The Ca2+/calmodulin-dependent kinase II is expressed in smooth muscle and believed to mediate intracellular calcium handling and calcium-dependent gene transcription. CaMKII is activated by Angiotensin-II.
Calcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function.
Specimen part, Treatment
View SamplesThe brain renin-angiotensin system (RAS) stimulates resting metabolic rate in part through a mechanism involving suppression of the circulating RAS. This effect appears to be mediated through a reduction in angiotensin AT2 receptor (AT2R) signaling within inguinal fat. To examine the molecular mechanisms underlying this effect, mice with hyperactivity of the brain RAS (“sRA” mice, expressing human renin via the synapsin promoter and human angiotensinogen via its own promoter) and littermate controls were chronically infused with vehicle or the AT2R specific agonist, CGP-42112a (CGP, 90 ng/hr, 8 wk, sc). To identify altered signaling pathways, total RNA was isolated from inguinal adipose tissue and transcript abundance was quantitated by RNA-Seq. Overall design: Four groups of mice were studied: controls receiving either a saline infusion (CON) or a specific angiotensin type 2 receptor agonist (CON_CGP), transgenic mice with specific activation of the brain renin-angiotensin receiving either a saline infusion (SRA) or a specific angiotensin type 2 receptor agonist (SRA_CGP). A sample size of N=3-4 was used for each of the four groups.
Suppression of Resting Metabolism by the Angiotensin AT2 Receptor.
Sex, Specimen part, Cell line, Subject
View SamplesAnalysis of gene expression profile in peritoneal macrophage extracted from LPS or PBS challenged DUSP3-/- and WT mice. DUSP3 deletion protects mice from sepsis and endotoxemia. We performed a microarray analysis to get insights into the differentially regulated pathways between WT and KO under inflammatory conditions.
DUSP3 Genetic Deletion Confers M2-like Macrophage-Dependent Tolerance to Septic Shock.
Sex, Age, Specimen part
View SamplesInformed by the genetic alterations observed in human GBM, we engineered a novel, lentiviral injection mediated, mouse model of proneural GBM.
A recombinant lentiviral PDGF-driven mouse model of proneural glioblastoma.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Specimen part, Treatment
View SamplesIdentification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma.
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Specimen part, Treatment
View SamplesIdentification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma.
PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-Mediated Survival of Proneural Glioma Cells.
Specimen part
View SamplesSpleen conventional dendritic cells from NOD mice show a lower overall response to CpG-A compared to B6 cDCs.
Despite Increased Type 1 IFN, Autoimmune Nonobese Diabetic Mice Display Impaired Dendritic Cell Response to CpG and Decreased Nuclear Localization of IFN-Activated STAT1.
Sex, Specimen part
View SamplesEffect of injury and Pseudomonas aeruginosa inoculation in Drosophila melanogaster
Involvement of skeletal muscle gene regulatory network in susceptibility to wound infection following trauma.
Sex, Time
View SamplesThe Pseudomonas aeruginosa MvfR-dependent QS regulatory pathway controls the expression of key virulence genes; and is activated via the extracellular signals 4-hydroxy-2-heptylquinoline (HHQ) and 3,4-dihydroxy-2-heptylquinoline (PQS), whose syntheses depend on anthranilic acid (AA), the primary precursor of 4-hydroxy-2-alkylquinolines (HAQs). We identified halogenated AA analogs that specifically inhibited HAQ biosynthesis and disrupted MvfR-dependent gene expression. These compounds restricted P. aeruginosa systemic dissemination and mortality in mice, without perturbing bacterial viability, and inhibited osmoprotection, a widespread bacterial function.
Inhibitors of pathogen intercellular signals as selective anti-infective compounds.
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