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accession-icon GSE32445
Identical gene regulation patterns of triiodothyronine (T3) and selective thyroid hormone receptor modulator GC-1
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identical gene regulation patterns of T3 and selective thyroid hormone receptor modulator GC-1.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

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accession-icon GSE32443
Identical gene regulation patterns of triiodothyronine (T3) and selective thyroid hormone receptor modulator GC-1 [Affymetrix]
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Synthetic selective thyroid hormone (TH) receptor (TR) modulators (STRMs) exhibit beneficial effects on dyslipidemias in animals and humans and reduce obesity, fatty liver and insulin resistance in preclinical animal models. STRMs differ from native THs in preferential binding to the TR subtype versus TR, increased uptake into liver and reduced uptake into other tissues. However, selective modulators of other nuclear receptors (NRs) exhibit important gene-selective actions which have been attributed to differential effects on receptor conformation and dynamics and these effects can have profound influences in animals and humans. While there are suggestions that STRMs could exhibit such gene-specific actions, the extent to which these effects are actually observed in vivo has not been explored. Here, we show that saturating concentrations of the main active form of TH, triiodothyronine (T3), and the prototype STRM GC-1 induce identical gene-sets in livers of euthyroid and hypothyroid mice and a human cultured hepatoma cell line that only expresses TR, HepG2. We find one case in which GC-1 exhibits a modest gene-specific reduction in potency versus T3, at angiopoietin-like factor 4 (ANGPTL4) in HepG2. Investigation of the latter effect confirms that GC-1 acts through TR to directly induce this gene. However, this gene-selective GC-1 activity is not related to unusual T3 response element (TRE) sequence, unlike previously documented promoter-selective STRM actions. Together, our data suggest that T3 and GC-1 exhibit almost identical gene regulation properties and that gene-selective actions of GC-1 and similar STRMs will be subtle and rare.

Publication Title

Identical gene regulation patterns of T3 and selective thyroid hormone receptor modulator GC-1.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE8868
Comparison of splenic and small intestine lamina propria macrophages
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The intestinal immune system must elicit robust immunity against harmful pathogens but restrain immune responses directed against commensal microbes and dietary antigens. The mechanisms that maintain this dichotomy are poorly understood. Here we describe a population of CD11b+F4/80+CD11c macrophages in the lamina propria (LP) that express several anti-inflammatory molecules including interleukin 10 (IL-10), but little or no pro-inflammatory cytokines, even upon stimulation with Toll-like receptor (TLR) ligands. These macrophages induced, in a manner dependent on IL-10, retinoic acid and exogenous transforming growth factor-, differentiation of FoxP3+ regulatory T cells. In contrast, LP CD11b+ dendritic cells elicited IL-17 production. This IL-17 production was suppressed by LP macrophages, indicating that a dynamic interplay between these subsets may influence the balance between immune activation and tolerance.

Publication Title

Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17-producing T cell responses.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE9686
Human colon expression in healthy, CD, treated CD, and UC
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Activation of inflammatory pathways in human IBD

Publication Title

Activation of an IL-6:STAT3-dependent transcriptome in pediatric-onset inflammatory bowel disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE41588
Expression data for HT29 cells treated with 5-aza-deoxy-cytidine
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Parallel comparison of Illumina RNA-Seq and Affymetrix microarray platforms on transcriptomic profiles generated from 5-aza-deoxy-cytidine treated HT-29 colon cancer cells and simulated datasets.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE61140
Expression data from mouse arthritis tarsal joints
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Pathological bone changes differ considerably between inflammatory arthritic diseases, and most studies have focused on bone erosion. Collagen Induced Arthritis (CIA) is a model for Rheumatoid Arthritis, which, in addition to bone erosion, demonstrates bone formation at the time for clinical manifestations. The objective of this study was to use the CIA model to study bone remodelling by performing a gene expression profiling time-course study on the CIA model.

Publication Title

Kinetics of gene expression and bone remodelling in the clinical phase of collagen-induced arthritis.

Sample Metadata Fields

Specimen part

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accession-icon GSE41364
Expression data for HT29 cells treated with 5-aza-deoxy-cytidine [Affymetrix]
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The RNA samples from HT-29 (ATCC) colon cancer cell line were reverse transcribed into cDNAs and categorized in 3 groups with different concentrations of 5-aza-deoxy-cytidine (5-Aza); in each group three replicative 150 mm cultures were treated with: 1) dimethyl sulfoxide (vehicle alone, 0 M 5-Aza); 2) 5M 5-Aza and 3) 10 M 5-Aza; for five days

Publication Title

Parallel comparison of Illumina RNA-Seq and Affymetrix microarray platforms on transcriptomic profiles generated from 5-aza-deoxy-cytidine treated HT-29 colon cancer cells and simulated datasets.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE13739
Golovinomyces orontii time course with Col-0 and eds16-1
  • organism-icon Arabidopsis thaliana
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Salicylic acid (SA) is a critical molecule mediating plant innate immunity with an important role limiting the growth and reproduction of the virulent powdery mildew (PM) Golovinomyces orontii on Arabidopsis thaliana. To investigate this later phase of the PM interaction, and the role played by SA, we performed replicated global expression profiling for wild type and SA biosynthetic mutant ics1 Arabidopsis from 0 to 7 days post infection. We found that ICS1-impacted genes comprise 3.8% of profiled genes with known molecular markers of Arabidopsis defense ranked very highly by the multivariate empirical Bayes statistic (T2 statistic ((Tai and Speed, 2006)). Functional analyses of T2-selected genes identified statistically significant PM-impacted processes including photosynthesis, cell wall modification, and alkaloid metabolism that are ICS1-independent. ICS1-impacted processes include redox, vacuolar transport/secretion, and signaling. Our data also supports a role for ICS1 (SA) in iron and calcium homeostasis and identifies components of SA crosstalk with other phytohormones. Through our analysis, 39 novel PMimpacted transcriptional regulators were identified. Insertion mutants in one of these regulators, PUX2, results in significantly reduced reproduction of the powdery mildew in a cell death independent manner. Though little is known about PUX2, PUX1 acts as a negative regulator of Arabidopsis CDC48 (Rancour et al., 2004; Park et al., 2007), an essential AAA-ATPase chaperone that mediates diverse cellular activities including homotypic fusion of ER and Golgi membranes, ER-associated protein degradation, cell cycle progression, and apoptosis. Future work will elucidate the functional role of the novel regulator PUX2 in PM resistance.

Publication Title

Temporal global expression data reveal known and novel salicylate-impacted processes and regulators mediating powdery mildew growth and reproduction on Arabidopsis.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP041265
Study of Foxp3 expression in tumor-associated macrophages
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Using 5 differents approaches, including RNA sequencing, we demonstrated that macrophages that specifically infiltrate renal tumors, express the immunosuppressive transcription factor Foxp3. Overall design: Examination of the Foxp3 mRNA expression in 3 different cell subsets (including CD4 T cells (CD4), type-1 macrophages (M1) and type-2 macrophages (M2))

Publication Title

Foxp3 expression in macrophages associated with RENCA tumors in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP150218
Light releases the TCP4-SAUR16/50 transcription module from the repression of PIF3 to facilitate cotyledon opening during de-etiolation [RNA-seq]
  • organism-icon Arabidopsis thaliana
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Etiolated Arabidopsis seedlings open their cotyledons and halt rapid elongation of hypocotyl when exposed to light (de-etiolation). Major light responsive components in this process have been identified and signaling pathways revealed, yet how the organ-specific light responses are achieved remains unknown. Here we report that a developmental regulator TCP4 (TEOSINTE BRANCHED1, CYCLOIDEA, and PCF) participates in photomorphogenesis and facilitates light-induced cotyledon-opening. We demonstrate that TCP4-like transcriptional factors, which predominantly express in cotyledons of both light and dark seedlings, activate SAUR16 and SAUR50 in response to light. Light repressor PIF3 (or PIFs, phytochrome-interacting factors), which accumulates in etiolated seedlings and rapidly declines upon light exposure, inhibits TCP4 promoter-binding and prevents activation of SAUR16/50 in darkness. Our study reveals how an interplay between light responsive factors and developmental regulators leads to signal-dependent and tissue-specific regulation of gene expressions, which ultimately resulted in organ-specific light responses during de-etiolation. Overall design: Cotyledon mRNA profiles of 4-day-old dark grown Col, mTCP4#4 and mTCP4#10 seedlings were generated by deep sequencing.

Publication Title

The Transcription Factors TCP4 and PIF3 Antagonistically Regulate Organ-Specific Light Induction of <i>SAUR</i> Genes to Modulate Cotyledon Opening during De-Etiolation in Arabidopsis.

Sample Metadata Fields

Specimen part, Subject

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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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