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GSE52227
Gallus gallus
12 Downloadable Samples
Affymetrix Chicken Genome Array (chicken)
Description
The patterning of the facial midline involves early specification of neural crest cells to form skeletal tissues that support the upper jaw . In order to understand the molecular mechanisms involved we have taken advantage of a beak duplication model developed in the chicken embryo. Here we can induce the transformation of the side of the beak into a second midline that is easily identifiable by the formation of a supernumerary egg tooth. The phenotype is induced by implanting two microscopic beads, one soaked in retinoic acid and the other soaked in Noggin into the side of the head of the chicken embryo. Here we use microarrays to profile expression of maxillary mesenchyme 16h after placing the beads. A subset of genes were validated using in situ hybridization and QPCR. The aims of the study are to test the function of these genes using retroviral transgenesis, knockdown with morpholinos or expression of secreted proteins and their application to the embryo.
Publication Title
Identification and functional analysis of novel facial patterning genes in the duplicated beak chicken embryo.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Innate and adaptive immune cells modulate heart failure pathogenesis during viral myocarditis, yet their identity and functions remain poorly defined. In this study we characterized the phenotype, life-cycle and function of different conventional dendritic cells (cDC) populations in the heart, with focus on the 2 major subsets (CD103+ and CD11b+), which differentially rely on local proliferation and precursor recruitment to maintain tissue residency. Following viral infection of the myocardium, cDCs accumulate in the heart coincident with monocyte infiltration and loss of resident reparative embryonic-derived cardiac macrophages. cDC depletion abrogates antigen-specific CD8+ T cell proliferative expansion, transforming subclinical cardiac injury to overt heart failure. Importantly, these effects are mediated by BATF3-dependent CD103+ cDCs. Collectively, our findings definitively identify resident cardiac cDC subsets, define their origins, and implicate an essential role for CD103+ cDCs in antigen-specific T cell responses during viral myocarditis.
Publication Title
A CD103<sup>+</sup> Conventional Dendritic Cell Surveillance System Prevents Development of Overt Heart Failure during Subclinical Viral Myocarditis.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
We sought to obtain gene signature specific of high oxidative phsophorylation function.
Publication Title
Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
It has been hypothesized that chemotherapy resistant human acute myeloid leukemia (AML) cells are enriched in an immature phenotype, cellular quiescence and leukemic initiating cells (LICs). However, these hypotheses have never been validated completely in vivo. We have developed a physiologically relevant chemotherapeutic approach with cytosine arabinoside AraC using patient-derived xenograft (PDX) models. AraC-treated AML cells are not consistently enriched for either immature cells or quiescent cells. AraC treatment does not enrich for LICs as measured by limiting dilution in secondary transplantations. Rather chemotherapy resistant cells in vivo have high levels of reactive oxygen species (ROS) and a gene signature consistent with oxidative phosphorylation (OXPHOS). Treatment of human HIGH OXPHOS but not LOW OXPHOS AML cell lines showed chemotherapy resistance in vivo, showing that essential mitochondrial functions make significant contributions to AraC resistance in AML. Accordingly, targeting mitochondrial OXPHOS metabolism through the inhibition of mitochondrial protein synthesis, the electron transfer chain or fatty acid oxidation induced an energetic shift towards LOW OXPHOS and strongly enhanced anti-leukemic effects of AraC in AML cells. These results demonstrate that chemotherapy resistance in AML is not necessarily associated with stemness but is highly dependent on a distinct oxidative metabolism, and that the HIGH OXPHOS gene signature is a robust hallmark of the AraC response in PDX and a promising therapeutic avenue to treat AML residual disease.
Publication Title
Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
It has been hypothesized that chemotherapy resistant human acute myeloid leukemia (AML) cells are enriched in an immature phenotype, cellular quiescence and leukemic initiating cells (LICs). However, these hypotheses have never been validated completely in vivo. We have developed a physiologically relevant chemotherapeutic approach with cytosine arabinoside AraC using patient-derived xenograft (PDX) models. AraC-treated AML cells are not consistently enriched for either immature cells or quiescent cells. AraC treatment does not enrich for LICs as measured by limiting dilution in secondary transplantations. Rather chemotherapy resistant cells in vivo have high levels of reactive oxygen species (ROS) and a gene signature consistent with oxidative phosphorylation (OXPHOS). Treatment of human HIGH OXPHOS but not LOW OXPHOS AML cell lines showed chemotherapy resistance in vivo, showing that essential mitochondrial functions make significant contributions to AraC resistance in AML. Accordingly, targeting mitochondrial OXPHOS metabolism through the inhibition of mitochondrial protein synthesis, the electron transfer chain or fatty acid oxidation induced an energetic shift towards LOW OXPHOS and strongly enhanced anti-leukemic effects of AraC in AML cells. These results demonstrate that chemotherapy resistance in AML is not necessarily associated with stemness but is highly dependent on a distinct oxidative metabolism, and that the HIGH OXPHOS gene signature is a robust hallmark of the AraC response in PDX and a promising therapeutic avenue to treat AML residual disease.
Publication Title
Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism.
Sample Metadata Fields
Specimen part, Disease, Treatment, Subject
View Samples- Rattus norvegicus
- 8 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Polycystic ovarian syndrome (PCOS) is an endocrine disorder of the reproductive and metabolic axis in women during the reproductive age. In this study, we used a rat model exhibiting reproductive and metabolic abnormalities similar to human PCOS to unravel the molecular mechanisms underlining this complex syndrome.
Publication Title
Polycystic ovarian syndrome is accompanied by repression of gene signatures associated with biosynthesis and metabolism of steroids, cholesterol and lipids.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 24 Downloadable Samples
Illumina HiSeq 2500
Description
We used RNA-seq to monitor mRNA levels of all genes in response to hypoxia of wild-type yeast, S. cerevisiae (strain yMH914 with wildtype HAP1). To gain insights into how gene expression changes over time, cells were subjected to 100% nitrogen gas and collected after 0,5,10,30,60,120,180, and 240 minutes. Total RNA was extracted and mRNAs were enriched by polyA selection. The cDNA was prepared into a sequencing library, multiplexed and single-end sequenced by an Illumina HiSeq 2500 sequencer. After mapping with Tophat2, the number of reads per feature was calculated using HTSeq. Overall design: RNA-seq analysis of eight time points of a yeast strain grown in hypoxia. There are three biological replicates of the time course.
Publication Title
Time-Course Analysis of Gene Expression During the Saccharomyces cerevisiae Hypoxic Response.
Sample Metadata Fields
Subject
View Samples- Zea mays
- 16 Downloadable Samples
- Affymetrix Maize Genome Array (maize)
Description
Genome-wide transcriptome analysis was performed to understand the expression pattern of transcriptomes in tolerant and susceptible subtropical maize genotypes under waterlogging stress condition.
Publication Title
Genome-wide expression of transcriptomes and their co-expression pattern in subtropical maize (Zea mays L.) under waterlogging stress.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 4000
Description
We examined the patterns of gene expression of mouse thymic leukemias extracted from Mb1-CreDPB mice by RNA sequencing (RNA-seq). Our goal was to integrate RNA-seq data with whole-exome sequencing (WES) to determined secondary driver mutations of leukemogenesis in the absence of Spi-B and PU.1, Overall design: Thymic leukemias were isolated from diseased Mb1-CreDPB mice. In summary, thymuses were homogenized and red blood cells were removed with ACK buffer, washed with PBS and counted. The amount of 8 million cells were pelleted an RNA was extracted using Rneasy RNA Isolation Kit (Qiagen). RNA was quantified and the purity was checked by spectophotrometer. RNA was sent to subsequently sequencing procedures.
Publication Title
Driver mutations in Janus kinases in a mouse model of B-cell leukemia induced by deletion of PU.1 and Spi-B.
Sample Metadata Fields
Disease, Disease stage, Cell line, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
We were interesed in defining the gene signautre of volar skin.
Publication Title
To Control Site-Specific Skin Gene Expression, Autocrine Mimics Paracrine Canonical Wnt Signaling and Is Activated Ectopically in Skin Disease.
Sample Metadata Fields
No sample metadata fields
View Samples