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accession-icon GSE8646
The Hay Wells Syndrome-Derived TAp63alphaQ540L Mutant Has Impaired Transcriptional and Cell Growth Regulatory Activity
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

p63 mutations have been associated with several human hereditary disorders characterized by ectodermal dysplasia such as EEC syndrome, ADULT syndrome and AEC syndrome . The location and functional effects of the mutations that underlie these syndromes reveal a striking genotype-phenotype correlation. Unlike EEC and ADULT that result from missense mutations in the DNA-binding domain of p63, AEC is solely caused by missense mutations in the SAM domain of p63. We report a study on the TAp63a isoform, the first to be expressed during development of the embryonic epithelia, and on its naturally occurring Q540L mutant derived from an AEC patient. To assess the effects of the Q540L mutation, we generated stable cell lines expressing TAp63a wt, DeltaNp63 alpha or the TAp63 alpha-Q540L mutant protein and used them to systematically compare the cell growth regulatory activity of the mutant and wt p63 proteins and to generate, by microarray analysis, a comprehensive profile of differential gene expression. We found that the Q540L substitution impairs the transcriptional activity of TAp63a and causes misregulation of genes involved in the control of cell growth and epidermal differentiation.

Publication Title

The Hay Wells syndrome-derived TAp63alphaQ540L mutant has impaired transcriptional and cell growth regulatory activity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41141
Transcriptome analysis of liver samples from PPARa KO and control mice injected with HDAd-TFEB
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

TFEB controls cellular lipid metabolism through a starvation-induced autoregulatory loop.

Sample Metadata Fields

Specimen part

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accession-icon GSE41140
Transcriptome analysis of the injected Ppara-KO mice overexpressing TFEB specifically in liver
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Expression data from Ppara (peroxisome proliferator activated receptor alpha) KO mice injected with TFEB specifically in liver. In order to identify the effects of TFEB overexpression together with Ppara absence on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the injected mice

Publication Title

TFEB controls cellular lipid metabolism through a starvation-induced autoregulatory loop.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE41139
Transcriptome analysis of the injected mice overexpressing TFEB specifically in liver
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

In order to identify the effects of TFEB overexpression on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the injected mice

Publication Title

TFEB controls cellular lipid metabolism through a starvation-induced autoregulatory loop.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE36510
Expression data from wild-type mice starved as compared to wild-type control mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

In order to identify the effects of starvation on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the starved mice

Publication Title

TFEB controls cellular lipid metabolism through a starvation-induced autoregulatory loop.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE35015
Expression data from injected mice overexpressing TFEB specifically in liver
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

In order to identify the effects of transcription factor EB (TFEB) overexpression on the liver transcriptome, we performed Affymetrix GeneChip hybridization experiments on injected mice overexpressing TFEB specifically in the liver.

Publication Title

TFEB controls cellular lipid metabolism through a starvation-induced autoregulatory loop.

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon GSE62980
Expression data from mice after knockout or overexpression of Tcfeb in muscle
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcription Factor EB Controls Metabolic Flexibility during Exercise.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE62976
Expression data from Tcfeb KO mice specifically in muscle
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

In order to identify the effects of the absence of Tcfeb on the muscle transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the KO mice as compared with wt mice

Publication Title

Transcription Factor EB Controls Metabolic Flexibility during Exercise.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE64965
Expression profile of osteosarcoma cells in which Sox2 maintains cancer stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Sox2 is required to maintain osteosarcoma cell tumor initiation.Knockdown of Sox2 leads tpo loss of tumorigenic properties. To examine gene expression changes upon Sox2 knockdown, we performed microarray analysis on mouse osteosarcoma cells expressing scrambled or Sox2shRNA. We found that genes upregulated upon Sox2 knockdown included osteoblast diffrentiation genes and genes down regulated included cell cycle and RNA processing genes as well as YAP-TEAD target genes.

Publication Title

Sox2 antagonizes the Hippo pathway to maintain stemness in cancer cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE50698
DENV1-NS3hell single point mutations enhance viral replication and bypass Type I IFN anti-virus function in human dendritic cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Dengue is one of the most important arboviruses in the world, with 2.5 billion people living in areas under risk to contagious. Mosquitos from Aedes genus is the transmission vector of viral particles.

Publication Title

Single point mutations in the helicase domain of the NS3 protein enhance dengue virus replicative capacity in human monocyte-derived dendritic cells and circumvent the type I interferon response.

Sample Metadata Fields

Specimen part, Time

View Samples
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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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