publication_authors:Lucas DM Results

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Microarray (43)

Rna-seq (4)

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Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (43)

Illumina HiSeq 2000 (4)

Includes Publication (4)

GSE16381

Cytoprotective Nrf2 pathway is induced in chronically Txnrd1-deficient hepatocytes

Mus musculus
8 Downloadable Samples

Description

Metabolically active cells require robust mechanisms to combat oxidative stress. The cytoplasmic thioredoxin reductase/thioredoxin (Txnrd1/Txn1) system maintains reduced protein dithiols and provides electrons to some cellular reductases, including peroxiredoxins.

Publication Title

Cytoprotective Nrf2 pathway is induced in chronically txnrd 1-deficient hepatocytes.

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GSE25100

Expression data from CD19-positive splenic B cells isolated from 1-month old ID4+/-TCL1-tg and ID4+/+TCL1-tg mice

Mus musculus
5 Downloadable Samples

Description

The function of ID4 in CLL development was studied in vivo using TCL1 transgenic mouse model that develop leukemia similar to human CLL. TCL1 mice with ID4 single knockout gene have accelerated CLL progression.

Publication Title

Silencing of the inhibitor of DNA binding protein 4 (ID4) contributes to the pathogenesis of mouse and human CLL.

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GSE41706

Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

Mus musculus
6 Downloadable Samples

Description

G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age.

Publication Title

Downregulation of G protein-coupled receptor kinase 2 levels enhances cardiac insulin sensitivity and switches on cardioprotective gene expression patterns.

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SRP346110

Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy

Mus musculus
4 Downloadable Samples
Illumina HiSeq 2000

Description

Autophagy selectively degrades aggregation-prone misfolded proteins caused by defective cellular proteostasis. However, the complexity of autophagy may prevent the full appreciation of how its modulation could be used as a therapeutic strategy in disease management. Here we define a molecular pathway through which recombinant interleukin-1 receptor antagonist (IL-1Ra, anakinra) affects cellular proteostasis independently from the IL-1 receptor (IL-1R1). Anakinra promoted H2O2-driven autophagy through a xenobiotic sensing pathway involving the aryl hydrocarbon receptor that, activated through the indoleamine 2,3-dioxygenase 1-kynurenine pathway, transcriptionally activates NADPH Oxidase 4 independent of the IL-1R1. By coupling the mitochondrial redox balance to autophagy, anakinra improved the dysregulated proteostasis network in murine and human cystic fibrosis. We anticipate that anakinra may represent a therapeutic option in addition to its IL-1R1 dependent anti-inflammatory properties by acting at the intersection of mitochondrial oxidative stress and autophagy with the capacity to restore conditions in which defective proteostasis leads to human disease. Overall design: mRNA profiles of alveolar macrophages purified from C57BL/6 and Il1r1-/- mice treated or not with Anakinra

Publication Title

Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy.

Sample Metadata Fields

Specimen part, Genotype, Subject

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GSE29648

The impact of a phytoestrogen-rich diet on cardiac gene expression in the context of HCM

Mus musculus
10 Downloadable Samples

Description

A soy diet worsens the progression of an inherited form of hypertrophic cardiomyopathy (HCM) in male mice when compared to casein-fed mice. Females are largely resistant to this diet effect and better preserve cardiac function. We hypothesized that the abundant phytoestrogens found in soy are mainly responsible for this diet-dependent phenotype. Indeed, feeding male mice a phytoestrogen-supplemented casein-based diet can recapitulate the negative outcome seen when male mice are fed a standard soy-based diet.