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accession-icon GSE49981
Reciprocal transcriptional responses in the interaction between Arabidopsis thaliana and Tetranychus urticae.
  • organism-icon Arabidopsis thaliana
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

While pathogen-induced immunity is comparatively well characterized, far less is known about plant defense responses to arthropod herbivores. To date, most molecular-genetic studies of plant-arthropod interactions have focused on insects. However, plant-feeding (phytophagous) mites are also pests of diverse plants, and mites induce different patterns of damage to plant tissues than do well-studied insects (e.g., Lepidopteran larvae or aphids). The two-spotted spider mite, Tetranychus urticae, is among the most significant mite pests in agriculture. T. urticae is an extreme generalist that has been documented on a staggering number of plant hosts (more than 1,100), and is renowned for the rapid evolution of pesticide resistance. To understand reciprocal interactions between T. urticae and a plant host at the molecular level, we examined mite herbivory using Arabidopsis thaliana. Despite differences in feeding guilds, we found that transcriptional responses of A. thaliana to mite herbivory generally resembled those observed for insect herbivores. In particular, defense to mites was mediated by jasmonic acid (JA) biosynthesis and signaling. Further, indole glucosinolates dramatically increased mite mortality and development times. Variation in both basal and activated levels of these defense pathways might also explain differences in mite damage and feeding success between A. thaliana accessions. On the herbivore side, a diverse set of genes associated with detoxification of xenobiotics was induced upon exposure to increasing levels of in planta indole glucosinolates. Our findings provide molecular insights into the nature of, and response to, herbivory for a representative of a major class of arthropod herbivores.

Publication Title

Reciprocal responses in the interaction between Arabidopsis and the cell-content-feeding chelicerate herbivore spider mite.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE77791
Prospective randomized doubleblind assessment of transcriptome modulation by hydrocortisone in severe burn shock
  • organism-icon Homo sapiens
  • sample-icon 114 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Rationale: Despite shortening vasopressor use in shock, hydrocortisone administration remains controversial, with potential harm on the immune system. Few studies assessed hydrocortisone impact on the transcriptional response in shock, and we are lacking data in burns. Objectives: To assess the hydrocortisone-induced transcriptional modulation in severe burn shock, particularly on the immune response. Methods: We collected whole blood samples (n= 117) during a randomized controlled trial assessing the efficacy of hydrocortisone administration on burn shock. Using whole genome microarrays, we first compared burn patients from the placebo group (n=15) to healthy volunteers (n=13) to describe the transcriptional modulation induced by burn shock over the first week. Then we compared burn patients randomized for either hydrocortisone administration (n=15) or placebo (n=15) to assess hydrocortisone-induced modulation. Measurements and Main Results: Study groups were similar in terms of severity and major outcomes, but shock duration (significantly reduced in the hydrocortisone group). Many genes (n=2250) were differentially expressed between burn patients and healthy volunteers, with 85% of them exhibiting a profound and persistent modulation over seven days. Interestingly, we showed that hydrocortisone enhanced the shock-associated repression of adaptive, but also innate immunity. Conclusions: We found that the initial host response to burn shock encompasses a wide and persistent modulation of gene expression, with profound modulation of pathways associated with metabolism and immunity. Importantly, hydrocortisone administration may worsen the immunosuppression associated with severe injury. These data should be taken into account in the risk ratio of hydrocortisone administration in patients with inflammatory shock.

Publication Title

Transcriptome modulation by hydrocortisone in severe burn shock: ancillary analysis of a prospective randomized trial.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Treatment, Subject

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accession-icon SRP132709
Whole blood transcriptome analysis of Septic shock patients according to early therapy response
  • organism-icon Homo sapiens
  • sample-icon 64 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx, Illumina HiSeq 2500

Description

Septic shock is the most severe complication of sepsis, associated with high mortality. The patient's response to supportive therapy is very heterogeneous and the underlying mechanisms are still elusive. In order to identify which are the actors (genes and pathways) that play a role in establishing the response, we investigate the whole blood transcriptome in septic shock patients with positive and negative responses to early supportive hemodynamic therapy, assessed by changes in SOFA scores within the first 48 hours from ICU admission. We pinpointed genes and pathways that are differently modulated and enriched respectively within 48hrs between responders and non-responders. Overall design: We analyzed 31 patients (17 Responders and 14 Not Responders to early therapy). For each patient, 2 samples were collected. In particular the first sample (T1) collected within 16 hours from ICU admission whereas the second (T2) collected within 48 hours from ICU admission. Experimental groups (Responders and Not Responders) are defined accordingly with SOFA scores improvements within 48 hours.

Publication Title

Identification of a transcriptome profile associated with improvement of organ function in septic shock patients after early supportive therapy.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE64457
Marked alterations of neutrophil functions during sepsis-induced immunosuppression
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Severe septic syndromes deeply impair innate and adaptive immunity. While neutrophils represent the first line of defense against infection, little is known about their phenotype and functions during sepsis-induced immunosuppression. The objective of this study was thus to perform for the first time a global evaluation of neutrophil alterations in immunosuppressed septic patients based on phenotypic, functional and transcriptomic studies. In addition, the potential association of these parameters and deleterious outcomes was assessed.

Publication Title

Marked alterations of neutrophil functions during sepsis-induced immunosuppression.

Sample Metadata Fields

Disease

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accession-icon GSE95233
Fractalkine receptor CX3CR1 and leukocyte Ig-like receptor B2 LILRB2 are prognostic biomarkers in septic shock
  • organism-icon Homo sapiens
  • sample-icon 120 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Sepsis is a major health concern, with high morbidity and mortality workdwide. In order to identify prognostic biomarkers in septic shock patients, we performed a microarray study exploring the early modulation of gene expression according to day 28 mortality.

Publication Title

Modulation of LILRB2 protein and mRNA expressions in septic shock patients and after ex vivo lipopolysaccharide stimulation.

Sample Metadata Fields

Sex, Age, Time

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accession-icon SRP185822
Robust hematopoietic specification requires the ubiquitous Sp1 and Sp3 transcription factors [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Development requires the cooperation of tissue-specific and ubiquitously expressed transcription factors, such as Sp-family members. However, the molecular details of how ubiquitous factors participate in developmental processes are still unclear. We previously showed that during the differentiation of embryonic stem cells lacking Sp1 DNA binding activity (Sp1deltaDBD/deltaDBD cells), early blood progenitors are formed. However, gene expression during differentiation becomes progressively deregulated and terminal differentiation is severely compromised. Here we studied the cooperation of Sp1 and its closest paralogue Sp3 in hematopoietic development and demonstrate that Sp1 and Sp3 binding sites largely overlap. Sp3 cooperates with Sp1deltaDBD/deltaDBD but is unable to support hematopoiesis in the complete absence of Sp1. Using single cell gene expression analysis, we show that the lack of Sp1 DNA binding leads to a distortion of cell fate decision timing, indicating that stable chromatin bi nding of Sp1 is required to maintain robust differentiation trajectories. Overall design: RNA-Seq in ESC, Flk, HE1, HE2 and progenitor cells with WT, Sp1deltaDBD or Sp3KO

Publication Title

Robust hematopoietic specification requires the ubiquitous Sp1 and Sp3 transcription factors.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP185853
Robust hematopoietic specification requires the ubiquitous Sp1 and Sp3 transcription factors
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Development requires the cooperation of tissue-specifically and ubiquitously expressed transcription factors, such as Sp-family members. However, the molecular details of how ubiquitous factors participate in developmental processes are still unclear. We previously showed that during the differentiation of embryonic stem cells lacking Sp1 DNA binding activity (Sp1DDBD/DDBD cells), early blood progenitors are formed. However, gene expression during differentiation becomes progressively deregulated and terminal differentiation is blocked. Here we studied the cooperation of Sp1 and its homologue Sp3 in hematopoietic development and demonstrate that Sp1 and Sp3 binding sites largely overlap. Sp3 cooperates with Sp1DDBD/DDBD cells but is unable to support hematopoiesis in the complete absence of Sp1. Using single cell gene expression analysis, we show that the lack of Sp1 DNA binding leads to a distortion of cell fate decision timing, indicating that stable chromatin binding of Sp1 is required to maintain robust differentiation trajectories. Overall design: Chromium 10X - Single-cell RNA-seq of Sp1 wild-type and Sp1 DNA binding domain mutant cells

Publication Title

Robust hematopoietic specification requires the ubiquitous Sp1 and Sp3 transcription factors.

Sample Metadata Fields

Specimen part, Subject

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accession-icon E-MEXP-1787
Transcription profiling by array of Arabidopsis ccr1 mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Regulation of carotenoid composition and shoot branching in Arabidopsis by a chromatin modifying histone methyltransferase, SDG8<br></br>Comparison of transcript profiles between wild type Columbia and ccr1 (carotenoid and chloroplast regulatory) mutant, which contains a mutation in At1g77300 (SDG8)

Publication Title

Regulation of carotenoid composition and shoot branching in Arabidopsis by a chromatin modifying histone methyltransferase, SDG8.

Sample Metadata Fields

Age

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accession-icon GSE42765
MLLT10 gene recombinations in pediatric T-Acute Lymphoblastic Leukemia
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

MLLT10, a 24 exons gene at 10p12, is known in leukemogenesis as partner of MLL or PICALM and recently NAP1L1. We identified HNRNPH1 and DDX3X, genes involved in RNA processing, as new MLLT10 partners in 2 cases of pediatric NOTCH1 positive T-ALL. HNRNPH1/5q35 encodes for a member of the ubiquitously expressed heterogeneous nuclear ribonucleoprotein (hnRNP) subfamily of RNA binding protein. DDX3X/Xp11.3, belongs to the big family of RNA helicases with a DEAD box domain.

Publication Title

New MLLT10 gene recombinations in pediatric T-acute lymphoblastic leukemia.

Sample Metadata Fields

Disease

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accession-icon GSE115971
Study of vascular endothelial-specific and inducible vascular endothelial-specific deletion of Major Facilitator Superfamily Domain containing 2a (Mfsd2a) in mice.
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Brain development requires a massive increase in brain lipogenesis and accretion of the essential omega-3 fatty acid docosahexaenoic acid (DHA). Brain acquisition of DHA is primarily mediated by the transporter Major Facilitator Superfamily Domain containing 2a (Mfsd2a) expressed in the endothelium of the blood-brain barrier. Mfsd2a transports DHA and other polyunsaturated fatty acids esterified to lysophosphatidylcholine (LPC-DHA). However, the function of Mfsd2a and DHA in brain development is incompletely understood. Using vascular endothelial-specific (2aECKO) and inducible vascular endothelial-specific (2aiECKO) deletion of Mfsd2a in mice, we found Mfsd2a to be uniquely required postnatally at the blood-brain barrier for normal brain growth and DHA accretion, with DHA deficiency preceding the onset of microcephaly. Gene expression profiling analysis of these DHA deficient brains indicated that Srebp-1 and Srebp-2 pathways were highly elevated.

Publication Title

The lysolipid transporter Mfsd2a regulates lipogenesis in the developing brain.

Sample Metadata Fields

Specimen part

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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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