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accession-icon GSE18969
Ontogeny of CD24 expression in the human fetal kidney
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

CD24, or heat stable antigen, is a cell surface sialoglycoprotein expressed on immature cells that disappears after the cells have reached their final differentiation stage. CD24 may be important in human embryonic kidney epithelial cell differentiation. In mice, CD24 expression is up-regulated in the early metanephros and localized to developing epithelial structures but the role and expression of CD24 in the developing human kidney has not been well described. In normal human fetal kidneys from 8 to 38 weeks gestation, CD24 expression was up-regulated and restricted to the early epithelial aggregates of the metanephric blastema and to the committed proliferating tubular epithelia of the S-shape nephron; however individual CD24+ cells were identified in the interstitium of later gestation and postnatal kidneys. In freshly isolated cells, FACS analysis demonstrated distinct CD24+ and CD24+133+ cell populations, constituting up to 16% and 14% respectively of the total cells analyzed. Isolated and expanded CD24+ clones displayed features of an epithelial progenitor cell line. Early fetal urinary tract obstruction resulted in an upregulation of CD24 expression, both in developing epithelial structures of early gestation kidneys and in the cells of the injured tubular epithelium of the later gestation kidneys. These results highlight the cell specific expression of CD24 in the developing human kidney and dysregulation in fetal urinary tract obstruction.

Publication Title

Ontogeny of CD24 in the human kidney.

Alternate Accession IDs

E-GEOD-18969

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE3583
Huntington's disease: Gene expression changes caused by Hdh CAG mutation or 3-nitropropionic acid in striatal cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Affymetrix MG430 2.0 expression levels of wild-type (STHdhQ7/Q7), 3NP-treated wild-type (STHdhQ7/Q7+3-NP), and mutant (STHdhQ111/Q111) striatal cells

Publication Title

Unbiased gene expression analysis implicates the huntingtin polyglutamine tract in extra-mitochondrial energy metabolism.

Alternate Accession IDs

E-GEOD-3583

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE16856
Identifying mutant genes in the LNCaP and 22Rv1 prostate cancer cell lines
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used a modification of GINI analysis to identify genes containing premature translation termination codons (PTC) generated by nonsense or frameshift mutations in prostate cancer cell lines. The analysis was performed in two steps. In the first step nonsense mediated mRNA decay (NMD) was inhibited in prostate cancer cell lines using incubation with medium containing caffeine for 4 hours. Gene expression analysis of caffeine treated or untreated cells after this step detects mRNA accumulation that takes place for genes containing PTC and as well as for genes that show induction of transciption due to stress caused by NMD inhibition. In the second step either both transcription and NMD or transcription only are blocked by incubating cell in a medium containing either both actinomycin D and caffeine or actinomacin D only for 4 hours. Gene expression analysis after this second step detects mRNA degradation for genes containing PTC as well as for genes that show induction of transciption due to stress caused by NMD inhibition. The efficiency of mRNA degradation for genes containing PTC during this step depends on whether NMD is inhibited or not. The efficiency of mRNA degradation for stress response genes does not depend on whether NMD is inhibited or not.

Publication Title

Par-3 partitioning defective 3 homolog (C. elegans) and androgen-induced prostate proliferative shutoff associated protein genes are mutationally inactivated in prostate cancer cells.

Alternate Accession IDs

E-GEOD-16856

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE5486
Using GINI2 to identify novel mutations in candidate tumor suppressor genes in colon cancer cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Inhibition of the nonsense mediated decay (NMD) mechanism in cells results in stabilization of transcripts carrying premature translation termination codons. A strategy referred to as gene indentification by NMD inhibition (GINI) has been proposed to identify genes carrying nonsense mutations (Noensie & Dietz, 2001). Genes containing frameshift mutations in colon cancer cell line have been identifying mutatnt genes using GINI, we have now further improved the strategy. In this approach, inhibition of NMD with emetine is complemented with inhibiting NMD by blocking the phosphorylation of the hUpf1 protein with caffeine. In addition, to enhance the GINI strategy, comparing mRNA level alterations produced by inhibiting transcription alone or inhbiiting transcription together with NMD following caffeine pretreatment were used for the efficient identification of false positives produced as a result of stress response to NMD inhibition. To demonstrate the improved efficiency of this approach, we analyzed colon cancer cell lines showing microstellite instability. Bi-allelic inactivating mutations were found in the FXR1, SEC1L1, NCOR1, BAT3, PHD14, ZNF294, C190ORF5 genes as well as genes coding for proteins with yet unknown functions.

Publication Title

Identifying candidate colon cancer tumor suppressor genes using inhibition of nonsense-mediated mRNA decay in colon cancer cells.

Alternate Accession IDs

E-GEOD-5486

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon E-ATMX-32
Transcription profiling of SALK_084897 or SAIL_303_D08 Arabidopsis plants grown under normal conditions or with moderate light and drough treatment applied
  • organism-icon Arabidopsis thaliana
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

4 week old Arabidopsis plants, of ecotype Columbia, SALK_084897 or SAIL_303_D08 were either grown under normal conditions or grown under normal conditions for before having a moderate light and drought treatment applied. Light and drought treatment was applied by withholding water for 5 days prior to transfer to 300 uE m-2 s-1 light conditions. Samples were collected after 3 days of treatment or for the same age plants grown under normal conditions.

Publication Title

The absence of ALTERNATIVE OXIDASE1a in Arabidopsis results in acute sensitivity to combined light and drought stress.

Alternate Accession IDs

None

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE44599
ZNF365 promotes stability of fragile sites and telomeres
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Critically short telomeres activate cellular senescence or apoptosis, as mediated by the tumor suppressor p53, but in the absence of this checkpoint response, telomere dysfunction engenders chromosomal aberrations and cancer. Here, analysis of p53-regulated genes activated in the setting of telomere dysfunction identified Zfp365 (ZNF365 in humans) as a direct p53 target that promotes genome stability. Germline polymorphisms in the ZNF365 locus are associated with increased cancer risk, including those associated with telomere dysfunction. On the mechanistic level, ZNF365 suppresses expression of a subset of common fragile sites (CFS) including telomeres. In the absence of ZNF365, defective telomeres engage in aberrant recombination of telomere ends, leading to increased telomere sister chromatid exchange (T-SCE) and formation of anaphase DNA bridges, including ultra-fine DNA bridges (UFB), and ultimately increased cytokinesis failure and aneuploidy. Thus, the p53-ZNF365 axis contributes to genomic stability in the setting of telomere dysfunction.

Publication Title

ZNF365 promotes stability of fragile sites and telomeres.

Alternate Accession IDs

E-GEOD-44599

Sample Metadata Fields

Disease, Cell line, Treatment, Time

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accession-icon GSE36011
Cyclin-dependent protein kinase E;1 (CDKE;1) is an essential component for mitochondrial retrograde signalling in Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Stresses that target mitochondrial function lead to altered transcriptional responses for 100-1000s of genes genome wide, and are signalled via retrograde signalling pathways within the cell. rao1 mutants contain a mutation in a gene encoding a Cyclin-Dependant Kinase E;1 and cannot induce stress responsive genes (such as the mitochondrial alternative oxidase 1a) in response to mitochondrial dysfunction. We sought to define the global gene network regulated through RAO1 function in response to mitochondrial stress (mimicked through treatment of plants with antimycin A - a specific inhibitor of complex III in the mitochondrial electron transfer chain). We have defined global stress responses that are positively and negatively mediated by RAO1 function, as well as global stress responses to antimycin A treatment that are regulated independently of RAO1.

Publication Title

Cyclin-dependent kinase E1 (CDKE1) provides a cellular switch in plants between growth and stress responses.

Alternate Accession IDs

E-GEOD-36011

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon SRP153923
Chromatin-associated factors Dppa2 and Dppa4 guide epigenetic remodeling during reprogramming to pluripotency (RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

As somatic cells are converted to iPSCs, their chromatin undergoes wide-ranging rearrangements that affect the ratio of euchromatin-to-heterochromatin, DNA methylation patterns and the regulation of enhancers and promoters. The molecular machinery underlying this process remains largely unknown. Here, we show that Dppa2 and Dppa4, two thus far poorly characterized mES-specific factors, play a key role in resetting the epigenome to a pluripotent configuration. They function as a heterodimer, are induced in late reprogramming intermediates, and are required for reprogramming. When overexpressed with OSKM factors, Dppa2/4 yield reprogramming efficiencies exceeding 75% of the starting culture and accelerate reprogramming kinetics, generating iPSCs in as little as 4 days. When chromatinbound, Dppa2/4 initiate global chromatin decompaction via the DNA damage response pathway, which subsequently activates mES promoters and enhancers and enables an efficient progression to pluripotency. Our work provides critical insights into how the epigenome is remodeled during cell fate transitions. Overall design: Transcriptional regulation by the Dppa2 and Dppa4 investigated by ChIP-Seq and RNA-Seq

Publication Title

Dppa2/4 Facilitate Epigenetic Remodeling during Reprogramming to Pluripotency.

Alternate Accession IDs

GSE117172

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE57140
Expression data of Col:LUC Arabidopsis treated with antimycin A (AA) in the presence or absence of a synthetic auxin analogue
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Mitochondrial stress stimuli such as AA caused a transient suppression of auxin signaling and conversely, auxin treatment represses a part of the response to AA treatment.

Publication Title

A Functional Antagonistic Relationship between Auxin and Mitochondrial Retrograde Signaling Regulates Alternative Oxidase1a Expression in Arabidopsis.

Alternate Accession IDs

E-GEOD-57140

Sample Metadata Fields

Treatment

View Samples
accession-icon SRP134092
Snapshot of translation in mammalian cells that are depleted of polyamines or replete with polyamines
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Snapshot of translation in mammalian cells that are depleted of polyamines or replete with polyamines. Hek293T cells treated with DFMO or Spermidine. Overall design: DFMO vs. Spermidine treatment

Publication Title

Polyamine Control of Translation Elongation Regulates Start Site Selection on Antizyme Inhibitor mRNA via Ribosome Queuing.

Alternate Accession IDs

GSE111517

Sample Metadata Fields

Disease, Treatment, Subject

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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