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accession-icon GSE62821
EIF4E AND EIF4GI HAVE DISTINCT AND DIFFERENTIAL IMPRINTS ON MULTIPLE MYELOMA'S PROTEOME AND SIGNALING
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Accumulating data indicate translation plays a role in cancer biology, particularly its rate limiting stage of initiation. Despite this evolving recognition, the function and importance of specific translation initiation factors is unresolved. The eukaryotic translation initiation complex eIF4F consists of eIF4E and eIF4G at a 1:1 ratio. Although it is expected that they display interdependent functions, several publications suggest independent mechanisms. This study is the first to directly assess the relative contribution of eIF4F components to the expressed cellular proteome, transcription factors, microRNAs, and phenotype in a malignancy known for extensive protein synthesis- multiple myeloma (MM). Previously, we have shown that eIF4E/eIF4GI attenuation (siRNA/ Avastin) deleteriously affected MM cells' fate and reduced levels of eIF4E/eIF4GI established targets. Here, we demonstrated that eIF4E/eIF4GI indeed have individual influences on cell proteome. We used an objective, high throughput assay of mRNA microarrays to examine the significance of eIF4E/eIF4GI silencing to several cellular facets such as transcription factors, microRNAs and phenotype. We showed different imprints for eIF4E and eIF4GI in all assayed aspects. These results promote our understanding of the relative contribution and importance of eIF4E and eIF4GI to the malignant phenotype and shed light on their function in eIF4F translation initiation complex.

Publication Title

eIF4E and eIF4GI have distinct and differential imprints on multiple myeloma's proteome and signaling.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE21076
Arabidopsis thaliana/Hyaloperonospora arabidopsidis compatible interaction transcriptome
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

We used Arabidopsis full-genome microarrays to characterize plant transcript accumulations at different stages of infection with the biotrophic oomycete downy mildew pathogen, Hyaloperonospora arabidopsidis : initiation (< 1 dpi) and maintenance of infection (> 4 dpi).

Publication Title

An Arabidopsis (malectin-like) leucine-rich repeat receptor-like kinase contributes to downy mildew disease.

Sample Metadata Fields

Specimen part

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accession-icon SRP041507
Fine kinetic transcriptome analysis during jasmonate signaling
  • organism-icon Arabidopsis thaliana
  • sample-icon 72 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To study the role of the plant hormone jasmonate in regulating stress-induced allocation of photosynthetic products between growth- and defense-related processes, we used RNA-sequencing to query the Arabidopsis transcriptome at high temporal resolution over 24 h after treatment with the bacterial toxin coronatine (COR), a high-affinity agonist of the JA receptor, or with a mock solution to account for diurnal changes in gene expression. These data establish a fine-scale view of the kinetics of jasmonate signaling, as well as of the diurnal patterns of gene expression.

Publication Title

Temporal Dynamics of Growth and Photosynthesis Suppression in Response to Jasmonate Signaling.

Sample Metadata Fields

Age, Specimen part, Treatment, Time

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accession-icon SRP199768
Comparative transcriptomics between species attributes reactogenicity pathways induced by the capsular group B meningococcal vaccine, 4CMenB, to the membrane-bound endotoxin of its outer membrane vesicle component.
  • organism-icon Mus musculus
  • sample-icon 57 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Whole blood RNA-seq was leveraged to explore gene expression changes induced in mice 24 hours after immunisation with a second dose of a licensed vaccine against capsular group B meningococcus, one of the vaccines components, or one of several comparator groups. Overall design: mRNA was profiled from RNA extracted from mouse whole blood, 5-6 samples per group, using an Illumina HiSeq4000

Publication Title

Comparative transcriptomics between species attributes reactogenicity pathways induced by the capsular group B meningococcal vaccine, 4CMenB, to the membrane-bound endotoxin of its outer membrane vesicle component.

Sample Metadata Fields

Sex, Cell line, Subject

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accession-icon SRP108353
Endoplasmic reticulum–mitochondria junction is required for iron homeostasis
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

The Endoplasmic Reticulum–Mitochondria Encounter Structure (ERMES) is a protein complex that tethers the two organelles and creates the physical basis for communication between them. ERMES functions in lipid and calcium exchange between the ER and mitochondria, mitochondrial protein import and maintenance of mitochondrial morphology and genome. Here we report that ERMES is also required for iron homeostasis. Loss of ERMES components activates an Aft1-dependent iron deficiency response even in iron-replete conditions, leading to accumulation of excess iron inside the cell. This function is independent of ERMES known roles in calcium regulation, phospholipid biosynthesis or mitochondrial biology. A mutation in the vacuolar protein sorting 13 (VPS13) gene that rescues the glycolytic phenotype of ERMES mutants suppresses the iron deficiency response and iron accumulation. Our study reveals that proper communication between the ER and mitochondria is required for appropriate maintenance of cellular iron levels. Overall design: various mutants

Publication Title

Endoplasmic reticulum-mitochondria junction is required for iron homeostasis.

Sample Metadata Fields

Subject

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accession-icon SRP174994
Induction and Therapeutic Targeting of Human NPM1c+ Myeloid Leukemia in the Presence of Autologous Immune System in Mice
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: To understand the molecular mechanisms underlying NPM1c-mediated tumorigenesis by comparing the transcriptome of de novo generated bulk human leukemic cells and leukemic stem cells Overall design: Human hematopoietic stem/progenitor cells (HSPC) are transduced with lentiviruses expressing a mutated form of Nucleophosmin (NPM1c). Following engraftment into immunodeficient mice, transduced HSPCs give rise to human myeloid leukemia whereas untransduced HSPCs give rise to human immune cells in the same mice. The de novo AML, with CD123+ leukemic stem cells (LSC), resembles NPM1c+ AML from patients.

Publication Title

Induction and Therapeutic Targeting of Human NPM1c<sup>+</sup> Myeloid Leukemia in the Presence of Autologous Immune System in Mice.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE9487
Genome-wide expression profiling of cells infected with control or RPS14 shRNAs
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

We performed genome-wide expression profiling of cells infected with control or RPS14 shRNAs.

Publication Title

Identification of RPS14 as a 5q- syndrome gene by RNA interference screen.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE18737
Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE18669
Analysis of murine hematopoieitic stem cells, multipotent progenitors, PreMegE progenitors and mature CD4+ T cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

An investigation of the global gene expression signatures of murine hematopoietic stem cell differentiation during steady state hematopoiesis.

Publication Title

Epigenetic chromatin states uniquely define the developmental plasticity of murine hematopoietic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon E-TABM-450
Transcription profiling by array of human lung cancer cells after treatment with various inhibitors of LIMK1 and LIMK2
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

To investigate an unknown mechanism of cytotoxicity, A549 human lung-cancer cells were treated with compounds from a series of inhibitors developed against the human LIM kinases LIMK1 and LIMK2. Compounds 1 and 2 inhibit LIM kinase activity in vitro and affect cell proliferation and survival in vivo. Compounds 3 and 4 inhibit LIM kinases but do not affect cell survival or proliferation. Compounds 5 and 6 affect proliferation and survival but do not inhibit LIM kinases. Nocodazole was included as a comparator because the compounds were known to affect microtubule stability. A treatment of 7 hours was used to examine events prior to apoptosis, while the dose levels captured both cytotoxicity and inhibition of LIMKs (Compounds 1 and 2), LIMK inhibition alone ( Compounds 3 and 4) or cytotoxicity alone (Compounds 5, 6, and Nocodazole).

Publication Title

Identification of a nonkinase target mediating cytotoxicity of novel kinase inhibitors.

Sample Metadata Fields

Cell line, Subject, Compound

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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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