA2 leads to a progressive movement disorder in mice and has been linked to parkinsonian neurodegeneration in humans. Here we demonstrate that loss of HtrA2 results in transcriptional up-regulation of nuclear genes characteristic of the integrated stress response, including the transcription factor CHOP, selectively in the brain. We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death. CHOP expression is also significantly increased in Parkinsons disease patients brain tissue. We therefore propose that this brain-specific transcriptional response to stress may be important in the advance of neurodegenerative diseases.

Publication Title

Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE62746
Gene expression profile of GM-CSF derived bone marrow dendritic cell subsets after LPS stimulation
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

GM-CSF derived bone marrow cultures contain several subsets of CD11c+MHCII+ mononuclear phagocytes

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE7700
Genes regulated by YAP in normal breast cell line and breast cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Frequent loss of heterozygosity (LOH) at 11q22-23 in breast cancer strongly suggests that this region contains a tumor suppressor gene, yet to be identified. We and others have shown Yes-associated protein (YAP), which is located at 11q22.2, transactivates the p53 family member p73 upon DNA damage, suggesting a tumor suppressive function for YAP. Our analysis of breast tumor tissues by immunohistochemistry (IHC) showed loss of YAP protein expression in great portion of breast cancers.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE38410
Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation (mRNA)
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

The expansion of repressive epigenetic marks has been implicated in heterochromatin formation during embryonic development, but the general applicability of this mechanism is unclear. Here we show that nuclear rearrangement of repressive histone marks H3K9me3 and H3K27me3 into non-overlapping structural layers characterizes senescence-associated heterochromatic foci (SAHF) formation in human fibroblasts. However, the global landscape of these repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells heterochromatin can be formed through the spatial repositioning of pre-existing repressively marked histones. This model is reinforced by the correlation of pre-senescent replication timing with both the subsequent layered structure of SAHFs and the global landscape of the repressive marks, allowing us to integrate microscopic and genomic information. Furthermore, modulation of SAHF structure does not affect the occupancy of these repressive marks nor vice versa. These experiments reveal that high-order heterochromatin formation and epigenetic remodeling of the genome can be discrete events.

Publication Title

Independence of repressive histone marks and chromatin compaction during senescent heterochromatic layer formation.

Sample Metadata Fields

Sex, Cell line, Treatment

View Samples
accession-icon GSE42460
Budding yeast Wapl controls sister chromatid cohesion maintenance and the chromosome condensation status
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Budding yeast Wapl controls sister chromatid cohesion maintenance and chromosome condensation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE98957
Gene expression profile of CD141+DNGR-1+ dendritic cells (cDC1s) derived in vitro from multipotent lymphoid progenitors (MLP) or common myeloid progenitors (CMP)
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

CD141+DNGR-1+ cDC1 have a dual origin. Both MLP and CMP can differentiate in CD141+DNGR-1+ cDC1s.

Publication Title

Dendritic Cell Lineage Potential in Human Early Hematopoietic Progenitors.

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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Developed by the Childhood Cancer Data Lab

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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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