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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 SRP157936
Transcriptomic analysis of T84 colon carcinoma cell line treated with trametinib, JQ1 or their combination
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

T84 cells were treated with DMSO, 30nM trametinib (MEKi), 1µM JQ1 (BRD4i) or the combination of trametinib and JQ1 (combo) for 24h. Overall design: 3 replicates per condition were analyzed by RNA-seq.

Publication Title

Suppression of interferon gene expression overcomes resistance to MEK inhibition in KRAS-mutant colorectal cancer.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP157753
Transcriptomic analysis of trametinib-resistant HCT116 colorectal carcinoma cells compared to the parental control cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

HCT116 cells were treated with with increasing concentrations of trametinib over 2 months. Drug-resistant clones emerged and were cultured in the presence of 30 nmol/L trametinib. These cells exhibited a greater than 10-fold increase in the GI50 for trametinib compared to the parental cell line. RNA-seq of the resistant clone HCT116_R4 versus the parental cells identified differentially expressed genes potentially involved in resistance. Overall design: For the parental and resistant clone, 3 replicates each were analysed by RNA-seq.

Publication Title

Suppression of interferon gene expression overcomes resistance to MEK inhibition in KRAS-mutant colorectal cancer.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP127325
Patient-derived organoids (PDOs) model treatment response of metastatic gastrointestinal cancers.
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We report RNAseq data from subsequent passages of five organoid cultures. Overall design: RNA extracted from subsequent PDO passages was subjected to RNAseq.

Publication Title

Patient-derived organoids model treatment response of metastatic gastrointestinal cancers.

Sample Metadata Fields

Disease, Subject

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accession-icon GSE22925
Murine Bone Marrow Stromal Cell Response to Granulocyte Colony-Stimulating Factor
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Neutrophil homeostasis is maintained, in part, by the regulated release of neutrophils from the bone marrow. Constitutive expression of the chemokine CXCL12 by bone marrow stromal cells provides a key retention signal for neutrophils in the bone marrow through activation of its receptor CXCR4. Herein, we show that the ELR chemokines CXCL1 and CXCL2 are constitutively expressed by bone marrow endothelial cells and osteoblasts, and CXCL2 expression is induced in endothelial cells during granulocyte colony-stimulating factor (G-CSF)-induced neutrophil mobilization. Neutrophils lacking CXCR2, the receptor for CXCL1 and CXCL2, are preferentially retained in the bone marrow, reproducing a myelokathexis phenotype. Transient disruption of CXCR4 failed to mobilize CXCR2 neutrophils. However, doubly deficient neutrophils (CXCR2-/- CXCR4-/-) displayed constitutive mobilization, showing that CXCR4 plays a dominant role. Collectively, these data suggest that CXCR2 signaling is a second chemokine axis that interacts antagonistically with CXCR4 to regulate neutrophil release from the bone marrow.

Publication Title

CXCR2 and CXCR4 antagonistically regulate neutrophil trafficking from murine bone marrow.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE17089
Identification of direct transcriptional targets of V600EBRAF/MEK in melanoma
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

A375P melanoma cells were treated with 1uM of the MEK inhibitor PD184352 or 0.4uM of the V600EBRAF inhibitor PLX4720 for 2hr, 6hr and 24hrs.

Publication Title

Identification of direct transcriptional targets of (V600E)BRAF/MEK signalling in melanoma.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon SRP113332
Exome sequencing analysis of murine medulloblastoma models identifies Wdr11 as a potential tumor suppressor in Group 3 tumors
  • organism-icon Mus musculus
  • sample-icon 49 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We previoiusly identified WDR11 as a potential tumor suppressor in murine medulloblastoma models. To determine additional genes/pathways affected by WDR11 overexpression.To compare somatic mutations of murine models with human medulloblastoma (MB), we performed whole-exome sequencing of mouse tumors representing three distinct MB subgroups: Wnt, Sonic Hedgehog (Shh) and Group 3 (G3). 64 somatic mutations were identified and validated, including 40 predicted to cause amino acid changes. After filtering and cross-species analysis with 366 human MBs from four independent studies, human orthologs for 16 of the 40 mouse genes were found to harbor non-silent mutations in human MB. Loss-of-function Mll2 mutations detected in one mouse tumor were previously reported in 30 of 366 human MBs. In mice with G3 MB, one mouse that died at least 15 days earlier than the others had four novel candidate genes harboring non-silent somatic mutations, Lrfn2, Smyd1, Ubn2 and Wdr11. To test whether these genes had tumor suppressive activity, we constitutively overexpressed each wild type gene in murine G3 tumorspheres followed by intracranial implantation. Mice harboring mouse G3 MB overexpressing WDR11 showed extended survival compared to the other three genes. Genes in the KEGG WNT signaling pathway, including Ccnd1/2/3, Myc and Tcf7l1, were down-regulated in G3 MB tumorspheres overexpressing WDR11, consistent with reduced tumor progression. In conclusion, we demonstrated that common spontaneous mutations were shared between human and murine models of MB suggesting similar molecular mechanisms of tumorigenesis, and identified WDR11 as a protein with tumor suppressive activity in G3 MB. Overall design: Compare differentially expressed genes in WDR11 overexpression group versus control group.

Publication Title

Exome sequencing analysis of murine medulloblastoma models identifies WDR11 as a potential tumor suppressor in Group 3 tumors.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP108574
RNASeq to identify the in vivo mechanism of anti-Ox40 mAb treatment exacerbated lupus in NZB/W F1 Mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We''ve recently shown that we can accelerate disease in a model of SLE (the NZB/W F1 model) using an anti-Ox40 mAb treatment regimen. The disease acceleration is rapid (within 2 weeks) but its unclear, mechanistically, how OX40 functions to promote disease. To that end we want to perform RNASeq on the sorted OX40-expressing CD4 T cells during treatment to understand how they function in response to OX40 signaling in vivo Overall design: RNASeq was performed on FACS sorted CD4 T cells from the spleen and kidney of NZB/W F1 lupus mice following anti-Ox40 agonist mAb treatment and disease acceleration

Publication Title

The Ox40/Ox40 Ligand Pathway Promotes Pathogenic Th Cell Responses, Plasmablast Accumulation, and Lupus Nephritis in NZB/W F1 Mice.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP108573
RNASeq to identify the in vitro molecular signature of Ox40 signaling in conjunction with TCR signaling in CD4 T cells from NZB/W F1 Mice
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We''ve recently shown that we can accelerate disease in a model of SLE (the NZB/W F1 model) using an anti-Ox40 mAb treatment regimen. The disease acceleration is rapid (within 2 weeks) but its unclear, mechanistically, how Ox40 promotes disease. To that end we performed RNASeq on in vitro cultured CD4 T cells during Ox40 and TCR stimulation (in a reductionist setting) to understand how Ox40 signaling impacts cellular phenotype and function, including with and without TCR stimulation Overall design: RNASeq was performed on in vitro cultured CD4 T cells from the spleen of NZB/W F1 lupus prone mice, following anti-Ox40 mAb and anti-CD3/CD28 bead stimulation

Publication Title

The Ox40/Ox40 Ligand Pathway Promotes Pathogenic Th Cell Responses, Plasmablast Accumulation, and Lupus Nephritis in NZB/W F1 Mice.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE11303
Transcriptional responses of Escherichia coli k12 TPEN
  • organism-icon Escherichia coli
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

DNA microarrays were conducted on E. coli K12 cells stressed with 10 M in N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN). Overall, 260 genes varied in expression, 114 up-regulated and 146 down-regulated by Zn deprivation

Publication Title

Characterization of Zn(II)-responsive ribosomal proteins YkgM and L31 in E. coli.

Sample Metadata Fields

No sample metadata fields

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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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