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accession-icon GSE11440
Role of Caveolin 1, E-Cadherin, Enolase 2 and PKCa on resistance to methotrexate in human HT29 colon cancer cells
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A summary of the work associated to these microarrays is the following:

Publication Title

Role of caveolin 1, E-cadherin, Enolase 2 and PKCalpha on resistance to methotrexate in human HT29 colon cancer cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE27525
Expression data from diet-induced obesity Oma1-deficient mice.
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Transriptional profiling of white adipose tissue extracted from obese mice.

Publication Title

Loss of mitochondrial protease OMA1 alters processing of the GTPase OPA1 and causes obesity and defective thermogenesis in mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP198959
Small extracellular vesicles are key regulators of non-cell autonomous intercellular communication in senescence via the interferon protein, IFITM3
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Senescence is a cellular phenotype present in health and disease, characterized by a stable cell cycle arrest and an inflammatory response, denominated senescence-associated secretory phenotype (SASP). The SASP is important in influencing the behaviour of neighbouring cells and altering the microenvironment; yet, this role has been mainly attributed to soluble factors. Here, we show that both the soluble factors in addition to small extracellular vesicles (sEV) are capable of transmitting paracrine senescence to nearby cells. Analysis of individual cells internalizing sEV, using a Cre-reporter system, show a positive correlation between sEV uptake and senescence activation. Interestingly, we find an increase in the number of multivesicular bodies during senescence in vivo. sEV protein characterization by mass spectrometry (MS) followed by a functional siRNA screen identify the Interferon Induced Transmembrane Protein 3 (IFITM3) as partially responsible for transmitting senescence to normal cells. Altogether, we found that sEV contribute to paracrine senescence. Overall design: SASP related mRNA transcripts in HFFF2 treated with sEV from iRAS cells in comparison with HFFF2 treated with sEV from iC cells

Publication Title

Small Extracellular Vesicles Are Key Regulators of Non-cell Autonomous Intercellular Communication in Senescence via the Interferon Protein IFITM3.

Sample Metadata Fields

Disease, Subject

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accession-icon SRP122966
Transcriptome of lung tissue from C57BL/6 mice with or without neutrophil depletion at ZT04 and ZT16
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Our study looks at the dirsruption of lung circadian transcriptome that occurs when neutrophils are depleted (by application of antibodies (anti-Ly6G-1A8) to wildtype C57BL/6 mice, or Diphtheria toxin (DT) to neutrophil-specific DT-susceptible mice (MRP8-Cre;iDTR-flox)). Overall design: Lungs were harvested from neutrophil-depleted (antibody or DT) or non-depleted mice, in normal light-controlled mouse facility (ZT4) or 12h inverted light cabinets (ZT16). Experiments were carried out over 3 batches (July 2017, September 2017, and April 2018), with 3 or 4 mice per group. Antibody-depleted and non-depleted mice were tested for the July 2017 and September 2017 batches, whereas DT-depleted mice were tested only in April 2018.

Publication Title

Neutrophils instruct homeostatic and pathological states in naive tissues.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE65415
Expression analysis of EDS1-NLS
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

TIR-type nucleotide-binding leucine-rich repeat domain proteins (TNLs) constitute one major group of immune receptors in dicotyledonous plants. Under normal conditions, TNLs can detect non-self or modified-self within the plant cytoplasm to activate immune signaling characterized by extensive transcriptional reprogramming and efficiently counteracting pathogen infection. At the same time, TNLs, in negative epistatic interaction with a second endogeneous locus or allele are causal for induction of autoimmunity or hybrid necrosis. Both native, pathogen-induced TNL responses and autoimmunity are fully dependent on the plant-specific lipase-like protein EDS1, which is a central integrator for all TNL-mediated responses. EDS1 signals within structurally similar, but spatially distinct complexes with PAD4 and SAG101. We here analyzed stable transgenic lines expressing an EDS1 fusion with enforced nuclear localization. Even in absence of SAG101, nuclear-localized EDS1-PAD4 complexes are fully sufficient to function in basal and effector-triggered immunity. Furthermore, we show that nuclear EDS1, when expressed to high levels, can induce autoimmuity in combination with an RPP1-like gene cluster from ecotype Ler. RPP1-like genes are also implicated in several cases of hybrid necrosis, and we can identify the RPP1 paralog R8 as causal for autoimmunity induction by nuclear EDS1 and a previously characterized, EMS-induced mutation. This highlights the important role of EDS1-family proteins in the nuclear compartment in different immune-like responses.

Publication Title

Arabidopsis thaliana DM2h (R8) within the Landsberg RPP1-like Resistance Locus Underlies Three Different Cases of EDS1-Conditioned Autoimmunity.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE28800
Gene expression data from ABA, [5-(3,4-Dichlorophenyl)Furan-2-yl]-Piperidin-1-ylMethanethione (DFPM), and ABA+DFPM treated Arabidopsis thaliana seedlings.
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Coordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptation and survival. Initial abiotic stress can interfere with disease resistance signaling. Conversely, initial plant immune signaling may interrupt subsequent ABA signal transduction. However, the processes involved in cross talk between these signaling networks have not been determined. By screening a 9,600 compound chemical library, we identified a small molecule [5-(3,4-Dichlorophenyl)Furan-2-yl]-Piperidin-1-ylMethanethione that rapidly down-regulates ABA-dependent gene expression and also inhibits ABA-induced stomatal closure. Transcriptome analyses show that DFPM also stimulates expression of plant defense-related genes. Plate grown 12-day-old seedlings were transferred into 6 well plates with 1:5000 (V/V) DMSO in water as a control, 30uM DFPM, and 10uM ABA in water as a treatment for 6 hours. DFPM was added 30 min prior to ABA treatment. RNA was extracted using Trizol (Invitrogen, Carlsbad, CA, USA) and further purified using RNeasy Plant RNA purification kit (QIAgen, Valencia, CA, USA). Three biological replicates of ATH1 oligonucleotide arrays were hybridized with labeled samples from 1) wild-type Columbia (WT) untreated, 2) WT with 30uM DFPM treatment, 3) WT with 10uM ABA treatment, 4) WT with 30uM DFPM and 10uM ABA treatment. Each biological replicate was prepared by combining 7 independently-treated samples.

Publication Title

Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway.

Sample Metadata Fields

Age

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accession-icon SRP056146
Pancreatic cancer exosomes induce pre-metastatic niche formation in the liver
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Pancreatic cancers (PCs) are highly metastatic with poor prognosis, mainly due to delayed detection. We hypothesized that intercellular communication is critical for metastatic progression. Here, we show that PC-derived exosomes induce liver pre-metastatic niche formation in naïve mice and consequently increase liver metastatic burden. Uptake of PC-derived exosomes by Kupffer cells caused transforming growth factor ß secretion and upregulation of fibronectin production by hepatic stellate cells. This fibrotic microenvironment enhanced recruitment of bone marrow-derived macrophages. We found that macrophage migration inhibitory factor (MIF) was highly expressed in PC-derived exosomes, and its blockade prevented liver pre-metastatic niche formation and metastasis. Compared to patients whose pancreatic tumors did not progress, MIF was markedly higher in exosomes from stage I PC patients who later developed liver metastasis. These findings suggest that exosomal MIF primes the liver for metastasis and may be a prognostic marker for the development of PC liver metastasis. Overall design: Normal pancreas and Pancreatic cancer exosomes education of human von Kupffer cells in vitro

Publication Title

Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE64920
Caspase-2-dependent tumor suppression does not depend on the scaffold protein Raidd
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The receptor-interacting protein-associated ICH-1/CED-3 homologous protein with a death domain (Raidd) functions as a dual adaptor protein due to its bipartite nature, and is therefore thought to be a constituent of different multiprotein complexes including the PIDDosome, where it connects the cell death-related protease, Caspase-2, with the p53-induced protein with a death domain 1 (Pidd1). As such, Raidd has been implicated in DNA-damage-induced apoptosis as well as in tumor suppression, the latter based on its role as a direct activator of Caspase-2, known to delay lymphomagenesis caused by overexpression of c-Myc or loss of ATM kinase. As loss of Caspase-2 leads to an acceleration of tumor onset in the E-Myc mouse model we set out to interrogate the role of Raidd in this process in more detail. Our data obtained analyzing E-Myc/Raidd-/- mice indicate that Raidd is unable to protect from c-MYC-driven lymphomagenesis. Similarly, we failed to observe an effect of Raidd-deficiency on thymic lymphomagenesis induced by y-irradiation or fibrosarcoma development driven by 3-methylcholanthrene. The role of Caspase-2 as a tumor suppressor can therefore be uncoupled from its ability to interact and auto-activate upon binding to Raidd. Further, we provide supportive evidence that the tumor suppressive role of Caspase-2 is related to maintaining genomic integrity and allowing efficient p53-mediated signaling. Overall, our findings suggest that Raidd, although described to be the key-adapter allowing activation of the tumor suppressor Caspase-2, fails to suppress tumorigenesis in vivo.

Publication Title

The tumor-modulatory effects of Caspase-2 and Pidd1 do not require the scaffold protein Raidd.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE68038
Comparison of cultured chondrocytes from knee and proximal interphalangeal joints
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Osteoarthritis (OA) of the hand is a common disease resulting in pain and impaired function. The pathogenesis of hand OA (HOA) is elusive and models to study it have not been described so far. Culture of chondrocytes is a model to study the development of cartilage degeneration, which is a hallmark of OA and well established in OA of the knee and hip. In the current study we investigated the feasibility human chondrocyte culture derived from proximal interphalangeal (PIP) finger joints of dissecting room cadavers. Index and middle fingers without signs of osteoarthritis were obtained from 30 cadavers using two different protocols. Hyaline cartilage from both articulating surfaces of the proximal interphalangeal (PIP) joint was harvested and digested in collagenase. Cultured chondrocytes were monitored for contamination, viability, and expression of chondrocyte specific genes. Chondrocytes derived from knee joints of the cadavers were cultured under identical conditions. Gene expression comparing chondrocytes from PIP and knee joints was carried out using Affymetrix GeneChip Human 2.0 ST arrays. The resulting differentially expressed genes were validated by real-time PCR and immunohistochemistry.Chondrocytes harvested up to 101 hours after death of the donors were viable. mRNA expression of collagen 2A1, aggrecan and Sox9 was significantly higher in chondrocytes as compared to cultured fibroblasts. Comparison of gene expression by chondrocytes from PIP and knee joints yielded 528 differentially expressed genes. Chondrocytes from the same joint region had a higher grade of similarity than chondrocytes of the same individual. These results were validated using real-time PCR and immunohistochemistry.We demonstrate for the first time a reliable method for culture of chondrocytes derived from PIP joints. PIP chondrocytes show a specific gene expression pattern and could be used as tool to study cartilage degeneration in HOA.

Publication Title

Chondrocyte cultures from human proximal interphalangeal finger joints.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE98265
Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis
  • organism-icon Homo sapiens
  • sample-icon 27 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

Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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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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