Objective Previous studies showed that genetic deletion or pharmacological blockade of the Receptor for Advanced Glycation Endproducts (RAGE) prevents the early structural changes in the glomerulus associated with diabetic nephropathy (DN). To overcome limitations of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the contribution of RAGE to DN in the OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function.
Deletion of the receptor for advanced glycation end products reduces glomerulosclerosis and preserves renal function in the diabetic OVE26 mouse.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesQuaking are RNA binding proteins, which are known to regulate the expression of different genes at the post-transcriptional level. Genetic interference with quaking a (qkia) and quaking c (qkic) leads to major myofibril defects during zebrafish development, without affecting early muscle differentiation. In order to understand how qkia and qkic jointly regulate myofibril formation, we performed a comparative analysis of the transcriptome of qkia/qkic (qkia mutant injected with qkic morpholino) versus control embryos. We show that Quaking activity is required for accumulation of the muscle-specific tropomyosin 3 transcript, tpm3.1. Whereas interference with tmp3.1 function disrupts myofibril formation, reintroducing tpm3.1 transcripts into embryos with reduced Quaking activity can restore structured myofibrils. Thus, we identify tropomyosin as an essential component in the process of myofibril formation and as a relay downstream of the regulator proteins Quaking. Overall design: Transcriptome of control versus qkia/qkic embryos at 24-26hpf. Biological triplicate were prepared for both condition (3x2 samples).
Quaking RNA-Binding Proteins Control Early Myofibril Formation by Modulating Tropomyosin.
No sample metadata fields
View SamplesIn several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS.
Systems genetics of susceptibility to obesity-induced diabetes in mice.
Sex, Age
View SamplesImmunosurveillance of secondary lymphoid organs (SLO) is performed by central memory T cells that recirculate through blood. Resident memory T cells (TRM) remain parked in nonlymphoid tissues and often stably express CD69. We recently identified TRM within SLO, and this study addresses knowledge gaps in their origin and phenotype. Parabiosis of dirty mice revealed that CD69 expression is insufficient to infer stable residence. Using selective depletion strategies, parabiosis, imaging, tissue grafting, and photoactivatable T cells, we report that restimulation of TRM within the skin or mucosa results in a substantial increase in TRM that patrol all regions of draining lymph nodes. SLO TRM were derived from nonlymphoid tissue residents. Transcriptional profiling and flow cytometry revealed a refined phenotype shared between both nonlymphoid and SLO TRM. These data demonstrate the nonlymphoid origin of SLO TRM and suggest vaccination strategies by which memory CD8 T cell immunosurveillance can be regionalized to specific lymph nodes.
T Cells in Nonlymphoid Tissues Give Rise to Lymph-Node-Resident Memory T Cells.
Specimen part
View SamplesTo investigate the role of YAP/TAZ as factors able to convert differentiated cells into stem cells of the same tissue, we compared the expression profiles of mammary organoids (yOrg) obtained by doxycycline-inducible expression of YAP in luminal differentiated mammary cells with original luminal differentiated mammary cells (Lum) and organoids from native mammary stem cells (Org).
Induction of Expandable Tissue-Specific Stem/Progenitor Cells through Transient Expression of YAP/TAZ.
Specimen part
View SamplesTranscriptome analysis comparing naive, protective and non-protective spleen memory CD8 T lymphocytes were conducted to identify key functions associated with memory CD8-mediated immune protection. Memory CD8 T cells generated in response to influenza or vaccinia infection (Flu-memory and VV-memory) were compared to inflammatory memory cells (TIM) that were generated by peptide in inflammatory context. Gene expression analysis was performed on quiescent and re-stimulated CD8 T cells.
Immune signatures of protective spleen memory CD8 T cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.
Specimen part
View SamplesThe effect of CTCFL mutation on the transcriptional program in testes
The male germ cell gene regulator CTCFL is functionally different from CTCF and binds CTCF-like consensus sites in a nucleosome composition-dependent manner.
Specimen part
View SamplesStem cell antigen-1 (Sca-1 or Ly6A) is a member of the Ly6 family of glycosyl phostidylinositol (GPI)-anchored cell surface proteins. To determine the potential mechanisms by which Sca-1 regulates cell migration, adhesion, and tumor development; we performed an Affymetrix mouse genome 430A 2.0 array on cDNA comparing shLuc and shSca-1 from cells grown in vitro.
Stem cell antigen-1 (sca-1) regulates mammary tumor development and cell migration.
Specimen part, Cell line
View SamplesExposure to PFOA during gestation altered the expression of genes related to fatty acid catabolism in both the fetal liver and lung. In the fetal liver, the effects of PFOA were robust and also included genes associated with lipid transport, ketogenesis, glucose metabolism, lipoprotein metabolism, cholesterol biosynthesis, steroid metabolism, bile acid biosynthesis, phospholipid metabolism, retinol metabolism, proteosome activation, and inflammation. These changes are consistent with activation of PPAR alpha. Non-PPAR alpha related changes were suggested as well.
Gene expression profiling in the lung and liver of PFOA-exposed mouse fetuses.
No sample metadata fields
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