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accession-icon GSE99869
Loss of arginine methylation in Saccharomyces cerevisiae leads to the dysregulation of phosphate-associated genes and processes
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Hmt1p is the predominant arginine methyltransferase in Saccharomyces cerevisiae. Its substrate proteins are involved in transcription, transcriptional regulation, nucleocytoplasmic transport and RNA splicing. Functionally, Hmt1p-catalysed methylation can also modulate protein-protein interactions. Despite Hmt1p being well-characterised, the effects of its knockout on the proteome and transcriptome have not been reported. SILAC-based analyses of the hmt1 proteome, in mid-log exponential growth, revealed a decreased abundance of phosphate-associated proteins including Pho84p (phosphate transporter), Pho8p (vacuolar alkaline phosphatase), Pho3p (acid phosphatase) along with Vtc1p, Vtc3p and Vtc4p (subunits of the vacuolar transporter chaperone complex). RNA-Seq and microarray analysis revealed a downregulation of phosphate-responsive genes in hmt1, including PHO5, PHO11 and PHO12 (acid phosphatases), PHO84 and PHO89 (phosphate transporters) and VTC3 (vacuolar transporter chaperone). Consistent with these observations, we observed a dysregulation of phosphate homeostasis in hmt1, with a general decrease in extracellular phosphatase production and a decrease in total Pi in phosphate replete medium. We show that the transcription factor Pho4p, responsible for activation of the PHO pathway, can be methylated by Hmt1p at Arg-241 and is the likely cause of phosphate dysregulation in hmt1. However, the methylation of Pho4p does not affect its nucleocytoplasmic localisation. We propose that the methylation of Pho4p may affect either its capacity to multimerise, its capacity to interact with Pho2p or target DNA, or may affect Pho4p phosphorylation at Ser-242 and/or Ser 243. Our study highlights a previously unknown function of Hmt1p in the regulation of phosphate homeostasis and suggests a means by which sensing of AdoMet may affect intracellular phosphate concentration.

Publication Title

Knockout of the Hmt1p Arginine Methyltransferase in <i>Saccharomyces cerevisiae</i> Leads to the Dysregulation of Phosphate-associated Genes and Processes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE19615
Integrated genomic and function characterization of the 8q22 gain
  • organism-icon Homo sapiens
  • sample-icon 113 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Integrated DNA and expression array analysis in primary human breast tumors identified chromosome 8q22 copy number gain and a suite of over-expressed genes in this region highly relevant to subsequent recurrence.

Publication Title

Amplification of LAPTM4B and YWHAZ contributes to chemotherapy resistance and recurrence of breast cancer.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE16391
GGI: a potential predictor of relapse for endocrine-treated breast cancer patients in the BIG 1-98 trial
  • organism-icon Homo sapiens
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: We have previously shown that the Gene expression Grade Index (GGI) was able to identify two subtypes of estrogen receptor (ER)-positive tumors that were associated with statistically distinct clinical outcomes in both untreated and tamoxifen-treated patients. Here, we aim to investigate the ability of the GGI to predict relapses in postmenopausal women who were treated with tamoxifen (T) or letrozole (L) within the BIG 1-98 trial.

Publication Title

The Gene expression Grade Index: a potential predictor of relapse for endocrine-treated breast cancer patients in the BIG 1-98 trial.

Sample Metadata Fields

Age, Specimen part, Disease stage, Treatment

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accession-icon GSE81068
Expression profile of Epstein Barr Virus infected mammary epithelial cells and Breast tumors
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Whether the human tumor virus, Epstein-Barr virus (EBV) promotes breast cancers remains controversial and a potential mechanism has remained elusive. Here we show EBV can infect primary mammary epithelial cells (MECs) that express the attachment receptor, CD21. EBV infection leads to the expansion of early MEC progenitor cells with a stem cell phenotype and enforces a differentiation block. When MECs were implanted as xenografts, EBV infection cooperated with activated Ras and accelerated the formation of breast cancer. Infection in EBV-related tumors was of a latency type II pattern, including expression of latent membrane proteins 1 (LMP1) and 2 (LMP2), similar to nasopharyngeal carcinoma (NPC). A human gene expression signature for EBVness was generated based on the RNA expression profile of the EBV infected primary mammary epithelial cells, tumors. This was signature associated with high grade (40 vs 13.5%) estrogen-receptor-negative status (31.8 vs. 10.5%, p53 mutation (37.5 vs 14.5%) and poor survival. In 11/33 (33%) of tumors positive for EBVness EBV-DNA was found in tumor cells by fluorescent in situ hybridization for the viral LMP1 and BXLF2 genes, while only 4/36 (11%) of EBVness-negative tumors tested positive for EBV DNA. An analysis of the TCGA breast cancer data revealed a correlation of EBVness with presence of the APOBEC mutational signatures consistent with past viral infection. We conclude that a contribution of EBV to breast cancer etiology via a hit-and-run mechanism is plausible, in which EBV infection predisposes mammary epithelial cells to malignant transformation, but is not required for the maintenance of the malignant phenotype.

Publication Title

Epstein-Barr Virus Infection of Mammary Epithelial Cells Promotes Malignant Transformation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE80809
Expression data from lung CD11b+ conventional dendritic cells in the steady-state and following exposure to house dust mite allergens
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Using mouse lung resident conventional CD11b+ dendritic cells (CD11b+ cDCs) in the context of house-dust mite (HDM)-driven allergic airway sensitization as a model, we aimed here to identify transcriptional events regulating the pro-Th2 activity of cDCs.

Publication Title

Interferon response factor-3 promotes the pro-Th2 activity of mouse lung CD11b<sup>+</sup> conventional dendritic cells in response to house dust mite allergens.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE53031
Gene expression profiling of human breast cancer during pregnancy
  • organism-icon Homo sapiens
  • sample-icon 167 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Using a dataset of 54 pregnant and 113 age/stage-matched non-pregnant breast cancer patients with complete clinical and survival data; we evaluated the pattern of hot spot somatic mutations and performed transcriptomic profiling using Sequenom and Affymetrix, respectively. Breast cancer molecular subtypes were defined using PAM50 and 3-Gene classifiers. We performed Gene set enrichment analysis (GSEA) to evaluate pathways associated with diagnosis during pregnancy. We investigated the differential expression of cancer-related genes and published gene sets according to pregnancy. We finally investigated genes associated with disease-free survival.

Publication Title

Biology of breast cancer during pregnancy using genomic profiling.

Sample Metadata Fields

Age, Disease stage

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accession-icon GSE43710
Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia
  • organism-icon Mus musculus
  • sample-icon 62 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

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

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accession-icon GSE43708
Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC), from wild-type, IFNAR1-/-, IL28Ra-/- and IFNAR1-/- IL28Ra-/- double ko
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection

Publication Title

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

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accession-icon GSE43709
Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC), from both wild-type and MAVS-/- mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection

Publication Title

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE43707
Expression data from Influenza A infected mouse primary tracheal epithelial cell cultures (MTEC)
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays to detail the global programme of gene expression in response to Influenza A (PR8) infection

Publication Title

Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia.

Sample Metadata Fields

Specimen part

View Samples
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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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