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accession-icon GSE71084
Fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation
  • organism-icon Mus musculus, Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE71083
Fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation [Rn]
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Determination of the mechanism by which fibrinogen, a central blood coagulation protein drives immunological responses targeted to the CNS. Results identify the factors involved in the regulation and provide mechanistic basis.

Publication Title

Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE71082
Fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation [Mm]
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Determination of the mechanism by which fibrinogen, a central blood coagulation protein drives immunological responses targeted to the CNS. Results identify the factors involved in the regulation and provide mechanistic basis.

Publication Title

Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE104448
Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_12h_Fibrinogen]
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Determination of the mechanism by which fibrinogen, a central blood coagulation protein, regulates OPC functions and remyelination in the CNS.

Publication Title

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE104449
Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage [Rat_OPC_48h_Fibrinogen]
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Determination of the mechanism by which fibrinogen, a central blood coagulation protein, regulates OPC functions and remyelination in the CNS.

Publication Title

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE104450
Fibrinogen activates BMP signaling in oligodendrocyte progenitor cells (OPCs) and inhibits remyelination after vascular damage
  • organism-icon Rattus norvegicus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Fibrinogen Activates BMP Signaling in Oligodendrocyte Progenitor Cells and Inhibits Remyelination after Vascular Damage.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE94589
Gene Expression In Drosophila Hearts Harboring Ion Channel Mutations
  • organism-icon Drosophila melanogaster
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Age-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations

Publication Title

Age-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE52334
Comparative transcriptome analysis of DFAT cells after the treatment with Y-27632 and the transfection of Mkl1 siRNA
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Cellular differentiation is regulated through activation and repression of defined transcription factors. A hallmark of differentiation is a pronounced change in cell shape, which is determined by dynamics of the actin cytoskeleton. In de-differentiated fat (DFAT) cells and 3T3-L1 cells, we showed that treatment with the ROCK inhibitor Y-27632, by inducing remodeling of the actin cytoskelton, causes adipocyte differentiation. In addition, we found that depletion of MKL1, an actin binding transcriptional coactivator, elicits adipogenesis.

Publication Title

Regulation of MKL1 via actin cytoskeleton dynamics drives adipocyte differentiation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE60436
Gene Expression Profile of Fibrovascular Membrane Associated with Proliferative Diabetic Retinopathy
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

Proliferative diabetic retinopathy (PDR) is a vision-threatening disorder characterized by the formation of cicatricial fibrovascular membranes leading to traction retinal detachment. Despite the recent advance in the treatment of PDR such as vitreoretinal surgery with use of anti-vascular endothelial growth factor (VEGF) drug as an adjunct, it still remains vision-threatening disease.

Publication Title

Microarray analysis of gene expression in fibrovascular membranes excised from patients with proliferative diabetic retinopathy.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon SRP084383
Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development [RNAseq]
  • organism-icon Rattus norvegicus
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes. The secretions and plasma contained altered microRNAs whose targets were linked with changes in gene expression in the fetal brain and with human schizophrenia loci. Molecular and morphological changes in vivo and in vitro were prevented by a single dose of MitoQ bound to nanoparticles, which were shown to localise and prevent oxidative stress in the placenta but not in the fetus. We suggest the possibility of developing preventative treatments that target the placenta and not the fetus to reduce risk of psychiatric disease in later life. Overall design: 16 samples (4 biological replicates per group) were analysed using RNA sequencing. The 4 groups were: Normoxia+Saline (control sample), Normoxia+MitoQ-NP, Hypoxia+Saline and Hypoxia+MitoQ-NPs. Pair-wise comparison between all groups was performed.

Publication Title

Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development.

Sample Metadata Fields

No sample metadata fields

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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