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accession-icon GSE96733
Ubc9 overexpression and SUMO1 deficiency blunt inflammation after intestinal ischemia/reperfusion.
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Clariom S Array (clariomsmouse)

Description

The intestinal epithelium constitutes a crucial defense to the potentially life-threatening effects of gut microbiota. However, due to a complex underlying vasculature, hypoperfusion and resultant tissue ischemia pose a particular risk to function and integrity of the epithelium. The small ubiquitin-like modifier (SUMO) conjugation pathway critically regulates adaptive responses to metabolic stress and is of particular significance in the gut, as inducible knockout of the SUMO-conjugating enzyme Ubc9 results in rapid intestinal epithelial disintegration. Here we analyzed the pattern of individual SUMO isoforms in intestinal epithelium and investigated their roles in intestinal ischemia/reperfusion (I/R) damage. Immunostaining revealed that epithelial SUMO2/3 expression was almost exclusively limited to crypt epithelial nuclei in unchallenged mice. However, intestinal I/R or overexpression of Ubc9 caused a remarkable enhancement of epithelial SUMO2/3 staining along the crypt-villus axis. Unexpectedly, a similar pattern was found in SUMO1 knockout mice. Ubc9 transgenic mice, but also SUMO1 knockout mice were protected from I/R injury as evidenced by better preserved barrier function and blunted inflammatory responses. PCR array analysis of microdissected villus-tip epithelia revealed a specific epithelial contribution to reduced inflammatory responses in Ubc9 transgenic mice, as key chemotactic signaling molecules such as IL17A were significantly downregulated. Together, our data indicate a critical role particularly of the SUMO2/3 isoforms in modulating responses to I/R and provide the first evidence that SUMO1 deletion activates a compensatory process that protects from ischemic damage.

Publication Title

Ubc9 overexpression and SUMO1 deficiency blunt inflammation after intestinal ischemia/reperfusion.

Alternate Accession IDs

E-GEOD-96733

Sample Metadata Fields

Treatment

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accession-icon SRP182100
A Myt1 family transcription factor defines neuronal fate by repressing non-neuronal genes
  • organism-icon Caenorhabditis elegans
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Cellular differentiation requires both activation of target cell programs and repression of non-target cell programs. Transcriptional repressors such as RE1-silencing transcription factor (REST) and Hairy/Enhancer of Split (Hes) repress neuronal genes in non-neuronal cells. However, it is unknown whether transcriptional repressors of non-neuronal genes in neuronal precursors are required to specify neuronal fate during development. The Myt1 family of zinc finger transcription factors contributes to fibroblast to neuron reprogramming in vitro by repressing Notch signaling. Here, we show that ztf-11 (Zinc-finger Transcription Factor-11), the sole Caenorhabditis elegans Myt1 homolog, is required for neurogenesis in multiple neuronal lineages, including an in vivo developmental epithelial-to-neuronal transdifferentiation event. ztf-11 is exclusively expressed in all neuronal precursors with remarkable specificity at single cell resolution. Loss of ztf-11 leads to upregulation of non-neuronal genes and reduced neurogenesis. Ectopic expression of ztf-11 in epidermal lineages is sufficient to produce additional neurons. Our genetic and genomic experiments show that ZTF-11 indeed functions as a transcriptional repressor to suppress the activation of non-neuronal genes in neurons; however, it does not function via repression of Notch signaling. Instead, ZTF-11 binds to the MuvBco-repressor complex, which we show is also required for neurogenesis. These results dovetail with ability of Myt1l (Myt1-like) to drive neuronal transdifferentiation in vitro in vertebrate systems. Together, we identified an evolutionarily conserved mechanism to specify neuronal cell fate by repressing non-neuronal genes. Overall design: 4 biological replicates each under 2 experemental conditions (ztf-11 KD and negative control) were used for total of 8 samples

Publication Title

A Myt1 family transcription factor defines neuronal fate by repressing non-neuronal genes.

Alternate Accession IDs

GSE125694

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon SRP114957
RNAseq of FACS-sorted C.elegans neurons from wildtype and thoc-5(wy822) mutant animals.
  • organism-icon Caenorhabditis elegans
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We sorted approx. 10000 neurons per sample from day one adult worms. We collected two wildtype samples and three thoc-5(wy822) mutant samples. Overall design: RNAseq of FACS-sorted C.elegans neurons from wildtype and thoc-5(wy822) mutant animals.

Publication Title

The THO Complex Coordinates Transcripts for Synapse Development and Dopamine Neuron Survival.

Alternate Accession IDs

GSE102300

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE64857
Gene expression data from patients with colorectal cancer
  • organism-icon Homo sapiens
  • sample-icon 81 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarray analyses for the identification of differences in gene expression patterns have increased our understanding of the molecular genetic events in colorectal cancer.

Publication Title

A molecular signature for the prediction of recurrence in colorectal cancer.

Alternate Accession IDs

E-GEOD-64857

Sample Metadata Fields

Sex

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accession-icon GSE19820
Expression data from rat pluripotent stem (PS) cells
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Various pluripotent stem (PS) cells can be isolated from early developing embryos in mouse. Among these, two kinds of PS cells were isolated from mouse blastocysts: conventional embryonic stem (ES) cells with domed morphology that are maintained with LIF and BMP for self-renewal, and FAB-ES cells with flat morphology that need bFGF, activinA and BIO for self-renewal. Here, we report a novel PS cell line from rat blastocysts, which is distinguishable from conventional ES cells but is morphologically similar to mouse epiblast stem cell (EpiSC) lines. We used microarrays to detail the global program of gene expression of rES and rPS.

Publication Title

The heterogeneity and dynamic equilibrium of rat embryonic stem cells.

Alternate Accession IDs

E-GEOD-19820

Sample Metadata Fields

Specimen part

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accession-icon GSE53735
Expression data for murine colon carcinoma cell line CT26.WT stimulated with S100a8 or S100a9 recombinant protein
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Damage-associated molecular pattern (DAMP) molecules S100A8 and S100A9 with well-known functions in inflammation, tumor growth and metastasis. It has been found to have promote tumor cell proliferation activity at low concentration . However, the mechanism underlying this remains unclear. In the current study, we performed genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with S100a8 or S100a9 recombinant protein stimulation in murine colon carcinoma cell line CT26.WT.

Publication Title

Inflammation-induced S100A8 activates Id3 and promotes colorectal tumorigenesis.

Alternate Accession IDs

E-GEOD-53735

Sample Metadata Fields

Cell line

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accession-icon GSE61989
Expression data from HUVEC with YAP siRNA knockdown
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

YAP knockdown in HUVEC elicits proliferation and cell cycle preogression defects. YAP deficient cells caused arrest in G1 and defects in S-phase entry. The microarray analysis was conducted to identify potential YAP targets that are involved in HUVEC cell cycle regulation

Publication Title

YAP regulates S-phase entry in endothelial cells.

Alternate Accession IDs

E-GEOD-61989

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE16923
Expression data from wild-type, Dgcr8 knockout and Dicer knockout ES cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dgcr8 and Dicer are both important components of the microRNA biogenesis pathway while Dicer is also implicated in biogenesis of other types of small RNAs such as siRNAs and mirtrons. Here we performed microarray analysis of WT, Dgcr8 and Dicer knockout ES cells to identify mRNAs differentially regulated upon loss of Dgcr8 and Dicer.

Publication Title

Genomic analysis suggests that mRNA destabilization by the microprocessor is specialized for the auto-regulation of Dgcr8.

Alternate Accession IDs

E-GEOD-16923

Sample Metadata Fields

Specimen part

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accession-icon SRP056038
Tex10 Coordinates Epigenetic Control of Super-Enhancer Activity for Pluripotency and Reprogramming [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Super-enhancers (SEs) are large clusters of transcriptional enhancers that are co-occupied by multiple lineage specific transcription factors driving expression of genes that define cell identity. In embryonic stem cells (ESCs), SEs are highly enriched for Oct4, Sox2, and Nanog in the enhanceosome assembly and express enhancer RNAs (eRNAs). We sought to dissect the molecular control mechanism of SE activity and eRNA transcription for pluripotency and reprogramming. Starting from a protein interaction network surrounding Sox2, a key pluripotency and reprogramming factor that guides the ESC-specific enhanceosome assembly and orchestrates the hierarchical transcriptional activation during the final stage of reprogramming, we discovered Tex10 as a novel pluripotency factor that is evolutionally conserved and functionally significant in ESC self-renewal, early embryo development, and reprogramming. Tex10 is enriched at SEs in a Sox2-dependent manner and coordinates histone acetylation and DNA demethylation of SEs. Our study sheds new light on epigenetic control of SE activity for cell fate determination. Overall design: RNA sequencing analysis was performed in mouse embryonic stem cells with Luciferase and Tex10 knockdown. RNA-seq Experiments were carry out in two biological replicates.

Publication Title

Tex10 Coordinates Epigenetic Control of Super-Enhancer Activity in Pluripotency and Reprogramming.

Alternate Accession IDs

GSE66734

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42255
Gene expression changes in response to aging compared to heat stress, oxidative stress and ionizing radiation in Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Gene expression changes in response to aging, hyperoxia, hydrogen peroxide, ionizing radiation, and heat stress were compared using microarrays. While aging shared features with each stress, aging was more similar to the stresses most associated with oxidative stress (hydrogen peroxide, hyperoxia, ionizing radiation) than to heat stress. Aging is associated with down-regulation of numerous mitochondrial genes, including electron-transport-chain (ETC) genes and mitochondrial metabolism genes, and a sub-set of these changes was also observed upon hydrogen peroxide stress and ionizing radiation stress. Aging shared the largest number of gene expression changes with hyperoxia. The extensive down-regulation of mitochondrial and ETC genes during aging is consistent with an aging-associated failure in mitochondrial maintenance, which may underlie the oxidative stress-like and proteotoxic stress-like responses observed during aging.

Publication Title

Gene expression changes in response to aging compared to heat stress, oxidative stress and ionizing radiation in Drosophila melanogaster.

Alternate Accession IDs

E-GEOD-42255

Sample Metadata Fields

Sex, Age

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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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