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accession-icon GSE14319
Genetic Control of Cellular Quiescence in S. pombe
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Transition from proliferation to quiescence brings about extensive changes in cellular behavior and structure. However, genes critical for establishing and/or for maintaining quiescence are largely unknown. The fission yeast S. pombe is found as an excellent model for studying this problem, because it becomes quiescent under nitrogen starvation. Here we characterize 610 temperature-sensitive (ts) mutants, and identify 33 genes required for entry into and the maintenance of quiescence. These genes cover a broad range of cellular functions in the cytoplasm, membrane and the nucleus, encoding proteins for stress-responsive and cell cycle kinase signaling pathway, actin-bound and osmo-controlling endosome formation, RNA transcription, splicing and ribosome biogenesis, chromatin silencing, biosynthesis of lipid and ATP, cell wall and membrane morphogenesis, protein trafficking and vesicle fusion. We specifically highlight Fcp1, CTD phosphatase of RNA polymerase II, which differentially affects transcription of genes involved in quiescence and proliferation. We propose that the transcriptional role of Fcp1 is central to differentiate quiescence from proliferation.

Publication Title

Genetic control of cellular quiescence in S. pombe.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE139286
MicroRNA 1253 regulation of WAVE2 and its relevance to health disparities in hypertension
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The prevalence of hypertension among African Americans (AAs) in the US is among the highest of any demographic and affects over two-thirds of AA women. Previous data from our laboratory suggests substantial differential gene expression of mRNAs and microRNAs (miRNAs) in peripheral blood mononuclear cells (PBMCs) isolated from AA and white women with or without hypertension. We hypothesized that differential gene expression by race may contribute to racial differences in hypertension. We found that the Wiskott-Aldrich syndrome protein Verprolin homologous-2 (WAVE2) is differentially-expressed in AA women with hypertension, along with several other members of the actin cytoskeleton signaling pathway that plays a role in cell shape and branching of actin filaments. We performed an in silico miRNA target prediction analysis that suggested miRNA miR-1253 regulates WAVE2. Transfection of miR-1253 mimics into human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs) significantly repressed WAVE2 mRNA and protein levels (P<0.05), and a luciferase reporter assay confirmed that miR-1253 regulates the WAVE2 3’ UTR (P<0.01). miR-1253 over-expression in HUVECs significantly increased HUVEC lamellipodia formation (P<0.01), suggesting the miR-1253/WAVE2 interaction may play a role in endothelial cell shape and actin cytoskeleton function. Together, we have identified novel roles for miR-1253 and WAVE2 in a hypertension-related disparities context. This may ultimately lead to the discovery of additional actin-related genes which are important in the vascular-related complications of hypertension and influence the disproportionate susceptibility to hypertension among AAs in general and AA women in particular.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE75461
Pediatric AML classification according to C/EBP expression
  • organism-icon Homo sapiens
  • sample-icon 85 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

We examined if pediatric AMLs rank-ordered according to C/EBP expression showed the activation of similar pathways. AML samples were dichotomized into groups including the upper quartile (Q1) and the lower three quartiles (Q2-4) according to their C/EBP expression values. Moreover, AML samples were associated to French-American-British (FAB) classification.

Publication Title

CREB engages C/EBPδ to initiate leukemogenesis.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE74183
Clinical and biological characterization of children with FLT3-ITD-mutated acute myeloid leukemia
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

We examined if the minimal residual disease (MRD) and the Allelic Ratio (AR) of FLT3 internal tandem duplication (ITD) mutated patients may be prognostic factors. We correlated these parameters both with event free survival (EFS), with incidence of relapse and with gene expression profile (GEP). GEP showed that patients with high-ITD-AR or persistent MRD had different expression profiles. Results indicated that the ITD-AR levels and the MRD after I induction course are associated with transcriptional oncogenic profiles, which highlight differences in epigenetic control that may explain the variability in outcome among FLT3-ITD patients

Publication Title

Characterization of children with FLT3-ITD acute myeloid leukemia: a report from the AIEOP AML-2002 study group.

Sample Metadata Fields

Specimen part, Disease

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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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