refine.bio
  • Search
      • Normalized Compendia
      • RNA-seq Sample Compendia
  • Docs
  • About
  • My Dataset
github link
Showing
of 1568 results
Sort by

Filters

Technology

Platform

accession-icon GSE3350
SLR/IAA14-dependent auxin induced lateral root initiation
  • organism-icon Arabidopsis thaliana
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Lateral root initiation was used as a model system to study the mechanisms behind auxin-induced cell division. Genome-wide transcriptional changes were monitored during the early steps of lateral root initiation. Inclusion of the dominant auxin signaling mutant solitary root1 (slr1) identified genes involved in lateral root initiation that act downstream of the AUX/IAA signaling pathway. Interestingly, key components of the cell cycle machinery were strongly defective in slr1, suggesting a direct link between AUX/IAA signaling and core cell cycle regulation. However, induction of the cell cycle in the mutant background by overexpression of the D-type cyclin (CYCD3;1) was able to trigger complete rounds of cell division in the pericycle that did not result in lateral root formation. Therefore, lateral root initiation can only take place when cell cycle activation is accompanied by cell fate respecification of pericycle cells. The microarray data also yielded evidence for the existence of both negative and positive feedback mechanisms that regulate auxin homeostasis and signal transduction in the pericycle, thereby fine-tuning the process of lateral root initiation.

Publication Title

Cell cycle progression in the pericycle is not sufficient for SOLITARY ROOT/IAA14-mediated lateral root initiation in Arabidopsis thaliana.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE104063
Aged gut microbiota contributes to systemical inflammaging after transfer to germ-free mice
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study gut microbiota from young or old conventional mice was transferred to young germ-free mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyers patches, and mesenteric lymph nodes from conventionalized germ-free mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here we show by transferring aged microbiota to young germ-free mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the germ-free mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young germ-free mice.

Publication Title

Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE85913
Gender and strain dependent differences in intestinal immunology correlate with differences in microbiota composition
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Sex and strain dependent differences in mucosal immunology and microbiota composition in mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE85911
Gender and strain dependent differences in intestinal immunology correlate with differences in microbiota composition (colon)
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

A dysbiosis in the intestinal microbiome plays a role in the pathogenesis of several immunological diseases. These diseases often show a gender bias, suggesting gender differences in immune responses and in the intestinal microbiome. We hypothesized that gender differences in immune responses are associated with gender differences in microbiota. We demonstrated mouse strain dependent gender differences in the intestinal microbiome. Interestingly, a cluster of colonic genes (related to humoral and cell-mediated immune responses) correlated oppositely with microbiota species abundant in B6 females and in BALB/c males. This suggests that with different genetic backgrounds, gender associated immune responses are differentially regulated by microbiota. The net result was the same, since both mouse strains showed similar gender induced differences in immune cell populations in the mesenteric lymph nodes. Therefore, host-microbe interactions might be more complicated than assumed, as bacterial-species adaptations might be highly dependent on the genetic make-up of the individual.

Publication Title

Sex and strain dependent differences in mucosal immunology and microbiota composition in mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE85912
Gender and strain dependent differences in intestinal immunology correlate with differences in microbiota composition (ileum)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

A dysbiosis in the intestinal microbiome plays a role in the pathogenesis of several immunological diseases. These diseases often show a gender bias, suggesting gender differences in immune responses and in the intestinal microbiome. We hypothesized that gender differences in immune responses are associated with gender differences in microbiota. We demonstrated mouse strain dependent gender differences in the intestinal microbiome. Interestingly, a cluster of colonic genes (related to humoral and cell-mediated immune responses) correlated oppositely with microbiota species abundant in B6 females and in BALB/c males. This suggests that with different genetic backgrounds, gender associated immune responses are differentially regulated by microbiota. The net result was the same, since both mouse strains showed similar gender induced differences in immune cell populations in the mesenteric lymph nodes. Therefore, host-microbe interactions might be more complicated than assumed, as bacterial-species adaptations might be highly dependent on the genetic make-up of the individual.

Publication Title

Sex and strain dependent differences in mucosal immunology and microbiota composition in mice.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE84495
Fibroblast growth factor 21 reflects liver fat accumulation and dysregulation of signalling pathways in the liver of C57BL/6J mice
  • organism-icon Mus musculus
  • sample-icon 78 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Fibroblast growth factor 21 (Fgf21) has emerged as a potential plasma marker to diagnose non-alcoholic fatty liver disease (NAFLD). To study the molecular processes underlying the association of plasma Fgf21 with NAFLD, we explored the liver transcriptome data of a mild NAFLD model of aging C57BL/6J mice at 12, 24, and 28 months of age. The plasma Fgf21 level significantly correlated with intrahepatic triglyceride content. At the molecular level, elevated plasma Fgf21 levels were associated with dysregulated metabolic and cancer-related pathways. The up-regulated Fgf21 levels in NAFLD were implied to be a protective response against the NAFLD-induced adverse effects, e.g. lipotoxicity, oxidative stress and endoplasmic reticulum stress. An in vivo PPARalpha challenge demonstrated the dysregulation of PPARalpha signalling in the presence of NAFLD, which resulted in a stochastically increasing hepatic expression of Fgf21. Notably, elevated plasma Fgf21 was associated with declining expression of Klb, Fgf21s crucial co-receptor, which suggests a resistance to Fgf21. Therefore, although liver fat accumulation is a benign stage of NAFLD, the elevated plasma Fgf21 likely indicated vulnerability to metabolic stressors that may contribute towards progression to end-stage NAFLD. In conclusion, plasma levels of Fgf21 reflect liver fat accumulation and dysregulation of metabolic pathways in the liver.

Publication Title

Fibroblast growth factor 21 reflects liver fat accumulation and dysregulation of signalling pathways in the liver of C57BL/6J mice.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE70169
The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways
  • organism-icon Homo sapiens, Saccharomyces cerevisiae
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE59426
Expression data from Arabidopsis wild type and ibr1 ibr3 ibr10 triple mutant seedlings root tip segments treated with indole-3-butyric acid (IBA)
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The root cap-specific conversion of the auxin precursor indole-3-butyric acid (IBA) into the main auxin indole-3-acetic acid (IAA) generates a local auxin source which subsequently modulates both the periodicity and intensity of auxin response oscillations in the root tip of Arabidopsis, and consequently fine-tunes the spatiotemporal patterning of lateral roots. To explore downstream components of this signaling process, we investigated the early transcriptional regulations happening in the root tip during IBA-to-IAA conversion in Col-0 and ibr1 ibr3 ibr10 triple mutant after 6 hours of IBA treatment.

Publication Title

Root Cap-Derived Auxin Pre-patterns the Longitudinal Axis of the Arabidopsis Root.

Sample Metadata Fields

Age, Specimen part, Treatment

View Samples
accession-icon SRP068739
Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconNextSeq 500, Illumina HiSeq 2500

Description

In this study we studied the presence of tumor cells that underwent epithelial-to-mesenchymal transition within polyoma middle T antigen (PyMT) breast tumors. For this we dissociated tumors and isolated Ecad positive tumor cells by FACS sorting. We confirmed that PyMT tumors contain a small set of tumor cells that have undergone EMT in the primary tumor and that E-cadherin can be used as a marker on single cell level for mesenchymal status in this model. Overall design: (i) We isolated primary tumors from mice, dissociated the tumors and FACS-sorted for single Ecad positive tumor cells, after this we performed single cell sequencing of the cells. (ii) We isolated CTCs and solid tumor cells from mice, dissociated the tumors and FACS-sorted for single Ecad positive and negative cells, after this we performed single cell sequencing of the cells.

Publication Title

Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE76003
Effects of Gut Microbiota Manipulation by Antibiotics on Host Metabolism in Obese Humans: a Randomized Double-blind Placebo-controlled Trial
  • organism-icon Homo sapiens
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

The gut microbiota has been implicated in obesity and cardiometabolic diseases, although evidence in humans is scarce. We investigated how gut microbiota manipulation by antibiotics (7-day administration of amoxicillin, vancomycin, or placebo) affects host metabolism in 57 obese, prediabetic men. Vancomycin, but not amoxicillin, decreased bacterial diversity and reduced Firmicutes involved in short-chain fatty acid and bile acid metabolism, concomitant with altered plasma and/or fecal metabolite concentrations. Adipose tissue gene expression of oxidative pathways was upregulated by antibiotics, whereas immune-related pathways were downregulated by vancomycin. Antibiotics did not affect tissue-specific insulin sensitivity, energy/substrate metabolism, postprandial hormones and metabolites, systemic inflammation, gut permeability, and adipocyte size. Importantly, energy harvest, adipocyte size, and whole-body insulin sensitivity were not altered at 8-week follow-up, despite a still considerably altered microbial composition, indicating that interference with adult microbiota by 7-day antibiotic treatment has no clinically relevant impact on metabolic health in obese humans.

Publication Title

Effects of Gut Microbiota Manipulation by Antibiotics on Host Metabolism in Obese Humans: A Randomized Double-Blind Placebo-Controlled Trial.

Sample Metadata Fields

Sex, Specimen part, Disease, Disease stage, Treatment, Subject, Time

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

Powered by Alex's Lemonade Stand Foundation

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.

BSD 3-Clause LicensePrivacyTerms of UseContact