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accession-icon GSE22971
Expression data from MMP-8 wild type and KO mice with or without arthritis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Rheumatoid arthritis is an autoimmune disease in which joint inflammation lead to progressive cartilage and bone destruction. Matrix metalloproteinases (MMP) implicated in homeostasis of extracellular matrix (ECM) play a central role in cartilage degradation. The aim of this study was to investigate the role of MMP-8 (collagenase-2) suppression in the K/BxN serum-transfer arthritis model.

Publication Title

Matrix metalloproteinase-8 deficiency increases joint inflammation and bone erosion in the K/BxN serum-transfer arthritis model.

Sample Metadata Fields

Specimen part

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accession-icon GSE51044
Gamma-secretase inhibitor plus fludarabine in CLL
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Combination of GSI with fludarabine has a synergistic antileukemic effect in primary NOTCH1-mutated CLL cells

Publication Title

The γ-secretase inhibitor PF-03084014 combined with fludarabine antagonizes migration, invasion and angiogenesis in NOTCH1-mutated CLL cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE32609
Transcriptional profiling of liver samples from Lmna Gly609Gly knock-in mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. We report herein a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. By using this animal model, we have developed an antisense morpholinobased therapy that prevents the pathogenic Lmna splicing, dramatically reducing the accumulation of progerin and its associated nuclear defects. Treatment of mutant mice with these morpholinos led to a marked amelioration of their progeroid phenotype and substantially extended their life span, supporting the effectiveness of antisense oligonucleotidebased therapies for treating human diseases of accelerated aging.

Publication Title

Splicing-directed therapy in a new mouse model of human accelerated aging.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP131004
RNA-Seq in human T-cell lymphoblastic lymphoma samples and control thymuses
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Precursor T-cell lymphoblastic neoplasms are aggressive haematological neoplasm that most often manifest with extensive marrow and blood affectation (T-cell acute lymphoblastic leukaemia or T-ALL) or less commonly as a thymic mass with limited bone marrow infiltration (T-cell lymphoblastic lymphoma or T-LBL). Here we show data from RNA-Seq in a sample series of T-LBL from Spanish patients.The goal was to determine the levels of expression of coding genes and microRNAs, and to identify all genetic variants including SNVs, indels, and fusion transcripts. Overall design: Expression data were determined by comparson of each tumour sample with two control thymuses (404 and 405). Genetic variants were determined by comparison of tumour sequences with canonical ENSEMBL normal-references of each gene.

Publication Title

RNA-Seq reveals the existence of a CDKN1C-E2F1-TP53 axis that is altered in human T-cell lymphoblastic lymphomas.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE44272
The Long-HER Study
  • organism-icon Homo sapiens
  • sample-icon 53 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Trastuzumab improves survival outcomes in patients with HER2+ metastatic breast cancer. Some of these patients may become long-term survivors. The Long-Her study was designed to identify clinical and molecular markers that could differentiate long-term survivors from patients having early progression to trastuzumab.

Publication Title

The Long-HER study: clinical and molecular analysis of patients with HER2+ advanced breast cancer who become long-term survivors with trastuzumab-based therapy.

Sample Metadata Fields

Age, Disease

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accession-icon GSE40529
Expression data from untreated and DSS-treated Adamts12 WT and KO mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Adamts12-deficient mice undergo more severe colitis than WT mice after induction with DSS.

Publication Title

ADAMTS-12 metalloprotease is necessary for normal inflammatory response.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE11632
Transcriptional profiling of Tmprss6-deficient mouse liver
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Matriptase-2 (Tmprss6), a recently described member of the TTSP family, is an essential regulator of iron homeostasis. Tmprss6-/- mice display an overt phenotype of alopecia and a severe iron deficiency anemia. These hematological alterations found in Tmprss6-/- mice are accompanied by a marked up-regulation of hepcidin, a negative regulator of iron export into plasma.

Publication Title

Membrane-bound serine protease matriptase-2 (Tmprss6) is an essential regulator of iron homeostasis.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE65173
NF-B activation impairs somatic cell reprogramming in ageing
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st), Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

NF-κB activation impairs somatic cell reprogramming in ageing.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE65172
NF-B activation impairs somatic cell reprogramming in ageing [MSCs]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Transcriptional profiling of human control and Nstor-Guillermo Progeria Syndrome (NGPS) mesenchymal stem cells (MSCs).

Publication Title

NF-κB activation impairs somatic cell reprogramming in ageing.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Treatment

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accession-icon GSE27525
Expression data from diet-induced obesity Oma1-deficient mice.
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Transriptional profiling of white adipose tissue extracted from obese mice.

Publication Title

Loss of mitochondrial protease OMA1 alters processing of the GTPase OPA1 and causes obesity and defective thermogenesis in mice.

Sample Metadata Fields

Age, 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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