Gene expression profiling in a mouse model for African trypanosomiasis

Kierstein, S.; Noyes, Harry; Naessens, Jan; Nakamura, Yoshio; Pritchard, Claire; Gibson, John P.; Kemp, Stephen J.; Brass, Andy

doi:10.1038/sj.gene.6364345

Cited by 20 publications

(20 citation statements)

References 39 publications

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“…Clone IL 1180 [81] was grown in sub-lethally irradiated Sprague–Dawley rats, and trypanosomes were isolated from infected rat blood by anion exchange column [82]. Mice were infected by intraperitoneal injection (1×10 4 parasites in 200 µl of phosphate-buffered saline (pH 8.0) containing 1.5% glucose).…”

Section: Methodsmentioning

confidence: 99%

Claudin 13, a Member of the Claudin Family Regulated in Mouse Stress Induced Erythropoiesis

et al. 2010

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Mammals are able to rapidly produce red blood cells in response to stress. The molecular pathways used in this process are important in understanding responses to anaemia in multiple biological settings. Here we characterise the novel gene Claudin 13 (Cldn13), a member of the Claudin family of tight junction proteins using RNA expression, microarray and phylogenetic analysis. We present evidence that Cldn13 appears to be co-ordinately regulated as part of a stress induced erythropoiesis pathway and is a mouse-specific gene mainly expressed in tissues associated with haematopoietic function. CLDN13 phylogenetically groups with its genomic neighbour CLDN4, a conserved tight junction protein with a putative role in epithelial to mesenchymal transition, suggesting a recent duplication event. Mechanisms of mammalian stress erythropoiesis are of importance in anaemic responses and expression microarray analyses demonstrate that Cldn13 is the most abundant Claudin in spleen from mice infected with Trypanosoma congolense. In mice prone to anaemia (C57BL/6), its expression is reduced compared to strains which display a less severe anaemic response (A/J and BALB/c) and is differentially regulated in spleen during disease progression. Genes clustering with Cldn13 on microarrays are key regulators of erythropoiesis (Tal1, Trim10, E2f2), erythrocyte membrane proteins (Rhd and Gypa), associated with red cell volume (Tmcc2) and indirectly associated with erythropoietic pathways (Cdca8, Cdkn2d, Cenpk). Relationships between genes appearing co-ordinately regulated with Cldn13 post-infection suggest new insights into the molecular regulation and pathways involved in stress induced erythropoiesis and suggest a novel, previously unreported role for claudins in correct cell polarisation and protein partitioning prior to erythroblast enucleation.

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Section: Methodsmentioning

confidence: 99%

Claudin 13, a Member of the Claudin Family Regulated in Mouse Stress Induced Erythropoiesis

et al. 2010

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“…ABHD1 mRNA levels are also regulated under several other conditions. For example, liver ABHD1 is upregulated in mice challenged with parasitic infection [6]. ABHD1 expression in mouse liver and small intestine is significantly down-regulated by transgenic activation of Notch signaling, which transcriptionally drives cell differentiation [7].…”

Section: Introductionmentioning

confidence: 99%

Mammalian alpha beta hydrolase domain (ABHD) proteins: Lipid metabolizing enzymes at the interface of cell signaling and energy metabolism

Lord

Thomas

Brown

2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

136

145

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Dysregulation of lipid metabolism underlies many chronic diseases such as obesity, diabetes, cardiovascular disease, and cancer. Therefore, understanding enzymatic mechanisms controlling lipid synthesis and degradation is imperative for successful drug discovery for these human diseases. Genes encoding α/β hydrolase fold domain (ABHD) proteins are present in virtually all reported genomes, and conserved structural motifs shared by these proteins predict common roles in lipid synthesis and degradation. However, the physiological substrates and products for these lipid metabolizing enzymes and their broader role in metabolic pathways remain largely uncharacterized. Recently, mutations in several members of the ABHD protein family have been implicated in inherited inborn errors of lipid metabolism. Furthermore, studies in cell and animal models have revealed important roles for ABHD proteins in lipid metabolism, lipid signal transduction, and metabolic disease. The purpose of this review is to provide a comprehensive summary surrounding the current state of knowledge regarding mammalian ABHD protein family members. In particular, we will discuss how ABHD proteins are ideally suited to act at the interface of lipid metabolism and signal transduction. Although, the current state of knowledge regarding mammalian ABHD proteins is still in its infancy, this review highlights the potential for the ABHD enzymes as being attractive targets for novel therapies targeting metabolic disease.

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“…Protection or susceptibility against cerebral malaria (50), susceptibility to multiple sclerosis (51), trypanosomaiasis (52), HIV (53), and hepatitis B and C virus (54,55) are influenced by IFNAR polymorphisms.…”

Section: Disease Associationsmentioning

confidence: 99%