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SRP109649
Arabidopsis thaliana
40 Downloadable Samples
Illumina 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.
Sample Metadata Fields
Treatment, Subject
View Samples- Arabidopsis thaliana
- 56 Downloadable Samples
- Illumina 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.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 424 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Transcriptome analysis of post-mortem brain tissue specimens from three brain regions (BRs), entorinal, temporal and frontal cortices, of 71 Japanese brain-donor subjects to identify genes relevant to the expansion of neurofibrillary tangles. In total, 213 brain tissue specimens (= 71 subjects 3 BRs) were involved in this study. The spreading of neurofibrillary tangles (NFTs), intraneuronal aggregates of highly phosphorylated microtubule-associated protein tau, across the human brain is correlated with the cognitive severity of Alzheimers disease (AD). To identify genes relevant to NFT expansion defined by the Braak stage, we conducted exon array analysis with an exploratory sample set consisting of 213 human post-mortem brain tissue specimens from the entorinal, temporal and frontal cortices of 71 brain-donor subjects: Braak NFT stages 0 (N = 13), III (N = 20), IIIIV (N = 19) and VVI (N = 19). We identified eight genes, RELN, PTGS2, MYO5C, TRIL, DCHS2, GRB14, NPAS4 and PHYHD1, associated with the Braak stage. The expression levels of three genes, PHYHD1, MYO5C and GRB14, exhibited reproducible association on real-time quantitative PCR analysis. In another sample set, including control subjects (N = 30) and patients with late-onset AD (N = 37), dementia with Lewy bodies (N = 17) and Parkinson disease (N = 36), the expression levels of two genes, PHYHD1 and MYO5C, were obviously associated with late-onset AD. Proteinprotein interaction network analysis with a public database revealed that PHYHD1 interacts with MYO5C via POT1, and PHYHD1 directly interacts with amyloid beta-peptide 42. It is thus likely that functional failure of PHYHD1 and MYO5C could lead to AD development.
Publication Title
Genes associated with the progression of neurofibrillary tangles in Alzheimer's disease.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- 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.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- 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.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- 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.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- 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.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Mus musculus
- 100 Downloadable Samples
- Illumina 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.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 21 Downloadable Samples
- 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.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- IonTorrentProton
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.
Sample Metadata Fields
No sample metadata fields
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