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accession-icon SRP065396
PIWI slicing and EXD1 drive biogenesis of nuclear piRNAs from cytosolic targets of the mouse piRNA pathway
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

PIWI-interacting RNAs (piRNAs) guide PIWI proteins to suppress transposable elements in animal gonads. Here we demonstrate that in the mouse embryonic male germline, endonucleolytic cleavage (slicing) of a transcript by cytosolic MILI acts as a trigger to initiate its further 5??3? processing into non-overlapping fragments. These fragments accumulate as new piRNAs within the nuclear PIWI protein MIWI2. We identify Exonuclease domain-containing 1 (EXD1) as a partner of the established MIWI2 piRNA biogenesis factor TDRD12. Although EXD1 homodimers are inactive as a nuclease, it functions as an RNA adapter within a PET (PIWI-EXD1-Tdrd12) complex. Loss of Exd1 impacts biogenesis of MIWI2 piRNAs and displays a reduction in sequences generated by MILI slicing. This results in selective depletion of repeat piRNAs that target active retrotransposons like LINE1, which are de-repressed in the mutant. We propose that PIWI slicing and EXD1 promote coordination of nucleo-cytoplasmic silencing via piRNA biogenesis. Overall design: Immunoprecipitated or total small RNAs were purified and sequenced from P0 mouse testis of Exd1+/- and Exd1 -/- mice. Testes of three males were pooled together and MILI and MIWI2 immunoprecipitation was performed or total small RNAs were purified. Two replicas from different pools were prepared. For Rosa26-pi reporter mouse P0 testes of three males were pooled together and MILI and MIWI2 immunoprecipitation was performed.

Publication Title

PIWI Slicing and EXD1 Drive Biogenesis of Nuclear piRNAs from Cytosolic Targets of the Mouse piRNA Pathway.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE11184
Gamma-secretase inhibitors reverse glucocorticoid resistance in T-ALL
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Gamma-secretase inhibitors (GSIs), which block the activation of NOTCH receptors, are being tested in the treatment of T-cell acute lymphoblastic leukemia (T-ALL). Thus far, limited antileukemic cytotoxicity and severe gastrointestinal toxicity have restricted the clinical application of these targeted drugs. Here we show that combination therapy with GSIs plus glucocorticoids can improve the antileukemic effects of GSIs and reduce their gut toxicity in vivo. Inhibition of NOTCH1 signaling in glucocorticoid-resistant T-ALL restored glucocorticoid receptor auto-up-regulation and induced apoptotic cell death through induction of BIM expression. Additionally, cotreatment with glucocorticoids induced Ccnd2 upregulation in the gut which protected mice from the intestinal secretory metaplasia typically induced by loss of NOTCH signaling. These results support a role for glucocorticoids plus GSIs in the treatment of glucocorticoid-resistant T-ALL.

Publication Title

Gamma-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE7067
Synergistic interaction of gamma-secretase inhibitor therapy and glucocorticoids in T-ALL
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Glucocorticoids are an essential component of the treatment of lymphoid malignancies and resistance to glucocorticoid therapy constitutes a prominent clinical problem in relapsed and refractory lymphoblastic leukemias. Constitutively active NOTCH signaling is involved in the pathogenesis of over 50% of T-cell lymphoblastic leukemia (T-ALL) which harbor activating mutations in the NOTCH1 gene. Aberrant NOTCH1 signaling has been shown to protect normal thymocytes from glucocorticoid induced cell death. Here we analyzed the interaction of glucocorticoid therapy with inhibition of NOTCH signaling in the treatment of T-ALL. Gamma-secretase inhibitors (GSI), which block the activation of NOTCH receptors, amplified the transcriptional changes induced by glucocorticoid treatment, including glucocorticoid receptor autoinduction and restored sensitivity to dexamethasone in glucocorticoid-resistant T-ALL cells. Apoptosis induction upon inhibition of NOTCH signaling and activation of the glucocorticoid receptor was dependent on transcriptional upregulation of BIM and subsequent activation of the mitochondrial/intrinsic cell death pathway. Finally, we used a mouse xenograft model of T-ALL to demonstrate that combined treatment with dexamethasone and a GSI results in improved antileukemic effects in vivo. These studies provide insight in the mechanisms of glucocorticoid resistance and serve as rationale for the use of glucocorticoid and GSIs in combination in the treatment of T-ALL.

Publication Title

Gamma-secretase inhibitors reverse glucocorticoid resistance in T cell acute lymphoblastic leukemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE63259
Comparison of gene expression in aorta and CD115+ isolated circulating cells from apoE-/- versus apoE-/-LTbR-/- mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Affymetrix Microarrays were used to analyse gene expression in aortas and circulating CD115+ cells of ApoE- and ApoE/Lymphotoxin beta receptor (LTbR)-double-deficent mice fed a Western diet from 8 to 12 weeks of age in order to identify regulated genes and pathways leading to reduced atherosclerosis in ApoE-/-/LTbR-/- mice compared to ApoE-/- littermate controls.

Publication Title

Deficiency in lymphotoxin β receptor protects from atherosclerosis in apoE-deficient mice.

Sample Metadata Fields

Sex, Age

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accession-icon GSE26713
Integrated transcript and genome analyses reveal NKX2-1 and MEF2C as potential oncogenes in T-ALL
  • organism-icon Homo sapiens
  • sample-icon 116 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To identify novel oncogenic pathways in T-cell acute lymphoblastic leukemia (T-ALL), we combined expression profiling of 117 pediatric patient samples and detailed molecular cytogenetic analyses including the Chromosome Conformation Capture on Chip (4C) method. Two T-ALL subtypes were identified that lacked rearrangements of known oncogenes. One subtype associated with cortical arrest, expression of cell cycle genes and ectopic NKX2-1 or NKX2-2 expression for which rearrangements were identified. The second subtype associated with immature T-cell development and high expression of the MEF2C transcription factor as consequence of rearrangements of MEF2C, transcription factors that target MEF2C or MEF2C-associated cofactors. We propose NKX2-1, NKX2-2 and MEF2C as T-ALL oncogenes that are activated by various rearrangements.

Publication Title

Integrated transcript and genome analyses reveal NKX2-1 and MEF2C as potential oncogenes in T cell acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE8166
Transcriptome Profile of the Vascular Endothelial Cell Response to Candida albicans
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We perform microarray analysis of HUVECs upon stimulation with virulent wildtype C. albicans strain SC5314 or its efg1/efg1 cph1/cph1 hyphal-deficient derivative strain CAN34 to compare the gene expression profiles elicited from HUVECs in response to these strains. In addition, these responses are compared to that of TNF-alpha induced responses to determine which responses are Candida-specific.

Publication Title

Transcriptome profile of the vascular endothelial cell response to Candida albicans.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE18300
Hypoxia related splice variants in HNSCC
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

The identifcation of alternatively spliced transcript variants specific to particular biological processes in tumours should increase our understanding of cancer. Hypoxia is an important factor in cancer biology and associated splice variants may present new markers to help with planning treatment. A method was developed to analyse alternative splicing in exon array data, using probeset multiplicity to identify genes with changes in expression across their loci, and a combination of the splicing index and a new metric based on the variation of reliability weighted fold changes to detect changes in the splicing patterns. The approach was validated on a cancer/normal sample dataset in which alternative splicing events had been confirmed using RT-PCR. We then analysed ten head and neck squamous cell carcinomas using exon arrays and identified differentially expressed splice variants in five samples with high versus five with low levels of hypoxia-associated genes (Winter et al, 2007; Cancer Res 67:3441-9). The analysis identified a splice variant of LAMA3 (Laminin 3), LAMA3-A, known to be involved in tumour cell invasion and progression. The full-length transcript of the gene (LAMA3-B) did not appear to be hypoxia-associated. The results were confirmed using qualitative real time PCR. In a series of 59 prospectively-collected head and neck tumours (Winter et al, 2007; Cancer Res 67:3441-9), expression of LAMA3-A had prognostic significance whereas LAMA3-B did not. This work illustrates the potential for alternatively spliced transcripts to act as biomarkers of disease prognosis with improved specificity for particular tissues or conditions over assays which do not discriminate between splice variants.

Publication Title

Exon array analysis of head and neck cancers identifies a hypoxia related splice variant of LAMA3 associated with a poor prognosis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE92355
Effects of POTEF-AS1 knockdown in prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified POTEF-AS1 is an androgen-regulated non-coding RNA gene.

Publication Title

Androgen-induced lncRNA POTEF-AS1 regulates apoptosis-related pathway to facilitate cell survival in prostate cancer cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE33070
Adipose tissue gene expression associated with weight gain in kidney transplant recipients
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The aim of this study was to investigate the association of gene expression profiles in subcutaneous adipose tissue with percent of total body weight change in 26 kidney transplant recipients.

Publication Title

Expression levels of obesity-related genes are associated with weight change in kidney transplant recipients.

Sample Metadata Fields

Sex, Race

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accession-icon GSE58309
The role of AR-associated factors in androgen signaling
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified androgen-regulated genes, CTBP2, FOXP1 and RUNX1. These factors interact with AR ligand dependently.

Publication Title

CtBP2 modulates the androgen receptor to promote prostate cancer progression.

Sample Metadata Fields

Cell line, Treatment

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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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