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accession-icon SRP109649
Transcriptome profiling of mutants of CALMODULIN-LIKE (CML) family genes and CALMODULIN-BINDING PROTEIN 60 (CBP60) family genes in response to Pseudomonas syringae pv maculicola ES4326
  • organism-icon Arabidopsis thaliana
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We observed that mutations in CBP60a, CML46, CML47 and WRKY70 enhanced plant resistance to Pma likely through different mechanisms. To investigate their contributions to enhanced resistance at the transcriptome level, we designed this experiment to measure their response to Pma using the SMART-3Seq method. Overall design: Mature leaves of Arabidopsis plants of seven different genotypes were infiltrated with mock or Pma. Samples were collected 24 hours after treatment. Each experiment contains one sample consisted of two leaves for each genotype-treatment combination. In total three independent experiments were conducted.

Publication Title

WRKY70 prevents axenic activation of plant immunity by direct repression of SARD1.

Alternate Accession IDs

GSE100187

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE68443
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity
  • organism-icon Mus musculus
  • sample-icon 18 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

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.

Alternate Accession IDs

E-GEOD-68443

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE68429
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Analysis of brown adipose tissue from Yin Yang 1 (YY1) brown fat specific knockout mice fed a high fat diet for 3 months. YY1 deficiency in brown adipose tissue leads to strong thermogenic deficiency. The goal was to identify the genes controlled by YY1 responsible of brown fat defective function.

Publication Title

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.

Alternate Accession IDs

E-GEOD-68429

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE70562
Brown fat-specific YY1 deficiency effect on subcutaneous white adipose tissue
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Analysis of visceral white adipose tissue (EWAT) from Yin Yang 1 adipose-specific knockout mice exposed to cold (4C) for 4 days.

Publication Title

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.

Alternate Accession IDs

E-GEOD-70562

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE68382
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Analysis of subcutaneous adipose tissue (IWAT) from Yin Yang 1 brown fat specific knockout mice fed a high fat diet for 2 weeks. The goal was to identify a gene signature of IWAT browning in YY1 mutant mice.

Publication Title

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.

Alternate Accession IDs

E-GEOD-68382

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon SRP137014
Comparative Transcriptomics of STR/ort, C57BL/6 and MRL/MpJ Knee Joints
  • organism-icon Mus musculus
  • sample-icon 100 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Injuries to the anterior cruciate ligament (ACL) often result in post-traumatic osteoarthritis (PTOA). PTOA accounts for ~12% of all osteoarthritis (OA) cases, yet the mechanisms contributing to OA after joint injury are not well understood. To better understand the molecular mechanisms behind PTOA development following ACL injury, we profiled ACL injury-induced gene expression changes in knee joints of three mouse strains with varying susceptibility to PTOA: STR/ort (highly susceptible), C57BL/6 (moderately susceptible) and super-healer MRL/MpJ (not susceptible) and identified genes differentially expressed between these strains at 0-day [before injury], 1-day, 1-week, and 2-weeks post-injury. This study highlights many new potential therapeutic targets and OA biomarkers. Overall design: Comparative transcriptomics to understand the molecular changes associated with early stages of PTOA development in STR/ort, C57BL/6 and MRL/MpJ mice and to identify genes that contribute to increased OA susceptibility in STR/ort and resistance to PTOA in MRL/MpJ.

Publication Title

Comparative Transcriptomics Identifies Novel Genes and Pathways Involved in Post-Traumatic Osteoarthritis Development and Progression.

Alternate Accession IDs

GSE112641

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment, Subject

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accession-icon GSE87437
Gene expression data of primary Osteosarcomas
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Affymetrix gene expression data of 21 high-grade osteosarcomas located in the extremities.This gene expression profiling was performed in order to evaluate the expression of candidate prognostic and therapeutic targets in high-grade osteosarcoma.

Publication Title

Targeting CDKs with Roscovitine Increases Sensitivity to DNA Damaging Drugs of Human Osteosarcoma Cells.

Alternate Accession IDs

E-GEOD-87437

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP058490
A positive regulatory loop between a Wnt-regulated non-coding RNA and ASCL2 controls intestinal stem cell fate
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIonTorrentProton

Description

The canonical Wnt pathway plays a central role in stem cell maintenance, differentiation and proliferation in the intestinal epithelium. Constitutive, aberrant activity of the TCF4/ß-catenin transcriptional complex is the primary transforming factor in colorectal cancer. Despite significant recent inroads, the full complement of Wnt target genes and the mechanisms of regulation remain incompletely understood. Here we identify a nuclear long non-coding RNA, termed WiNTRLINC1, as a direct target of TCF4/ß-catenin in colorectal cancer cells. WiNTRLINC1 positively regulates the expression of its close neighbor ASCL2, a transcription factor that controls intestinal stem cell fate. WiNTRLINC1 interacts with TCF4/ß-catenin to mediate the juxtaposition/physical contact of its own promoter with the regulatory regions of ASCL2. ASCL2, in turn, regulates WiNTRLINC1 expression. This feedforward regulatory loop controls stem cell-related gene expression and is highly amplified in colorectal cancer. Overall design: Derivatives of Ls174T colon cancer cells, overexpressing the Tet repressor were used for the construction of inducible overexpressing a shRNA against the WiNTRLINC1 long non coding RNA upon treatment with doxyxycline. siRNAs against WiNTRLINC1 were designed with the siDesign center tool from Dharmacon and their sequences were used for the construction of the shRNA stem loop structure as described in EMBO Rep. 2003 Jun;4(6):609-15. The modified pTER vector was used as a backbone for constructing the shRNA cassette as described in EMBO Rep. 2003 Jun;4(6):609-15. Positive cell clones were screened with RT-PCR in order to validate the efficiency of the knockdown of WiNTRLINC1. The Ls174T derivative cell line inducibly overexpressing a shRNA against ASCL2 has been described previously in Cell. 2009 Mar 6;136(5):903-12. RNA deep sequencing was performed in the WiNTRLINC1 KD and ASCL2 KD cells compared to controls cells in order to detect changes in gene expression due to the loss of either WiNTRLINC1 or ASCL2.

Publication Title

A Positive Regulatory Loop between a Wnt-Regulated Non-coding RNA and ASCL2 Controls Intestinal Stem Cell Fate.

Alternate Accession IDs

GSE69036

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP104760
Interactions between effector-triggered immunity (ETI) and pattern-triggered immunity (PTI) in an Arabidopsis dde2 ein2 pad4 sid2 mutant
  • organism-icon Arabidopsis thaliana
  • sample-icon 56 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We observed inhibition of the hypersensitive response (a typical ETI response) by PTI signaling in an Arabidopsis quadruple mutant dde2 ein2 pad4 sid2 (quad). Thus, we designed an experiment to see the interaction between ETI and PTI signaling at the transcriptome level. The Arabidopsis line dde2 ein2 pad4 sid2 Ed-AvrRpt2 (quadAvrRpt2) was used (Ed-AvrRpt2, estradiol-inducible AvrRpt2 transgene). In this plant line, ETI can be elicited by estradiol (Ed) treatment via in planta expression of AvrRpt2. Transcriptome responses to PTI only, ETI only, and PTI+ETI together were recorded. Overall design: quadAvrRpt2 was treated with one of (1) Mock, (2) flg22 to elicit PTI response only, (3) Ed to elicit ETI response only via AvrRpt2, (4) flg22+Ed to elicit both PTI and ETI responses together. At 0 (untouched), 60, 120, 180, and 300 minutes after treatment, treated plant leaves were harvested for RNA-seq analysis. Three independent experiments were performed (rep1-rep3).

Publication Title

A plant effector-triggered immunity signaling sector is inhibited by pattern-triggered immunity.

Alternate Accession IDs

GSE98075

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE40041
Jnk1 in murine hepatic stellate cells is a crucial mediator of liver fibrogenesis
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Hepatic fibrosis is a wound-healing response to chronic liver injury, which may result in cirrhosis and liver failure. The c-Jun N-terminal kinase-1 (JNK1) gene has been shown to be involved in liver fibrosis. Here, we aimed to investigate the molecular mechanism and identify the cell-type involved in mediating the JNK1-dependent effect on liver fibrogenesis Wild-type (WT), JNK1/ and JNK1hepa (hepatocyte-specific deletion of JNK1) mice were subjected to bile duct ligation (BDL). Additionally, we performed bone marrow transplantations (BMT), isolated primary hepatic stellate cells (HSCs) and studied their activation in vitro. Serum markers of liver damage (liver transaminases, alkaline phosphatase and bilirubin) and liver histology revealed reduced injury in JNK1/ compared to WT and JNK1hepa mice. Hepatocyte cell death and proliferation was reduced in JNK1/ compared to WT and JNK1hepa. Parameters of liver fibrosis such as Sirius Red staining as well as Collagen IA1 and SMA expression were down-regulated in JNK1/ compared to WT and JNK1hepa livers, 4 weeks after BDL. To delineate the essential cell-type, we performed BMT of WT and JNK1-/- into JNK1-/- and WT mice, respectively. BMT experiments excluded bone marrow derived cells from having a major impact on the JNK1-dependent effect on fibrogenesis. Hence, we investigated primary HSCs from JNK1/ livers showing reduced transdifferentiation compared with WT and JNK1hepa-derived HSCs. We conclude that JNK1 in HSCs plays a crucial role in hepatic fibrogenesis and thus represents a promising target for cell-directed treatment options for liver fibrosis.

Publication Title

Jnk1 in murine hepatic stellate cells is a crucial mediator of liver fibrogenesis.

Alternate Accession IDs

E-GEOD-40041

Sample Metadata Fields

Sex, Age, Specimen part, Treatment, 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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